Pub Date : 2023-01-05DOI: 10.1177/1721727x221149534
Leilei Tang, Lingdi Zhang, Xuan Mei, Jiawen Yu, Guojun Jiang
Acute Exacerbation Chronic Obstructive Pulmonary Disease (AECOPD) is associated with an acute worsening of respiratory symptoms that have effects on lung function, quality of life and health economic burden. In addition, the development of pulmonary infections is a common complication of Chronic Obstructive Pulmonary Disease (COPD). In the pathophysiology of AECOPD, interleukin (IL)-6 is a pleiotropic cytokine that can be produced by inflammatory and primary lung epithelial cells in response to a variety of different stimuli. We aim to investigate the correlation between serum cytokine levels and AECOPD with pulmonary infection. 37 AECOPD patients diagnosed with pulmonary infection and 33 patients diagnosed with AECOPD only were selected. All COPD patients were diagnosed according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria. Serum samples for C-reactive protein (CRP) and cytokines were obtained from the patients immediately after admission. Serum concentrations of cytokines were measured using a fluorescent bead immunoassay on a flow cytometer. Logistic regression was used to identify risk factors for AECOPD co-infection of the lungs. Serum characterization of our cohort showed patients with AECOPD and pulmonary infection had higher levels of IL-6 and IL-10 compared with the AECOPD group, and IL-6 was independently associated with AECOPD with pulmonary infection. ROC curve analysis showed that IL-6 was a useful predictor of the incidence of pulmonary infection in AECOPD patients. Our findings highlight the role of IL-6 in the pathogenesis of AECOPD with pulmonary infection.
{"title":"Pulmonary infection is associated with an increased IL-6 in acute exacerbation chronic obstructive pulmonary disease","authors":"Leilei Tang, Lingdi Zhang, Xuan Mei, Jiawen Yu, Guojun Jiang","doi":"10.1177/1721727x221149534","DOIUrl":"https://doi.org/10.1177/1721727x221149534","url":null,"abstract":"Acute Exacerbation Chronic Obstructive Pulmonary Disease (AECOPD) is associated with an acute worsening of respiratory symptoms that have effects on lung function, quality of life and health economic burden. In addition, the development of pulmonary infections is a common complication of Chronic Obstructive Pulmonary Disease (COPD). In the pathophysiology of AECOPD, interleukin (IL)-6 is a pleiotropic cytokine that can be produced by inflammatory and primary lung epithelial cells in response to a variety of different stimuli. We aim to investigate the correlation between serum cytokine levels and AECOPD with pulmonary infection. 37 AECOPD patients diagnosed with pulmonary infection and 33 patients diagnosed with AECOPD only were selected. All COPD patients were diagnosed according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria. Serum samples for C-reactive protein (CRP) and cytokines were obtained from the patients immediately after admission. Serum concentrations of cytokines were measured using a fluorescent bead immunoassay on a flow cytometer. Logistic regression was used to identify risk factors for AECOPD co-infection of the lungs. Serum characterization of our cohort showed patients with AECOPD and pulmonary infection had higher levels of IL-6 and IL-10 compared with the AECOPD group, and IL-6 was independently associated with AECOPD with pulmonary infection. ROC curve analysis showed that IL-6 was a useful predictor of the incidence of pulmonary infection in AECOPD patients. Our findings highlight the role of IL-6 in the pathogenesis of AECOPD with pulmonary infection.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41498952","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 : 2022-07-01DOI: 10.1177/1721727X221113399
Xiongying Zhang, Yalan Lai, Ling Guo
Objectives: Differential expression of microRNAs (miRNAs) has been confirmed to promote hypertrophic scar (HS) formation. However, this mechanism remains to be further elucidated. This paper investigated the effects of microRNA26a on HS of rabbit ears or its mechanism. Methods: The rabbit HS models were established and randomly assigned to either the experimental group (20 rabbits with treatment through triamcinolone acetonide) or the scar group (20 rabbits without treatment). In addition, 10 unmodeled rabbits were served as control group. The expression of microRNA-26a in HS tissues was detected via a stem-loop real-time polymerase chain reaction (RT-PCR). Results: According to RT-PCR, we showed the decreased expression of microRNA-26a in the scar group compared with that in the experimental group, and in the experimental group compared with that in the control group (p < .01). In addition, the expression of microRNA-26a was negatively correlated with scar thickness (STs), number of fibroblasts (NFs), Collagen I (Col I) level, Collagen III (Col III) level, Interleukin-6 (IL-6) level, and Tumor necrosis factor-alpha (TNF-α) level (all p < .01). Conclusions: Our findings revealed that the increase of microRNA-26a expression might alleviate excessive inflammation during the HS formation, inhibit fibroblast proliferation and collagen deposition in HS, and promote the treatment of HS.
