Immunity, Inflammation and Disease最新文献_第3页

Association of the Geriatric Nutritional Risk Index With Prognosis in Patients With Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention 经皮冠状动脉介入治疗急性冠状动脉综合征患者的老年营养风险指数与预后的关系

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-15 DOI: 10.1002/iid3.70321

Yuewen Qi, Xinchen Wang, Yan Liu, Ying Zhang, Qiyu Sun, Chen Wei, Ge Song, Jingyi Liu, Fei Shi, Lixian Sun

Background and Aims

The geriatric nutritional risk index (GNRI) has shown good predictive value for some diseases. However, its association with major adverse cardiovascular events (MACEs) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) remains uncertain. This study investigated the correlation between the GNRI and MACEs.

Patients and Methods

This was a prospective cohort study. We consecutively enrolled 1515 ACS patients who underwent PCI. The median duration of follow-up was 1000 days. The primary endpoints were MACEs, including all-cause mortality, severe heart failure rehospitalization, revascularization, acute myocardial infarction (AMI) recurrence, and restenosis/intrastent thrombosis.

Results

ROC curve analysis revealed an area under the curve of 0.603, with a GNRI cutoff value of 110.78. Cox regression analysis indicated that lower GNRI levels were independently associated with an increased risk of MACEs, a finding supported by risk score assessments. Kaplan–Meier survival curves and log-rank tests indicated significantly lower cumulative survival rates in patients with lower GNRI value. Lower GNRI levels were also correlated with a higher risk of rehospitalization and cardiovascular death, as confirmed by the competing risk model. These associations remained significant after adjustments (all p for interaction > 0.05). RCS analysis and trend tests (all p < 0.05) further supported these findings.

Conclusion

GNRI, as an indicator of nutritional status, was correlated with the risk of MACEs in ACS patients undergoing PCI, particularly in predicting cardiac death and rehospitalization, suggesting that the GNRI level may serve as a valid indicator for predicting poor prognosis in patients with ACS undergoing PCI.

背景与目的：老年营养风险指数（GNRI）对某些疾病具有较好的预测价值。然而，其与急性冠状动脉综合征（ACS）患者经皮冠状动脉介入治疗（PCI）的主要不良心血管事件（mace）的关系仍不确定。本研究探讨了GNRI与mace的相关性。患者和方法：这是一项前瞻性队列研究。我们连续入组1515例接受PCI治疗的ACS患者。中位随访时间为1000天。主要终点是mace，包括全因死亡率、严重心力衰竭再住院、血运重建、急性心肌梗死（AMI）复发和再狭窄/急性血栓形成。结果：ROC曲线分析显示曲线下面积为0.603，GNRI截断值为110.78。Cox回归分析表明，较低的GNRI水平与mace风险增加独立相关，这一发现得到了风险评分评估的支持。Kaplan-Meier生存曲线和log-rank检验显示，GNRI值较低的患者累积生存率明显较低。正如竞争风险模型所证实的那样，较低的GNRI水平也与较高的再住院和心血管死亡风险相关。调整后，这些关联仍然显著（相互作用p均为0.05）。结论：GNRI作为营养状况指标与ACS行PCI患者mace发生风险相关，特别是在预测心源性死亡和再住院方面，提示GNRI水平可作为预测ACS行PCI患者预后不良的有效指标。

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引用次数: 0

Concordance Analysis of ALEX-2, ImmunoCAP, and Prick Test for Respiratory Allergies in Lima, Peru 秘鲁利马地区呼吸过敏的alex2、ImmunoCAP和点刺试验的一致性分析。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-12 DOI: 10.1002/iid3.70325

César A. Galván, Rafael Durán, José Ignacio Larco, Juan Carlos Gomez de la Torre

Background

Accurate identification of respiratory allergen sensitization is essential for managing asthma and allergic rhinitis (AR). While Skin Prick Test (SPT) and ImmunoCAP are standard diagnostic tools, exploratory comparative data for the novel Allergy Explorer 2 (ALEX-2) test in Latin American populations remain scarce. While Skin Prick Test (SPT) and ImmunoCAP are standard diagnostic tools with limited allergen panels per test, the novel Allergy Explorer 2 (ALEX-2) multiplex platform can simultaneously assess multiple allergens. However, exploratory comparative data for ALEX-2 in Latin American populations remain scarce.

Methods

This prospective cross-sectional study evaluated the concordance between SPT, ImmunoCAP, and ALEX-2 in detecting respiratory allergen sensitization among 57 patients with asthma or AR recruited consecutively from a private allergy clinic in Lima, Peru. Concordance was assessed using Cohen's κ coefficient.

