Pub Date : 2024-01-01DOI: 10.1615/critrevimmunol.2024051340
Hao Yuan, Jing Tian, Lu Wen
Pneumonia is a common infection in elderly patients. We explored the correlations of serum interleukin-6 (IL-6) and ferritin (SF) levels with immune function/disease severity in elderly pneumonia patients. Study subjects included 151 pneumonia/58 healthy geriatrics, with their age/sex/body mass index (BMI)/disease course and severity/blood pressure/C-reactive protein (CRP)/procalcitonin (PCT)/smoking status documented. The disease severity was evaluated by pneumonia severity index (PSI). T helper 17 (Th17)/regulatory T (Treg) cell ratios and IL-6/SF/immunoglobulin G (IgG)/Th17 cytokine (IL-21)/Treg cytokine (IL-10) levels were assessed using flow cytometry/ELISA. The correlations between these indexes/independent risk factors in elderly patients with severe pneumonia were evaluated by Spearman/multivariate logistic regression analyses. Patients showed obvious differences in smoking and CRP/PCT levels. Pneumonia patients exhibited up-regulated Th17 cell ratio and serum IL-6/SF/IL-21/IL-10/IgG levels, down-regulated Treg cell ratio, and more evident differences were noted in severe cases. Serum IL-6/SF levels were positively correlated with disease severity, immune function, and IL-21/IL-10/IgG levels. Smoking history and IL-6/SF levels were identified as independent risk factors in severe pneumonia geriatrics. Collectively, serum IL-6 and SF levels in elderly pneumonia patients were conspicuously positively correlated with disease severity and IL-21/IL-10/IgG levels. CRP, PCT, IL-6, and SF levels were independent risk factors for severe pneumonia in elderly patients.
{"title":"Serum interleukin 6 and ferritin levels are the independent risk factors for pneumonia in elderly patients","authors":"Hao Yuan, Jing Tian, Lu Wen","doi":"10.1615/critrevimmunol.2024051340","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024051340","url":null,"abstract":"Pneumonia is a common infection in elderly patients. We explored the correlations of serum interleukin-6 (IL-6) and ferritin (SF) levels with immune function/disease severity in elderly pneumonia patients. Study subjects included 151 pneumonia/58 healthy geriatrics, with their age/sex/body mass index (BMI)/disease course and severity/blood pressure/C-reactive protein (CRP)/procalcitonin (PCT)/smoking status documented. The disease severity was evaluated by pneumonia severity index (PSI). T helper 17 (Th17)/regulatory T (Treg) cell ratios and IL-6/SF/immunoglobulin G (IgG)/Th17 cytokine (IL-21)/Treg cytokine (IL-10) levels were assessed using flow cytometry/ELISA. The correlations between these indexes/independent risk factors in elderly patients with severe pneumonia were evaluated by Spearman/multivariate logistic regression analyses. Patients showed obvious differences in smoking and CRP/PCT levels. Pneumonia patients exhibited up-regulated Th17 cell ratio and serum IL-6/SF/IL-21/IL-10/IgG levels, down-regulated Treg cell ratio, and more evident differences were noted in severe cases. Serum IL-6/SF levels were positively correlated with disease severity, immune function, and IL-21/IL-10/IgG levels. Smoking history and IL-6/SF levels were identified as independent risk factors in severe pneumonia geriatrics. Collectively, serum IL-6 and SF levels in elderly pneumonia patients were conspicuously positively correlated with disease severity and IL-21/IL-10/IgG levels. CRP, PCT, IL-6, and SF levels were independent risk factors for severe pneumonia in elderly patients.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"4 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139646859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1615/critrevimmunol.2024052462
Xiaoyu Qian, Lin Li, Liang Chen, Chao Shen, Jian Tang
Background: Thyroidectomy causes impaired blood supply to the parathyroid glands, which leads to hypoparathyroidism. Tanshinone IIA (Tan IIA) is helpful in blood activation and cardiovascular protection. Therefore, the efficacy of Tan IIA in improving hypoparathyroidism was explored in this study. Methods: New Zealand white rabbits were utilized to establish a unilateral parathyroid gland ischemia injury model. The model was created by selectively ligating the main blood supply vessel of one parathyroid gland, and the rabbits were then divided into three groups receiving 1, 5, and 10 mg/kg of Tan IIA. Serum calcium and parathyroid hormone (PTH) levels were measured using specialized assay kits. Immunohistochemistry was used to assess the microvessel density (MVD) in parathyroid glands. Western blotting (WB) was used to analyze protein expression related to the PI3K/AKT signaling pathway and the pathway-associated HIF-1α and VEGF. Moreover, MMP-2 and MMP-9 involved in angiogenesis were detected by WB. Results: Tan IIA treatment effectively restored serum calcium and PTH levels in a dose-dependent manner. Notably, MVD in the parathyroid glands increased significantly, especially at higher doses. The Tan IIA treatment also elevated the p-PI3K/PI3K and p-AKT/AKT ratios, indicating that the PI3K/AKT pathway was reactivated. Moreover, Tan IIA significantly restored the decreased expression levels of VEGF and HIF-1α caused by parathyroid surgery. Additionally, Tan IIA increased MMP-2 and MMP-9 levels. Conclusion: Tan IIA activates the PI3K/AKT pathway, promotes angiogenesis by modulating VEGF, HIF-1α, MMP-2, and MMP-9, thereby further enhancing MVD within the parathyroid glands. This study demonstrates that Tan IIA improved post-thyroidectomy hypoparathyroidism.