{"title":"Treatment of hypertrophic scar with injection of triamcinolone leads to increased microRNA-26a in a rabbit ear model","authors":"Xiongying Zhang, Yalan Lai, Ling Guo","doi":"10.1177/1721727X221113399","DOIUrl":"https://doi.org/10.1177/1721727X221113399","url":null,"abstract":"Objectives: Differential expression of microRNAs (miRNAs) has been confirmed to promote hypertrophic scar (HS) formation. However, this mechanism remains to be further elucidated. This paper investigated the effects of microRNA26a on HS of rabbit ears or its mechanism. Methods: The rabbit HS models were established and randomly assigned to either the experimental group (20 rabbits with treatment through triamcinolone acetonide) or the scar group (20 rabbits without treatment). In addition, 10 unmodeled rabbits were served as control group. The expression of microRNA-26a in HS tissues was detected via a stem-loop real-time polymerase chain reaction (RT-PCR). Results: According to RT-PCR, we showed the decreased expression of microRNA-26a in the scar group compared with that in the experimental group, and in the experimental group compared with that in the control group (p < .01). In addition, the expression of microRNA-26a was negatively correlated with scar thickness (STs), number of fibroblasts (NFs), Collagen I (Col I) level, Collagen III (Col III) level, Interleukin-6 (IL-6) level, and Tumor necrosis factor-alpha (TNF-α) level (all p < .01). Conclusions: Our findings revealed that the increase of microRNA-26a expression might alleviate excessive inflammation during the HS formation, inhibit fibroblast proliferation and collagen deposition in HS, and promote the treatment of HS.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45866644","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 : 2022-06-01DOI: 10.1177/1721727X221107232
X. Wen, Kui Huang, J. Li, Li-xue Wu, Bo Gao
Whether serum proprotein convertase subtilisin/kexin type 9 (PCSK9) affects the prognosis of patients after the percutaneous coronary intervention (PCI) in hypertension patients remains unknown. A total of 2350 acute myocardial infarction (AMI) subjects with hypertension after PCI were enrolled. Subjects were under 30-months follow-up and divided into the major cardiovascular adverse event (MACE) Group and the non-MACE Group. Cox regression analysis were performed for the risk factors of occurrence of MACE. The relationship between the level of PCSK9 and Gensin score was analyzed by Pearson correlation. Two hundred and thirty-two patients were divided to the MACE Group. Age over 55 (hazard ratio (HR) = 2.52; p = 0.032), smoking (HR = 1.02; p < 0.001), diabetes mellitus (HR = 1.35; p < 0.001) and PCSK9 levels over 1011.3 ng/mL (HR = 1.05; ptdf < 0.001) were risk factors of occurrence of MACE. Baseline levels of PCSK9 was significantly related with Gensini score in ST segment elevation myocardial infarction (STEMI) patients (r = 0.51), all patients (r = 0.37) and non-STEMI patients (r = 0.34, p < 0.001). A high baseline PCSK9 level was the risk factor of poor prognosis of AMI patients with hypertension after PCI. PCSK9 levels were associated with the Gensini score in STEMI patients. Trial registration: This trial was registered at clinicaltrials.gov as NCT04100434.