Results

The highest overall agreement was observed between ALEX-2 and SPT (κ = 0.5649, p < 0.0001), followed by ALEX-2 and ImmunoCAP (κ = 0.4911, p < 0.0001), and ImmunoCAP and SPT (κ = 0.4688, p < 0.0001). ALEX-2 and ImmunoCAP aligned on 7 of 10 allergens, while both ImmunoCAP and SPT, as well as ALEX-2 and SPT, agreed on 5 of 9 allergens. The strongest concordance was found for dust mites, particularly Dermatophagoides farinae (κ = 0.6323, p < 0.0001) between ALEX-2 and SPT.

Conclusions

ALEX-2 demonstrates moderate agreement with SPT and ImmunoCAP, with the highest concordance for dust mites, suggesting potential as a complementary diagnostic tool pending validation in diverse populations.

背景：准确识别呼吸道过敏原致敏对哮喘和变应性鼻炎（AR）的治疗至关重要。虽然皮肤点刺试验（SPT）和免疫cap是标准的诊断工具，但在拉丁美洲人群中，新型过敏探索者2 （alex2）试验的探索性比较数据仍然很少。虽然皮肤点刺试验（SPT）和免疫cap是标准的诊断工具，每次测试的过敏原面板有限，但新的过敏探索者2 （alex2）多重平台可以同时评估多种过敏原。然而，拉丁美洲人群中alex2的探索性比较数据仍然很少。方法：这项前瞻性横断研究评估了SPT、ImmunoCAP和alex2在检测呼吸道过敏原致敏方面的一致性，这些患者连续从秘鲁利马的一家私人过敏诊所招募了57名哮喘或AR患者。采用Cohen’s κ系数评价一致性。结果：alex2与SPT的总体一致性最高（κ = 0.5649, p）。结论：alex2与SPT和ImmunoCAP的一致性中等，其中尘螨的一致性最高，这表明alex2有潜力作为一种补充诊断工具，有待于在不同人群中验证。

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引用次数: 0

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-12 DOI: 10.1002/iid3.70322

Charles Nkansah, Felix Osei-Boakye, Samuel K. Appiah

Background

Alterations in hematological parameters in SARS-CoV-2 infection may contribute to disease severity and poor outcomes. This study reports the hematological profile of COVID-19 patients.

Methods

This was a cross-sectional study involving 169 confirmed COVID-19 patients conducted at Sunyani Teaching Hospital between January and August, 2022. Sociodemographic, clinical, and laboratory data were obtained. Full blood count was performed using an automated hematology analyzer, and systemic inflammatory indices were calculated.

Results

Participants were mostly young adults (51.5%), females (53.8%), resided in urban settings (41.4%), and aged 20-81 years with a median age of 35.0 (29.0–47.0) years. Overall, anemia was present in 60.4% of the COVID-19 patients (56.4% in males and 63.7% in females), with 23.7%, 23.7%, and 13.0% experiencing mild, moderate, and severe anemia, respectively. The COVID-19 patients mostly had normocytic normochromic anemia (50.3%), and 37.9% had macrocytic normochromic anemia. Older adults (6.600 times, p = 0.004), middle-aged adults (4.435 times, p = 0.034), and rural dwellers (3.759 times, p = 0.012) were associated with anemia among the COVID-19 patients. Thrombocytopenia was detected in 56.2% of the patients, and 36.7%, 16.0%, and 2.4% had mild, moderate and severe thrombocytopenia respectively. Leucocyte alterations among the patients included leucopenia (22.5%), leucocytosis (17.2%), neutropenia (40.8%), and lymphocytosis (39.6%). Total leucocyte count (AUC: 0.818, p < 0.001), absolute neutrophil count (AUC: 0.816, p < 0.001), and absolute lymphocyte count (AUC: 0.804, p < 0.001) predicted severe COVID-19 among the participants. Bicytopenia and pancytopenia were observed in 37.3% and 17.8%, respectively.

Conclusion

COVID-19 is associated with diverse and clinically relevant hematological abnormalities, remarkably anemia, thrombocytopenia, and leucocyte alterations, and usually relate with disease severity. Routine blood cell analysis is essential in the management of COVID-19, particularly in resource-limited settings.

背景：SARS-CoV-2感染患者血液学参数的改变可能与疾病严重程度和不良预后有关。本研究报告了COVID-19患者的血液学特征。方法：本研究是一项横断面研究，涉及2022年1月至8月在Sunyani教学医院进行的169例确诊的COVID-19患者。获得了社会人口学、临床和实验室数据。使用自动血液学分析仪进行全血细胞计数，并计算全身炎症指数。结果：研究对象以年轻人（51.5%）、女性（53.8%）、城市居民（41.4%）为主，年龄20 ~ 81岁，中位年龄为35.0（29.0 ~ 47.0）岁。总体而言，60.4%的COVID-19患者存在贫血（男性56.4%，女性63.7%），分别有23.7%、23.7%和13.0%的患者出现轻度、中度和重度贫血。新冠肺炎患者多为正红细胞性贫血（50.3%），大细胞性贫血占37.9%。老年人（6600次，p = 0.004）、中年人（4.435次，p = 0.034）、农村居民（3.759次，p = 0.012）与新冠肺炎患者贫血相关。56.2%的患者存在血小板减少，其中轻度、中度和重度血小板减少分别为36.7%、16.0%和2.4%。患者白细胞改变包括白细胞减少（22.5%）、白细胞增多（17.2%）、中性粒细胞减少（40.8%）和淋巴细胞增多（39.6%）。结论：COVID-19与多种临床相关的血液学异常相关，特别是贫血、血小板减少和白细胞改变，且通常与疾病严重程度有关。常规血细胞分析对于COVID-19的管理至关重要，特别是在资源有限的情况下。