{"title":"Mechanistic Insights into Tanshinone IIA in the Amelioration of Post-Thyroidectomy Hypoparathyroidism","authors":"Xiaoyu Qian, Lin Li, Liang Chen, Chao Shen, Jian Tang","doi":"10.1615/critrevimmunol.2024052462","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024052462","url":null,"abstract":"<b>Background:</b> Thyroidectomy causes impaired blood supply to the parathyroid glands, which leads to hypoparathyroidism. Tanshinone IIA (Tan IIA) is helpful in blood activation and cardiovascular protection. Therefore, the efficacy of Tan IIA in improving hypoparathyroidism was explored in this study.<br/>\u0000<b>Methods:</b> New Zealand white rabbits were utilized to establish a unilateral parathyroid gland ischemia injury model. The model was created by selectively ligating the main blood supply vessel of one parathyroid gland, and the rabbits were then divided into three groups receiving 1, 5, and 10 mg/kg of Tan IIA. Serum calcium and parathyroid hormone (PTH) levels were measured using specialized assay kits. Immunohistochemistry was used to assess the microvessel density (MVD) in parathyroid glands. Western blotting (WB) was used to analyze protein expression related to the PI3K/AKT signaling pathway and the pathway-associated HIF-1α and VEGF. Moreover, MMP-2 and MMP-9 involved in angiogenesis were detected by WB.<br/>\u0000<b>Results: </b>Tan IIA treatment effectively restored serum calcium and PTH levels in a dose-dependent manner. Notably, MVD in the parathyroid glands increased significantly, especially at higher doses. The Tan IIA treatment also elevated the p-PI3K/PI3K and p-AKT/AKT ratios, indicating that the PI3K/AKT pathway was reactivated. Moreover, Tan IIA significantly restored the decreased expression levels of VEGF and HIF-1α caused by parathyroid surgery. Additionally, Tan IIA increased MMP-2 and MMP-9 levels.<br/>\u0000<b>Conclusion: </b>Tan IIA activates the PI3K/AKT pathway, promotes angiogenesis by modulating VEGF, HIF-1α, MMP-2, and MMP-9, thereby further enhancing MVD within the parathyroid glands. This study demonstrates that Tan IIA improved post-thyroidectomy hypoparathyroidism.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"55 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140603029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1615/critrevimmunol.2024050754
Rongjin Zhou, Junguo Wang
We aimed to identify an effective metabolic subtype and risk score to predict survival and immunotherapy response in head and neck squamous cell carcinoma (HNSCC). Data were obtained from an online database. We screened significant prognostic metabolism-related genes between the normal and tumor groups using a series of bioinformatics methods. Based on the selected prognostic genes, we conducted a subtype analysis to identify significantly different subtypes in HNSCC. We then investigated survival, immune features, and hallmark differences among different subtypes. LASSO was utilized to identify optimal genes for the risk score model construction. Finally, distribution of the risk score samples was analyzed for different subtypes. A total of 32 significantly prognostic metabolism-related genes were screened, and all samples were grouped into two subtypes: cluster 1 and cluster 2. Cluster 1 had worse survival. Different immune cell infiltration (CD8 T cells, macrophages, and regulatory T cells) and immune checkpoint gene expression (PD-1 and CLAT-4) were observed between the two clusters. Twelve optimal genes were involved in risk score model, and high-risk group had poorer survival. Cluster 1 contained more high-risk samples (60%). Finally, four genes CAV1, GGT6, PYGL, and HS3ST1 were identified as significantly related to immune cells, and these genes were differentially expressed in the normal oral epithelial cells and HNSCC cells. The subtypes and risk score model in the study provide a promising biomarker for prognosis and immunotherapy response.