{"title":"Elevated plasma proprotein convertase subtilisin/kexin type-9 is associated with poor prognosis of acute myocardial infarction in hypertension patients","authors":"X. Wen, Kui Huang, J. Li, Li-xue Wu, Bo Gao","doi":"10.1177/1721727X221107232","DOIUrl":"https://doi.org/10.1177/1721727X221107232","url":null,"abstract":"Whether serum proprotein convertase subtilisin/kexin type 9 (PCSK9) affects the prognosis of patients after the percutaneous coronary intervention (PCI) in hypertension patients remains unknown. A total of 2350 acute myocardial infarction (AMI) subjects with hypertension after PCI were enrolled. Subjects were under 30-months follow-up and divided into the major cardiovascular adverse event (MACE) Group and the non-MACE Group. Cox regression analysis were performed for the risk factors of occurrence of MACE. The relationship between the level of PCSK9 and Gensin score was analyzed by Pearson correlation. Two hundred and thirty-two patients were divided to the MACE Group. Age over 55 (hazard ratio (HR) = 2.52; p = 0.032), smoking (HR = 1.02; p < 0.001), diabetes mellitus (HR = 1.35; p < 0.001) and PCSK9 levels over 1011.3 ng/mL (HR = 1.05; ptdf < 0.001) were risk factors of occurrence of MACE. Baseline levels of PCSK9 was significantly related with Gensini score in ST segment elevation myocardial infarction (STEMI) patients (r = 0.51), all patients (r = 0.37) and non-STEMI patients (r = 0.34, p < 0.001). A high baseline PCSK9 level was the risk factor of poor prognosis of AMI patients with hypertension after PCI. PCSK9 levels were associated with the Gensini score in STEMI patients. Trial registration: This trial was registered at clinicaltrials.gov as NCT04100434.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45057141","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 : 2022-05-01DOI: 10.1177/1721727X221105132
Yan Wu, Jun Ye, Chunhui Zhao, Ji Pang, Yue-ying Li, Xin-qing Lin
Introduction Protein kinase A (PKA) and protein kinase G (PKG) are the main downstream effectors of second messengers cAMP and cGMP, which play important roles in physiological and pathological processes. Recently, there are two findings: one is PKA catalytic subunits α (PKACα) and PKG II can be secreted, the other is that the two secretory protein kinases are associated with the progression of tumors. Previous data also demonstrate that the two kinases, as signal cascades, involved in inflammation-associated disorders. However, it remains unclear whether the secreted PKACα or PKG II could serve as diagnostic biomarkers for inflammation-associated disorders. Methods The serum from suffered coronary disease, diabetes, rheumatoid arthritis, and schizophrenia were collected. The serum PKACα and PKG II were detected by ELISA. All the patients were consent informed. Results Our results showed that the serum PKACα and PKG II had obvious changes in coronary disease, rheumatoid arthritis, schizophrenia patients. However, the trends was opposite, especially in rheumatoid arthritis. Conclusions Serum PKACα and PKG II could serve as potentially diagnostic biomarkers for some inflammation-associated disorders, such as coronary disease, rheumatoid arthritis, and schizophrenia.
{"title":"Extracellular protein kinase A and G are potential biomarkers of some inflammation-associated disorders","authors":"Yan Wu, Jun Ye, Chunhui Zhao, Ji Pang, Yue-ying Li, Xin-qing Lin","doi":"10.1177/1721727X221105132","DOIUrl":"https://doi.org/10.1177/1721727X221105132","url":null,"abstract":"Introduction Protein kinase A (PKA) and protein kinase G (PKG) are the main downstream effectors of second messengers cAMP and cGMP, which play important roles in physiological and pathological processes. Recently, there are two findings: one is PKA catalytic subunits α (PKACα) and PKG II can be secreted, the other is that the two secretory protein kinases are associated with the progression of tumors. Previous data also demonstrate that the two kinases, as signal cascades, involved in inflammation-associated disorders. However, it remains unclear whether the secreted PKACα or PKG II could serve as diagnostic biomarkers for inflammation-associated disorders. Methods The serum from suffered coronary disease, diabetes, rheumatoid arthritis, and schizophrenia were collected. The serum PKACα and PKG II were detected by ELISA. All the patients were consent informed. Results Our results showed that the serum PKACα and PKG II had obvious changes in coronary disease, rheumatoid arthritis, schizophrenia patients. However, the trends was opposite, especially in rheumatoid arthritis. Conclusions Serum PKACα and PKG II could serve as potentially diagnostic biomarkers for some inflammation-associated disorders, such as coronary disease, rheumatoid arthritis, and schizophrenia.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47567341","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 : 2022-05-01DOI: 10.1177/1721727X221106506
K. Ma, Yun Li, Xiaolin Dong, Jingjing Guo
Introduction: The homeostasis of intestinal epithelial cells (IECs) is disrupted in diabetes, leading to functional changes of the gastrointestinal tract and increasing the risk of diabetic enteropathy. Methods: The aim of this study is to explore the effect of autophagy on the expression of inflammatory factors under high glucose in vitro. The effect of glucose at different concentrations (5, 10, 30 and 50 Mm) on IEC-6 cells was analyzed. Dorsomorphin (AMPK antagonist) and GSK621 (AMPK agonist) were used to examine the relationship between the autophagy and the AMPK/ULK1 signaling pathway in IEC-6 cells. Results: Our results showed that the high glucose significantly inhibited the growth of IECs, and induced more shrinkage and necrosis of cells. Autophagy was inhibited by high glucose. Furthermore, the levels of cytokines, including IL-22, INF-γ, NOS2, and TNF-α, were significantly increased, which were positively correlated with glucose concentration. Additionally, we confirmed that Dorsomorphin down-regulated the expression of p-AMPK and autophagy protein compared with GSK621. Similar, cellular immunofluorescence also detected low autophagy expression. However, GSK621 and Rapamycin increased the level of autophagy and down-regulated the secretion of pro-inflammatory factors compared with Dorsomorphin. Conclusion: Therefore, our results demonstrate that AMPK mediated autophagy may regulate levels of inflammation in IECs and improve cell survival under high glucose.
{"title":"AMPK-mediated autophagy modulates the inflammatory cytokine expression in intestinal epithelial cells induced by high glucose","authors":"K. Ma, Yun Li, Xiaolin Dong, Jingjing Guo","doi":"10.1177/1721727X221106506","DOIUrl":"https://doi.org/10.1177/1721727X221106506","url":null,"abstract":"Introduction: The homeostasis of intestinal epithelial cells (IECs) is disrupted in diabetes, leading to functional changes of the gastrointestinal tract and increasing the risk of diabetic enteropathy. Methods: The aim of this study is to explore the effect of autophagy on the expression of inflammatory factors under high glucose in vitro. The effect of glucose at different concentrations (5, 10, 30 and 50 Mm) on IEC-6 cells was analyzed. Dorsomorphin (AMPK antagonist) and GSK621 (AMPK agonist) were used to examine the relationship between the autophagy and the AMPK/ULK1 signaling pathway in IEC-6 cells. Results: Our results showed that the high glucose significantly inhibited the growth of IECs, and induced more shrinkage and necrosis of cells. Autophagy was inhibited by high glucose. Furthermore, the levels of cytokines, including IL-22, INF-γ, NOS2, and TNF-α, were significantly increased, which were positively correlated with glucose concentration. Additionally, we confirmed that Dorsomorphin down-regulated the expression of p-AMPK and autophagy protein compared with GSK621. Similar, cellular immunofluorescence also detected low autophagy expression. However, GSK621 and Rapamycin increased the level of autophagy and down-regulated the secretion of pro-inflammatory factors compared with Dorsomorphin. Conclusion: Therefore, our results demonstrate that AMPK mediated autophagy may regulate levels of inflammation in IECs and improve cell survival under high glucose.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46512215","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 : 2022-01-01DOI: 10.1177/1721727X221093056
Feng Zhuo, Jun Li, Yong-Hong Wang, Ming Li, Fangnan Song, Yu-liang Liu, Zong-Yu Tao
Objectives Osteoarthritis (OA) is a chronic joint disease characterized by osteoproliferation and the degeneration and destruction of articular cartilage. Platelet-rich plasma (PRP) is rich in various growth factors that have been reported to promote bone defect repair. This study examined the specific role and mechanism of PRP in OA. Methods OA model cells were created by treating articular chondrocytes with IL-1β. After treatment of the model cells with PRP or/and a T-box transcription factor 3 (TBX3)-overexpression plasmid, TBX3 expression was monitored via RT-qPCR, western blotting, and immunofluorescence assays. IL-1β, IL-33, and Caspase-3 levels were detected with ELISA kits. Levels of NLRP3, Caspase-1, MMP9, MMP13, and COL2A1 expression were evaluated by western blotting, and cell proliferation was assessed by the CCK-8 assay. Results Our results showed that TBX3 expression was upregulated in IL-1β-induced articular chondrocytes. IL-1β stimulation induced inflammation and the production of matrix metalloproteinases, activated Caspase-3 and the NLRP3/Caspase-1 pathway, inhibited the proliferation of articular chondrocytes; however, all those affects mediated by IL-1β could be markedly reversed by PRP. We also found that PRP alleviated IL-1β-induced inflammation, apoptosis, and extracellular matrix degradation in articular chondrocytes by inhibiting TBX3. Our findings suggest that PRP alleviates OA progression in vitro by downregulating TBX3. Conclusion PRP suppressed OA progression in vitro by inhibiting TBX3, which may be its mechanism of action in treating OA.