{"title":"Identification of Metabolism-Related Prognostic Biomarkers and Immune Features of Head and Neck Squamous Cell Carcinoma","authors":"Rongjin Zhou, Junguo Wang","doi":"10.1615/critrevimmunol.2024050754","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024050754","url":null,"abstract":"We aimed to identify an effective metabolic subtype and risk score to predict survival and immunotherapy response in head and neck squamous cell carcinoma (HNSCC). Data were obtained from an online database. We screened significant prognostic metabolism-related genes between the normal and tumor groups using a series of bioinformatics methods. Based on the selected prognostic genes, we conducted a subtype analysis to identify significantly different subtypes in HNSCC. We then investigated survival, immune features, and hallmark differences among different subtypes. LASSO was utilized to identify optimal genes for the risk score model construction. Finally, distribution of the risk score samples was analyzed for different subtypes. A total of 32 significantly prognostic metabolism-related genes were screened, and all samples were grouped into two subtypes: cluster 1 and cluster 2. Cluster 1 had worse survival. Different immune cell infiltration (CD8 T cells, macrophages, and regulatory T cells) and immune checkpoint gene expression (PD-1 and CLAT-4) were observed between the two clusters. Twelve optimal genes were involved in risk score model, and high-risk group had poorer survival. Cluster 1 contained more high-risk samples (60%). Finally, four genes CAV1, GGT6, PYGL, and HS3ST1 were identified as significantly related to immune cells, and these genes were differentially expressed in the normal oral epithelial cells and HNSCC cells. The subtypes and risk score model in the study provide a promising biomarker for prognosis and immunotherapy response.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"40 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139461538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1615/critrevimmunol.2024051294
Huifei Lu, Fei He, Ying Huang, Zhongliang Wei
Postoperative sleep disturbance is a common issue that affects recovery in patients undergoing general anesthesia. Dexmedetomidine (Dex) has a potential role in improving postoperative sleep quality. Thus, we evaluated the effects of different doses of Dex on postoperative sleep disturbance and serum neurotransmitters in patients undergoing radical gastrectomy under general anesthesia. Patients were assigned to the control, NS, and Dex (Dex-L/M/H) groups based on different treatment doses [0.2, 0.4, 0.6 μg/(kg·h)]. The Athens Insomnia Scale (AIS) and ELISA kits were used to assess sleep disturbance and serum neurotransmitter (GABA, 5-HT, NE) levels before surgery and on postoperative days 1/4/7. The effects of different doses of Dex on postoperative sleep disturbance incidence and serum neurotransmitter levels were analyzed by Fisher exact test, one-way and repeated measures ANOVA. Patients had no differences in gender, age, body mass index, operation time, and bleeding volume. Different doses of Dex reduced the postoperative AIS score of patients under general anesthesia, improved their sleep, and increased serum levels of 5-HT, NE, and GABA. Furthermore, the effects were dose-dependent within the range of safe clinical use doses. Specifically, Dex at doses of 0.2, 0.4, 0.6 μg/(kg·h) reduced postoperative AIS score, elevated serum neurotransmitter levels, and reduced postoperative sleep disturbance incidence. Collectively, Dex has a potential preventive effect on postoperative sleep disturbance in patients undergoing general anesthesia for radical gastrectomy. The optimal dose of Dex is between 0.2 and 0.6 μg/(kg·h), which significantly reduces the incidence of pos
{"title":"Effects of different doses of dexmedetomidine on the prevention of postoperative sleep disturbance and serum neurotransmitter level in patients under general anesthesia","authors":"Huifei Lu, Fei He, Ying Huang, Zhongliang Wei","doi":"10.1615/critrevimmunol.2024051294","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024051294","url":null,"abstract":"Postoperative sleep disturbance is a common issue that affects recovery in patients undergoing general anesthesia. Dexmedetomidine (Dex) has a potential role in improving postoperative sleep quality. Thus, we evaluated the effects of different doses of Dex on postoperative sleep disturbance and serum neurotransmitters in patients undergoing radical gastrectomy under general anesthesia. Patients were assigned to the control, NS, and Dex (Dex-L/M/H) groups based on different treatment doses [0.2, 0.4, 0.6 μg/(kg·h)]. The Athens Insomnia Scale (AIS) and ELISA kits were used to assess sleep disturbance and serum neurotransmitter (GABA, 5-HT, NE) levels before surgery and on postoperative days 1/4/7. The effects of different doses of Dex on postoperative sleep disturbance incidence and serum neurotransmitter levels were analyzed by Fisher exact test, one-way and repeated measures ANOVA. Patients had no differences in gender, age, body mass index, operation time, and bleeding volume. Different doses of Dex reduced the postoperative AIS score of patients under general anesthesia, improved their sleep, and increased serum levels of 5-HT, NE, and GABA. Furthermore, the effects were dose-dependent within the range of safe clinical use doses. Specifically, Dex at doses of 0.2, 0.4, 0.6 μg/(kg·h) reduced postoperative AIS score, elevated serum neurotransmitter levels, and reduced postoperative sleep disturbance incidence. Collectively, Dex has a potential preventive effect on postoperative sleep disturbance in patients undergoing general anesthesia for radical gastrectomy. The optimal dose of Dex is between 0.2 and 0.6 μg/(kg·h), which significantly reduces the incidence of pos","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"167 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139562237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1615/critrevimmunol.2024051292