{"title":"Platelet-rich plasma inhibits inflammation, apoptosis, and the NLRP3/Caspase-1 pathway and induces matrix metalloproteinases and proliferation of IL-1β-induced articular chondrocytes by downregulating T-box transcription factor 3","authors":"Feng Zhuo, Jun Li, Yong-Hong Wang, Ming Li, Fangnan Song, Yu-liang Liu, Zong-Yu Tao","doi":"10.1177/1721727X221093056","DOIUrl":"https://doi.org/10.1177/1721727X221093056","url":null,"abstract":"Objectives Osteoarthritis (OA) is a chronic joint disease characterized by osteoproliferation and the degeneration and destruction of articular cartilage. Platelet-rich plasma (PRP) is rich in various growth factors that have been reported to promote bone defect repair. This study examined the specific role and mechanism of PRP in OA. Methods OA model cells were created by treating articular chondrocytes with IL-1β. After treatment of the model cells with PRP or/and a T-box transcription factor 3 (TBX3)-overexpression plasmid, TBX3 expression was monitored via RT-qPCR, western blotting, and immunofluorescence assays. IL-1β, IL-33, and Caspase-3 levels were detected with ELISA kits. Levels of NLRP3, Caspase-1, MMP9, MMP13, and COL2A1 expression were evaluated by western blotting, and cell proliferation was assessed by the CCK-8 assay. Results Our results showed that TBX3 expression was upregulated in IL-1β-induced articular chondrocytes. IL-1β stimulation induced inflammation and the production of matrix metalloproteinases, activated Caspase-3 and the NLRP3/Caspase-1 pathway, inhibited the proliferation of articular chondrocytes; however, all those affects mediated by IL-1β could be markedly reversed by PRP. We also found that PRP alleviated IL-1β-induced inflammation, apoptosis, and extracellular matrix degradation in articular chondrocytes by inhibiting TBX3. Our findings suggest that PRP alleviates OA progression in vitro by downregulating TBX3. Conclusion PRP suppressed OA progression in vitro by inhibiting TBX3, which may be its mechanism of action in treating OA.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45161526","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 : 2022-01-01DOI: 10.1177/1721727X221100602
Xiaonan Xu, Ni Zhang, Binde Li, Li Huang
Objective: To investigate the clinical value of Clostridium butyricum powders combined with zinc gluconate in the treatment of infectious diarrhea in children, clinical data of 86 children with infectious diarrhea were retrospectively analyzed. Methods: Both groups received routine treatments to reduce symptoms, among which the control group (n = 40) was given Clostridium butyricum powders, and the experiment group (n = 46) was given Clostridium butyricum powders and zinc gluconate. Patients in both groups were treated for 5 days. The clinical efficacy, recovery time, safety, serum levels of inflammatory markers (interleukin-6, interleukin-17, C-reactive protein), indicators of the intestinal mucosal function (diamine oxidase, D-lactate) and indicators to intestinal microecology (bifidobacteria, lactobacillus) before and after treatment were compared between the two groups. Results: The clinical efficacy in the experiment group (95.65%) was higher than that in the control group (77.50%, p < 0.05). The time of recovery from symptoms including diarrhea, abdominal pain and vomiting, and to normal body temperature in the experiment group were shorter than those in the control group (all p < .001). After treatment, the serum IL-6, IL-17, CRP levels and DAO, D-lactate levels in both groups were lower than those before treatment, and were lower in the experiment group than in the control group (all p < .001). After treatment, the intestinal bifidobacteria and lactobacillus levels in both groups were higher than those before treatment, and were higher in the experiment group than in the control group (all p < .01). There was no significant difference in the incidence of adverse reactions between the experiment group (8.70%) and the control group (2.50%). Conclusion: In this open-label study, Clostridium butyricum powders combined with zinc gluconate are significantly effective in treating children with infectious diarrhea, which is conducive to relieving early symptoms, downregulating serum inflammatory factor levels, improving intestinal mucosal function, regulating intestinal microecology, and ensuring the safety of patients.
{"title":"Clostridium butyricum powders combined with zinc gluconate on inflammatory factors and intestinal microecology in children with infectious diarrhea","authors":"Xiaonan Xu, Ni Zhang, Binde Li, Li Huang","doi":"10.1177/1721727X221100602","DOIUrl":"https://doi.org/10.1177/1721727X221100602","url":null,"abstract":"Objective: To investigate the clinical value of Clostridium butyricum powders combined with zinc gluconate in the treatment of infectious diarrhea in children, clinical data of 86 children with infectious diarrhea were retrospectively analyzed. Methods: Both groups received routine treatments to reduce symptoms, among which the control group (n = 40) was given Clostridium butyricum powders, and the experiment group (n = 46) was given Clostridium butyricum powders and zinc gluconate. Patients in both groups were treated for 5 days. The clinical efficacy, recovery time, safety, serum levels of inflammatory markers (interleukin-6, interleukin-17, C-reactive protein), indicators of the intestinal mucosal function (diamine oxidase, D-lactate) and indicators to intestinal microecology (bifidobacteria, lactobacillus) before and after treatment were compared between the two groups. Results: The clinical efficacy in the experiment group (95.65%) was higher than that in the control group (77.50%, p < 0.05). The time of recovery from symptoms including diarrhea, abdominal pain and vomiting, and to normal body temperature in the experiment group were shorter than those in the control group (all p < .001). After treatment, the serum IL-6, IL-17, CRP levels and DAO, D-lactate levels in both groups were lower than those before treatment, and were lower in the experiment group than in the control group (all p < .001). After treatment, the intestinal bifidobacteria and lactobacillus levels in both groups were higher than those before treatment, and were higher in the experiment group than in the control group (all p < .01). There was no significant difference in the incidence of adverse reactions between the experiment group (8.70%) and the control group (2.50%). Conclusion: In this open-label study, Clostridium butyricum powders combined with zinc gluconate are significantly effective in treating children with infectious diarrhea, which is conducive to relieving early symptoms, downregulating serum inflammatory factor levels, improving intestinal mucosal function, regulating intestinal microecology, and ensuring the safety of patients.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44105218","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 : 2022-01-01DOI: 10.1177/1721727X221139266
M. Abayneh, Dassaleng Muleta, Asnake Simieneh, Tadesse Duguma, Molla Asnake, Murtii Teressa, Biruktawit Endalkachew, Milkiyas Toru
This study was designed to assess the prevalence and factors associated with poor clinical outcome of acute respiratory infections (ARIs) among children less than five years of age at Mizan-Tepi university teaching public hospital in southwest district of Ethiopia. A prospective observational cohort study design was conducted from 01 June to August 30, 2020. Data related to socio-demographics, child nutritional status, clinical and environmental characteristics of patients were collected with structured questionnaire. Follow-up data were gathered from patient’s medical records using standard data collection tool. The data were analyzed using SPSS versions 25.0. In this study, 305 children of age less than five years were included. Of these, 124 (40.7%) of children were diagnosed with ARIs, of which 66 (53.2%) were female and 69 (55.6%) were age of 24–59 months. Of children diagnosed with ARIs, 21 (16.9%) were ended with poor clinical outcomes after completion of their treatment. In the multivariate analysis, age of children and presence of any other disease conditions (OR = 0.331; 95% CI: 0.123– 0.880; p= 0.024), exposure to indoor air pollution (OR = 0.344; 95% CI: 0.128– 0.925; p= 0.030), malnutrition (OR = 0.175; 95% CI: 0.058– 0.523; p= 0.002) and end point pneumonia (OR = 0.305; 95% CI: 0.113–0.821; p= 0.015) were found to be independent factors for poor outcome of under-five children with ARIs. Our findings highlight that timely detection, proper management and treatments as well as addressing other contributing factors are essentials in order to reduce prevalence and poor clinical outcomes of under five children with ARIs.