Qiang Shao, Lin Sun
C1q/tumor necrosis factor-related protein 3 (CTRP3) has been demonstrated to play a protective role in mice with severe acute pancreatitis (SAP). However, its clinical significance in SAP remains unknown. This study was conducted to explore the clinical values of serum C1q/tumor necrosis factor-related protein 3 (CTRP3) level in the diagnosis of cardiac dysfunction (CD) and intestinal mucosal barrier dysfunction (IMBD) in SAP. Through RT-qPCR, we observed decreased CTRP3 level in the serum of SAP patients. Serum CTRP3 level was correlated with C-reactive protein, procalcitonin, creatine, modified computed tomography severity index score, and Acute Physiology and Chronic Health Evaluation II score. The receiver-operating characteristic curve revealed that CTRP3 serum level < 1.005 was conducive to SAP diagnosis with 72.55% sensitivity and 60.00% specificity, CTRP3 < 0.8400 was conducive to CD diagnosis with 80.49% sensitivity and specificity 65.57%, CTRP3 < 0.8900 was conducive to IMBD diagnosis with 94.87% sensitivity and 63.49% specificity, and CTRP3 < 0.6250 was conducive to the diagnosis of CD and IMBD co-existence with 65.22% sensitivity and 89.87% specificity. Generally, CTRP3 was downregulated in the serum of SAP patients and served as a candidate biomarker for the diagnosis of SAP and SAP-induced CD and IMBD.
C1q/ 肿瘤坏死因子相关蛋白 3（CTRP3）已被证实在重症急性胰腺炎（SAP）小鼠体内发挥保护作用。然而，其在 SAP 中的临床意义仍然未知。本研究旨在探讨血清 C1q/肿瘤坏死因子相关蛋白 3（CTRP3）水平在诊断 SAP 中心脏功能障碍（CD）和肠粘膜屏障功能障碍（IMBD）中的临床价值。通过 RT-qPCR，我们观察到 SAP 患者血清中 CTRP3 水平下降。血清 CTRP3 水平与 C 反应蛋白、降钙素原、肌酸、改良计算机断层扫描严重程度指数评分以及急性生理学和慢性健康评估 II 评分相关。接受者工作特征曲线显示，CTRP3 血清水平 < 1.005 有利于 SAP 诊断，灵敏度为 72.55%，特异度为 60.00%；CTRP3 < 0.8400 有利于 CD 诊断，灵敏度为 80.49%，特异度为 65.57%，CTRP3 <0.8900有利于IMBD诊断，灵敏度为94.87%，特异度为63.49%，CTRP3 <0.6250有利于CD和IMBD并存的诊断，灵敏度为65.22%，特异度为89.87%。总体而言，CTRP3在SAP患者血清中下调，可作为诊断SAP和SAP诱发的CD和IMBD的候选生物标志物。
{"title":"Clinical significance of serum CTRP3 level in the prediction of cardiac dysfunction and intestinal mucosal barrier dysfunction in patients with severe acute pancreatitis","authors":"Qiang Shao, Lin Sun","doi":"10.1615/critrevimmunol.2024051292","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024051292","url":null,"abstract":"C1q/tumor necrosis factor-related protein 3 (CTRP3) has been demonstrated to play a protective role in mice with severe acute pancreatitis (SAP). However, its clinical significance in SAP remains unknown. This study was conducted to explore the clinical values of serum C1q/tumor necrosis factor-related protein 3 (CTRP3) level in the diagnosis of cardiac dysfunction (CD) and intestinal mucosal barrier dysfunction (IMBD) in SAP. Through RT-qPCR, we observed decreased CTRP3 level in the serum of SAP patients. Serum CTRP3 level was correlated with C-reactive protein, procalcitonin, creatine, modified computed tomography severity index score, and Acute Physiology and Chronic Health Evaluation II score. The receiver-operating characteristic curve revealed that CTRP3 serum level < 1.005 was conducive to SAP diagnosis with 72.55% sensitivity and 60.00% specificity, CTRP3 < 0.8400 was conducive to CD diagnosis with 80.49% sensitivity and specificity 65.57%, CTRP3 < 0.8900 was conducive to IMBD diagnosis with 94.87% sensitivity and 63.49% specificity, and CTRP3 < 0.6250 was conducive to the diagnosis of CD and IMBD co-existence with 65.22% sensitivity and 89.87% specificity. Generally, CTRP3 was downregulated in the serum of SAP patients and served as a candidate biomarker for the diagnosis of SAP and SAP-induced CD and IMBD.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"9 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139586345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To explore the protective effect and mechanism of mild hypothermia on lung tissue damage after cardiopulmonary resuscitation in pigs. Methods: In this experiment, we electrically stimulated 16 pigs (30±2kg) for 10 minutes to cause ventricular fibrillation. The successfully resuscitated animals were randomly divided into two groups, a mild hypothermia group and a control group. We took arterial blood 0.5h, 1h, 3h and 6h after ROSC recovery in the two groups of animals for blood gas analysis. We observed the structural changes of lung tissue under an electron microscope and calculate the wet weight/dry weight (W/D) ratio. We quantitatively analyzed the expression differences of representative inflammatory factors (IL-6 and TNF-α) through the Elisa test. We detected the expression levels of Bax, Bcl-2 and Caspase-3 proteins in lung tissues by Western blot. Results: The 3 h and 6 h after spontaneous circulation was restored, compared with the control group, PaO2/FiO2 decreased significantly (P <0.05). In addition, the pathological changes, lung W/D and lung MDA of the mild hypothermia group were better than those of the control group. The levels of IL-6 and TNF-α in the lung tissue of the mild hypothermia group were significantly lower than those of the control group (P <0.05). The content of Caspase-3 and Bax in the mild hypothermia group was significantly lower than that of the control group. Conclusion: Our experiments have shown that mild hypothermia can reduce lung tissue damage after cardiopulmonary resuscitation.