{"title":"Acute respiratory infections (ARIs) and factors associated with their poor clinical outcome among children under-five years attending pediatric wards of public hospital in Southwest district of Ethiopia: A prospective observational cohort study","authors":"M. Abayneh, Dassaleng Muleta, Asnake Simieneh, Tadesse Duguma, Molla Asnake, Murtii Teressa, Biruktawit Endalkachew, Milkiyas Toru","doi":"10.1177/1721727X221139266","DOIUrl":"https://doi.org/10.1177/1721727X221139266","url":null,"abstract":"This study was designed to assess the prevalence and factors associated with poor clinical outcome of acute respiratory infections (ARIs) among children less than five years of age at Mizan-Tepi university teaching public hospital in southwest district of Ethiopia. A prospective observational cohort study design was conducted from 01 June to August 30, 2020. Data related to socio-demographics, child nutritional status, clinical and environmental characteristics of patients were collected with structured questionnaire. Follow-up data were gathered from patient’s medical records using standard data collection tool. The data were analyzed using SPSS versions 25.0. In this study, 305 children of age less than five years were included. Of these, 124 (40.7%) of children were diagnosed with ARIs, of which 66 (53.2%) were female and 69 (55.6%) were age of 24–59 months. Of children diagnosed with ARIs, 21 (16.9%) were ended with poor clinical outcomes after completion of their treatment. In the multivariate analysis, age of children and presence of any other disease conditions (OR = 0.331; 95% CI: 0.123– 0.880; p= 0.024), exposure to indoor air pollution (OR = 0.344; 95% CI: 0.128– 0.925; p= 0.030), malnutrition (OR = 0.175; 95% CI: 0.058– 0.523; p= 0.002) and end point pneumonia (OR = 0.305; 95% CI: 0.113–0.821; p= 0.015) were found to be independent factors for poor outcome of under-five children with ARIs. Our findings highlight that timely detection, proper management and treatments as well as addressing other contributing factors are essentials in order to reduce prevalence and poor clinical outcomes of under five children with ARIs.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48907264","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}
Objectives Many researches showed that Erythropoietin-producing hepatocyte kinase receptor A1 (EphA1) can promote the occurrence and development of malignant tumors and may be related to tumor microenvironment. But most of them are phenomenon studies, and there are few in-depth and complete mechanism studies. This study aims to understand how EphA1 promotes the progression of malignant tumors by regulating tumor microenvironment (focusing on Interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF)) from two experimental dimensions of in vitro and in vivo by using genetic engineering technology. Material and Methods We used genetic engineering technology to enhance and knock down EphA1 gene expression in SGC-7901 cells, respectively, and analyzed its influence on cell function and the expression levels of VEGF and IL-6 in cells. Subsequently, we constructed human EphA1 gene overexpression, EphA1 gene silencing, and normal expression of human EphA1 gene subcutaneous transplanted tumor models of SGC-7901 cells nude mice, and analyzed the differences in tumor development and the changes in the expression levels of VEGF and ILl-6 in tumor tissues. Results After EphA1 gene expression was enhanced, the proliferation, invasion and migration of SGC-7901 cells were enhanced, and apoptosis was weakened, and the expression levels of VEGF and IL-6 were increased. While the opposite results were found when EphA1 gene expression were knocked down. Meanwhile, tumor formation time and growth rate of subcutaneous transplantation in nude mice were advanced and the expression levels of VEGF and IL-6 in tumor tissues were increased when EphA1 gene expression were overexpressed by genetic engineering technology. Similarly, the opposite effect occurred in transplanted tumor model when EphA1 gene was silenced. Conclusion Our study showed that EphA1 can up-regulating VEGF and IL-6 expression, thereby enhancing the inflammatory environment and angiogenesis in the tumor microenvironment, and this helps to promote the progression of SGC-7901 cells and its transplanted tumor.
{"title":"Erythropoietin-producing hepatocyte kinase receptor A1 facilitating the prgression of SGC-7901 cells and its transplanted tumor by increasing the expression of interleukin-6 and vascular endothelial growth factor in tumor microenvironment","authors":"Yong-Cang Wang, Wenjing Zheng, Wei Yu, Rui-liang Quan, Ya-jun Zhao","doi":"10.1177/1721727X221125612","DOIUrl":"https://doi.org/10.1177/1721727X221125612","url":null,"abstract":"Objectives Many researches showed that Erythropoietin-producing hepatocyte kinase receptor A1 (EphA1) can promote the occurrence and development of malignant tumors and may be related to tumor microenvironment. But most of them are phenomenon studies, and there are few in-depth and complete mechanism studies. This study aims to understand how EphA1 promotes the progression of malignant tumors by regulating tumor microenvironment (focusing on Interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF)) from two experimental dimensions of in vitro and in vivo by using genetic engineering technology. Material and Methods We used genetic engineering technology to enhance and knock down EphA1 gene expression in SGC-7901 cells, respectively, and analyzed its influence on cell function and the expression levels of VEGF and IL-6 in cells. Subsequently, we constructed human EphA1 gene overexpression, EphA1 gene silencing, and normal expression of human EphA1 gene subcutaneous transplanted tumor models of SGC-7901 cells nude mice, and analyzed the differences in tumor development and the changes in the expression levels of VEGF and ILl-6 in tumor tissues. Results After EphA1 gene expression was enhanced, the proliferation, invasion and migration of SGC-7901 cells were enhanced, and apoptosis was weakened, and the expression levels of VEGF and IL-6 were increased. While the opposite results were found when EphA1 gene expression were knocked down. Meanwhile, tumor formation time and growth rate of subcutaneous transplantation in nude mice were advanced and the expression levels of VEGF and IL-6 in tumor tissues were increased when EphA1 gene expression were overexpressed by genetic engineering technology. Similarly, the opposite effect occurred in transplanted tumor model when EphA1 gene was silenced. Conclusion Our study showed that EphA1 can up-regulating VEGF and IL-6 expression, thereby enhancing the inflammatory environment and angiogenesis in the tumor microenvironment, and this helps to promote the progression of SGC-7901 cells and its transplanted tumor.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49106644","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 : 2022-01-01DOI: 10.1177/1721727X221137488
Dan Y. Wu, F. Bao, Yong Huang
Mucosa-associated lymphoid tissue (MALT) lymphoma-induced hemophagocytic lymphohistiocytosis (HLH) has rarely been reported. Herein, we report the diagnosis and treatment process of a patient with MALT lymphoma-induced HLH who received chemotherapy after diagnosis and finally achieved partial remission. In this case, blood cells were only reduced to grade II at the time of diagnosis, and the patient was then treated with the R-CHOP regimen (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone). HLH responded well to treatment. Laboratory data indicative of HLH and blood chemistry results were steadily normalized, and hepatosplenomegaly resolved. One month after chemotherapy, the patient achieved partial remission. The results also showed that the treatment was successful. In conclusion, treatment of lymphoma-triggered HLH needs to balance HLH-specific and lymphoma-specific treatment. Once HLH is initially controlled or the decrease in blood cells is better than grade II, it should actively transition to lymphoma treatment.
{"title":"Mucosa-associated lymphoid tissue lymphoma-induced hemophagocytic lymphohistiocytosis: A case report","authors":"Dan Y. Wu, F. Bao, Yong Huang","doi":"10.1177/1721727X221137488","DOIUrl":"https://doi.org/10.1177/1721727X221137488","url":null,"abstract":"Mucosa-associated lymphoid tissue (MALT) lymphoma-induced hemophagocytic lymphohistiocytosis (HLH) has rarely been reported. Herein, we report the diagnosis and treatment process of a patient with MALT lymphoma-induced HLH who received chemotherapy after diagnosis and finally achieved partial remission. In this case, blood cells were only reduced to grade II at the time of diagnosis, and the patient was then treated with the R-CHOP regimen (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone). HLH responded well to treatment. Laboratory data indicative of HLH and blood chemistry results were steadily normalized, and hepatosplenomegaly resolved. One month after chemotherapy, the patient achieved partial remission. The results also showed that the treatment was successful. In conclusion, treatment of lymphoma-triggered HLH needs to balance HLH-specific and lymphoma-specific treatment. Once HLH is initially controlled or the decrease in blood cells is better than grade II, it should actively transition to lymphoma treatment.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49167233","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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