{"title":"The protective effect and mechanism of mild hypothermia on pig lung injury after cardiopulmonary resuscitation","authors":"Jinlin Ren, Fangfang Zhu, Dongdong Sang, Mulin Cong, Shujuan Jiang","doi":"10.1615/critrevimmunol.2024052420","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024052420","url":null,"abstract":"Objective: To explore the protective effect and mechanism of mild hypothermia on lung tissue damage after cardiopulmonary resuscitation in pigs. Methods: In this experiment, we electrically stimulated 16 pigs (30±2kg) for 10 minutes to cause ventricular fibrillation. The successfully resuscitated animals were randomly divided into two groups, a mild hypothermia group and a control group. We took arterial blood 0.5h, 1h, 3h and 6h after ROSC recovery in the two groups of animals for blood gas analysis. We observed the structural changes of lung tissue under an electron microscope and calculate the wet weight/dry weight (W/D) ratio. We quantitatively analyzed the expression differences of representative inflammatory factors (IL-6 and TNF-α) through the Elisa test. We detected the expression levels of Bax, Bcl-2 and Caspase-3 proteins in lung tissues by Western blot. Results: The 3 h and 6 h after spontaneous circulation was restored, compared with the control group, PaO2/FiO2 decreased significantly (P <0.05). In addition, the pathological changes, lung W/D and lung MDA of the mild hypothermia group were better than those of the control group. The levels of IL-6 and TNF-α in the lung tissue of the mild hypothermia group were significantly lower than those of the control group (P <0.05). The content of Caspase-3 and Bax in the mild hypothermia group was significantly lower than that of the control group. Conclusion: Our experiments have shown that mild hypothermia can reduce lung tissue damage after cardiopulmonary resuscitation.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"172 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139585635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1615/critrevimmunol.2024051316
Kang Zhang, Xiaoqun Chen
Objective: Zilongjin (ZLJ) is a common Traditional Chinese medicine for lung adenocarcinoma (LUAD) treatment. However, its mechanisms of action remain to be elucidated. Network pharmacology was used to explore underlying mechanisms of ZLJ on LUAD. Methods: The disease-related targets were found out from the GeneCards and DisGeNET databases. Active compounds and targets of ZLJ were obtained from the HIT, TCMSP, and TCMID databases. Then, the protein-protein interaction (PPI) network was built by STRING database to identify core-hub targets of ZLJ in LUAD. Next, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were employed to analyze the enriched regulatory pathways of targets. Molecular docking analysis were used to evaluate interactions between potential targets and active compounds. Finally, qRT-PCR method was further to verify the results of network pharmacology. Results: A total of 124 LUAD-related targets of ZLJ and 5 active compounds of ZLJ from the relevant databases were screened out. Among these target proteins, JUN, CDH1, PPARG, and FOS were core-hub genes in PPI network. GO and KEGG pathway enrichment analysis indicated that these targets might regulate the PPAR signaling pathway in LUAD. JUN, PPARG, and FOS levels were upregulated, while CDH1 level was downregulated in LUAD cells. Conclusion: This study discerned that ZLJ may target genes such as JUN, FOS, PPARG, and CDH1 via the PPAR signaling pathway in LUAD, offering foundational insights for further exploration of ZLJ in clinical applications.
{"title":"Exploring mechanism of Zilongjin in treating lung adenocarcinoma based on network pharmacology combined with experimental verification","authors":"Kang Zhang, Xiaoqun Chen","doi":"10.1615/critrevimmunol.2024051316","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024051316","url":null,"abstract":"Objective: Zilongjin (ZLJ) is a common Traditional Chinese medicine for lung adenocarcinoma (LUAD) treatment. However, its mechanisms of action remain to be elucidated. Network pharmacology was used to explore underlying mechanisms of ZLJ on LUAD.\u0000Methods: The disease-related targets were found out from the GeneCards and DisGeNET databases. Active compounds and targets of ZLJ were obtained from the HIT, TCMSP, and TCMID databases. Then, the protein-protein interaction (PPI) network was built by STRING database to identify core-hub targets of ZLJ in LUAD. Next, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were employed to analyze the enriched regulatory pathways of targets. Molecular docking analysis were used to evaluate interactions between potential targets and active compounds. Finally, qRT-PCR method was further to verify the results of network pharmacology.\u0000Results: A total of 124 LUAD-related targets of ZLJ and 5 active compounds of ZLJ from the relevant databases were screened out. Among these target proteins, JUN, CDH1, PPARG, and FOS were core-hub genes in PPI network. GO and KEGG pathway enrichment analysis indicated that these targets might regulate the PPAR signaling pathway in LUAD. JUN, PPARG, and FOS levels were upregulated, while CDH1 level was downregulated in LUAD cells.\u0000Conclusion: This study discerned that ZLJ may target genes such as JUN, FOS, PPARG, and CDH1 via the PPAR signaling pathway in LUAD, offering foundational insights for further exploration of ZLJ in clinical applications.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"59 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139551724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-01DOI: 10.1615/critrevimmunol.2023050325
Nisar Shaikh, Xiao-Bing Zhang, Maisa Abdalla, David Baylink, Xiaolei Tang
Regulatory T (Treg) cells hold promise for the ultimate cure of immune-mediated diseases. However, how to effectively restore Treg function in patients remains unknown. Previous reports suggest that activated dendritic cells (DCs) de novo synthesize locally high concentrations of 1,25-dihydroxy vitamin D, i.e., the active vitamin D or 1,25(OH)2D by upregulating the expression of 25-hydroxy vitamin D 1α-hydroxylase. Although 1,25(OH)2D has been shown to induce Treg cells, DC-derived 1,25(OH)2D only serves as a checkpoint to ensure well-balanced immune responses. Our animal studies have shown that 1,25(OH)2D requires high concentrations to generate Treg cells, which can cause severe side effects. In addition, our animal studies have also demonstrated that dendritic cells (DCs) overexpressing the 1α-hydroxylase de novo synthesize the effective Treg-inducing 1,25(OH)2D concentrations without causing the primary side effect of hypercalcemia (i.e., high blood calcium levels). This study furthers our previous animal studies and explores the efficacy of the 1α-hydroxylase-overexpressing DCs in inducing human CD4+FOXP3+ regulatory T (Treg) cells. We discovered that the Treg-inducing doses of 1,25(OH)2D were within a range, not the higher, the better. Additionally, our data corroborated that the 1α-hydroxylase-overexpressing DCs synthesized 1,25(OH)2D within this concentration range in vivo, thus facilitating effective Treg cell induction. Moreover, this study demonstrated that α-hydroxylase expression levels were pivotal for DCs to induce Treg cells because physiological 25(OH)D levels were sufficient for the engineered but not parental DCs to enhance Treg cell induction. Int
调节性 T（Treg）细胞有望最终治愈免疫介导疾病。然而，如何有效恢复患者的 Treg 功能仍是未知数。以前的报告表明，活化的树突状细胞（DC）通过上调 25- 羟基维生素 D 1α- 羟化酶的表达，在局部从头合成高浓度的 1,25-二羟基维生素 D，即活性维生素 D 或 1,25(OH)2D。虽然 1,25（OH）2D 已被证明能诱导 Treg 细胞，但 DC 衍生的 1,25（OH）2D 只是确保免疫反应平衡的一个检查点。我们的动物实验表明，1,25(OH)2D 需要高浓度才能生成 Treg 细胞，而高浓度会导致严重的副作用。此外，我们的动物实验还证明，过表达 1α- 羟化酶的树突状细胞（DCs）能从头合成有效的 Treg 诱导浓度的 1,25（OH）2D，而不会引起高钙血症（即高血钙）这一主要副作用。这项研究进一步推进了我们之前的动物实验，并探索了1α-羟化酶外表达的DC在诱导人类CD4+FOXP3+调节性T（Treg）细胞方面的功效。我们发现，1,25(OH)2D的Treg诱导剂量在一定范围内，并非越高越好。此外，我们的数据还证实，1α-羟化酶脱表达的DC在体内合成的1,25（OH）2D也在这个浓度范围内，从而促进了Treg细胞的有效诱导。此外，这项研究还证明了α-羟化酶的表达水平是DC诱导Treg细胞的关键，因为生理25(OH)D水平足以使工程DC而非亲代DC增强Treg细胞诱导。中
{"title":"Enhancing Human Treg Cell Induction through Engineered Dendritic Cells and Zinc Supplementation","authors":"Nisar Shaikh, Xiao-Bing Zhang, Maisa Abdalla, David Baylink, Xiaolei Tang","doi":"10.1615/critrevimmunol.2023050325","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2023050325","url":null,"abstract":"Regulatory T (Treg) cells hold promise for the ultimate cure of immune-mediated diseases. However, how to effectively restore Treg function in patients remains unknown. Previous reports suggest that activated dendritic cells (DCs) de novo synthesize locally high concentrations of 1,25-dihydroxy vitamin D, i.e., the active vitamin D or 1,25(OH)2D by upregulating the expression of 25-hydroxy vitamin D 1α-hydroxylase. Although 1,25(OH)2D has been shown to induce Treg cells, DC-derived 1,25(OH)2D only serves as a checkpoint to ensure well-balanced immune responses. Our animal studies have shown that 1,25(OH)2D requires high concentrations to generate Treg cells, which can cause severe side effects. In addition, our animal studies have also demonstrated that dendritic cells (DCs) overexpressing the 1α-hydroxylase de novo synthesize the effective Treg-inducing 1,25(OH)2D concentrations without causing the primary side effect of hypercalcemia (i.e., high blood calcium levels). This study furthers our previous animal studies and explores the efficacy of the 1α-hydroxylase-overexpressing DCs in inducing human CD4+FOXP3+ regulatory T (Treg) cells. We discovered that the Treg-inducing doses of 1,25(OH)2D were within a range, not the higher, the better. Additionally, our data corroborated that the 1α-hydroxylase-overexpressing DCs synthesized 1,25(OH)2D within this concentration range in vivo, thus facilitating effective Treg cell induction. Moreover, this study demonstrated that α-hydroxylase expression levels were pivotal for DCs to induce Treg cells because physiological 25(OH)D levels were sufficient for the engineered but not parental DCs to enhance Treg cell induction. Int","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"1 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138548199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-01DOI: 10.1615/critrevimmunol.2023051651
Peng Wan, Xiang Tan, Mengting Sheng, Yan Xiang, Peng Wang, Min Yu
Background The present study investigated that the roles and mechanisms of platelet-derived exosomes in sepsis-induced acute renal injury. Methods The blood samples of septic patients and healthy controls were collected for clinical examination. The plasma level of miR-223-3p and NLRP3 mRNA were analyzed by qRT-PCR and the serum IL-1β and creatinine levels were quantified by ELISA(Enzyme-linked immunosorbent assay). C57BL/6 mice injected with LPS(lipopolysaccharide) were employed as the animal model for sepsis-induced acute renal injury. Human coronary artery endothelial cells(HCAECs) were treated with TNF-α as a cellular model for sepsis-induced endothelial damages. Results The number of PMP(platelet-derived microparticles) in patients with sepsis was increased. The level of miR-223-3p in the platelet exosomes isolated from the serum sample in patients with sepsis was significantly lower than that of the healthy controls. The level of miR-223-3p was also decreased in the platelet exosomes of mouse model with sepsis-induced acute renal injury. Downregulating miR-223-3p promoted sepsis-induced acute renal injury in mice model, while the administration of miR-223-3p reduced the inflammation in endothelial cells of sepsis-induced acute renal injury. NLRP3 (NLR Family Pyrin Domain Containing 3) was identified as one target of miR-223-3p in the platelet exosomes of sepsis-induced acute kidney injury. MiR-223-3p attenuated NLRP3-induced pyroptosis in endothelial cell model of sepsis-induced acute kidney injury. Conclusion In summary, platelet exosome-derived miR-223-3p regulates NLRP3 inflammasome and pyroptosis of endothelial cells in model of sepsis-induced acute renal
{"title":"Platelet exosome-derived miR-223-3p regulates pyroptosis in the cell model of sepsis-induced acute renal injury by targeting mediates NLRP3","authors":"Peng Wan, Xiang Tan, Mengting Sheng, Yan Xiang, Peng Wang, Min Yu","doi":"10.1615/critrevimmunol.2023051651","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2023051651","url":null,"abstract":"Background The present study investigated that the roles and mechanisms of platelet-derived exosomes in sepsis-induced acute renal injury.\u0000Methods The blood samples of septic patients and healthy controls were collected for clinical examination. The plasma level of miR-223-3p and NLRP3 mRNA were analyzed by qRT-PCR and the serum IL-1β and creatinine levels were quantified by ELISA(Enzyme-linked immunosorbent assay). C57BL/6 mice injected with LPS(lipopolysaccharide) were employed as the animal model for sepsis-induced acute renal injury. Human coronary artery endothelial cells(HCAECs) were treated with TNF-α as a cellular model for sepsis-induced endothelial damages.\u0000Results The number of PMP(platelet-derived microparticles) in patients with sepsis was increased. The level of miR-223-3p in the platelet exosomes isolated from the serum sample in patients with sepsis was significantly lower than that of the healthy controls. The level of miR-223-3p was also decreased in the platelet exosomes of mouse model with sepsis-induced acute renal injury. Downregulating miR-223-3p promoted sepsis-induced acute renal injury in mice model, while the administration of miR-223-3p reduced the inflammation in endothelial cells of sepsis-induced acute renal injury. NLRP3 (NLR Family Pyrin Domain Containing 3) was identified as one target of miR-223-3p in the platelet exosomes of sepsis-induced acute kidney injury. MiR-223-3p attenuated NLRP3-induced pyroptosis in endothelial cell model of sepsis-induced acute kidney injury.\u0000Conclusion In summary, platelet exosome-derived miR-223-3p regulates NLRP3 inflammasome and pyroptosis of endothelial cells in model of sepsis-induced acute renal","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"65 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138537044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-01DOI: 10.1615/critrevimmunol.2023050473
Jianye Yang, Wenbin Hu, Jiaming Zhao
Objective. Homeobox A1 (HOXA1) is a protein coding gene involved in regulating immunity signaling. This study aims to explore the function and mechanism of HOXA1 in asthma. Methods. An asthma mouse model was established via ovalbumin (OVA) induction. Airway hyperresponsiveness was evaluated by the value of pause enhancement (Penh). Inflammatory cells in bronchoalveolar lavage fluid (BALF) were detected by Trypan blue and Wright staining. The pathological morphology of lung tissues was assessed by H&E staining. The IgE and inflammatory biomarkers (IL-1β, IL-6, IL-17, and TNF-α) in BALF and lung tissues were measured by ELISA. Western blot was performed to detect the expression of NF-κB pathway-related proteins. Results. HOXA1 was down-regulated in OVA-induced asthmatic mice. Overexpression of HOXA1 decreased Penh and relieved pathological injury of lung tissues in OVA-induced mice. Overexpression of HOXA1 also reduced the numbers of total cells, leukocytes, eosinophils, neutrophils, macrophages, and lymphocytes, as well as the levels of IgE, IL-1β, IL-6, IL-17, and TNF-α in BALF of OVA-induced mice. The inflammatory biomarkers were also decreased in lung tissues by HOXA1 overexpression. In addition, HOXA1 overexpression blocked the NF-κB signaling pathway in OVA-induced mice. Conclusion. Overexpression of HOXA1 relieved OVA-induced asthma in female mice by blocking the NF-κB signaling pathway.
{"title":"Overexpression Of Homeobox A1 Relieves Ovalbumin-Induced Asthma In Mice By Inhibiting The Nf-Κb Signaling Pathway","authors":"Jianye Yang, Wenbin Hu, Jiaming Zhao","doi":"10.1615/critrevimmunol.2023050473","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2023050473","url":null,"abstract":"Objective. Homeobox A1 (HOXA1) is a protein coding gene involved in regulating immunity signaling. This study aims to explore the function and mechanism of HOXA1 in asthma.\u0000Methods. An asthma mouse model was established via ovalbumin (OVA) induction. Airway hyperresponsiveness was evaluated by the value of pause enhancement (Penh). Inflammatory cells in bronchoalveolar lavage fluid (BALF) were detected by Trypan blue and Wright staining. The pathological morphology of lung tissues was assessed by H&E staining. The IgE and inflammatory biomarkers (IL-1β, IL-6, IL-17, and TNF-α) in BALF and lung tissues were measured by ELISA. Western blot was performed to detect the expression of NF-κB pathway-related proteins.\u0000Results. HOXA1 was down-regulated in OVA-induced asthmatic mice. Overexpression of HOXA1 decreased Penh and relieved pathological injury of lung tissues in OVA-induced mice. Overexpression of HOXA1 also reduced the numbers of total cells, leukocytes, eosinophils, neutrophils, macrophages, and lymphocytes, as well as the levels of IgE, IL-1β, IL-6, IL-17, and TNF-α in BALF of OVA-induced mice. The inflammatory biomarkers were also decreased in lung tissues by HOXA1 overexpression. In addition, HOXA1 overexpression blocked the NF-κB signaling pathway in OVA-induced mice.\u0000Conclusion. Overexpression of HOXA1 relieved OVA-induced asthma in female mice by blocking the NF-κB signaling pathway.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"47 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138629136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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