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引用次数: 0

Clinical Characteristics of Patients With Anti-Signal Recognition Particle Antibody: A Cohort Study 抗信号识别颗粒抗体患者的临床特征：一项队列研究。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-11 DOI: 10.1002/iid3.70297

Ameen Jubber, Maumer Durrani, Abdullah Almayahi, Kehinde Sunmboye

Background

Anti-signal recognition particle (anti-SRP) antibodies are myositis-specific autoantibodies associated with immune-mediated necrotizing myopathy. This study was undertaken to better understand how patients with anti-SRP antibodies have been managed at our tertiary centre and to assess the spectrum of clinical features and outcomes in routine clinical practice.

Methods

We conducted a retrospective evaluation of 25 patients with anti-SRP antibodies identified via line-blot immunoassay at a tertiary care centre (2019–2024). Demographic, clinical, serological, and imaging data were reviewed.

Results

The group of patients had a mean age of 60.1 years, with a female-to-male ratio of 10:15. Eight patients (32%) were diagnosed with myositis, primarily presenting with proximal muscle weakness. Interstitial lung disease was observed in 53% of the group of patients, and 50% of the subset of patients with myositis. Coexisting myositis-specific autoantibodies were present in 32%, and 48% had positive antinuclear antibody titres (≥ 1:400). Cardiac involvement was reported in two myositis patients. Corticosteroids, often combined with mycophenolate mofetil or other immunosuppressants, formed the basis of treatment.

Conclusion

Anti-SRP antibodies are associated with a heterogeneous clinical spectrum, with many patients lacking myositis features. There was a high prevalence of coexisting autoantibodies. Further studies are needed to elucidate the pathogenic role of anti-SRP and optimise management strategies.

背景：抗信号识别颗粒抗体是与免疫介导的坏死性肌病相关的肌炎特异性自身抗体。开展这项研究是为了更好地了解我们三级中心如何管理抗srp抗体患者，并评估常规临床实践中的临床特征和结果。方法：我们对一家三级医疗中心（2019-2024）25例通过线印迹免疫分析法鉴定出抗srp抗体的患者进行了回顾性评估。回顾了人口学、临床、血清学和影像学资料。结果：本组患者平均年龄60.1岁，男女比例为10:15。8例（32%）患者被诊断为肌炎，主要表现为近端肌无力。间质性肺疾病在53%的患者组中被观察到，50%的患者亚群患有肌炎。32%的患者存在肌炎特异性自身抗体，48%的患者抗核抗体阳性（≥1:400）。报告2例肌炎患者心脏受累。皮质类固醇通常与霉酚酸酯或其他免疫抑制剂联合使用，是治疗的基础。结论：抗srp抗体与异质性临床谱相关，许多患者缺乏肌炎特征。同时存在自身抗体的发生率高。需要进一步的研究来阐明抗srp的致病作用并优化管理策略。

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引用次数: 0

Role of Macrophages in Cardiac Remodeling: Cues From Zebrafish Heart 巨噬细胞在心脏重塑中的作用：来自斑马鱼心脏的线索。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-11 DOI: 10.1002/iid3.70282

Himanshu Gaur, Maram Hasan, Huseyin C. Yalcin

Background

Macrophages are a key component of innate immunity and regulate cardiac phenotypes by their polarization state. The classical M1 macrophages are activated by pro-inflammatory stimuli, whereas M2 macrophages are activated by anti-inflammatory stimuli. The balance between M1 and M2 polarization is important and tightly controlled to maintain tissue homeostasis.

Objective

This review aims to explain the diversity of the ability to regenerate among humans and zebrafish, the role of the immune system in heart regeneration, and macrophage function in normal conditions and disease. It also investigates age-related effects on macrophage function and therapeutic strategies to manipulate macrophage polarization in the treatment of heart injury.

Methods

Systematic review of the literature was conducted focusing on macrophage polarization, cardiac regeneration mechanisms, and immunomodulatory therapy.

Results

Macrophage polarization imbalances of M1-M2 are involved in inflammatory and cardiac disease. Mechanisms of macrophage function under various states and in various species are useful for insightful comprehension of novel therapy strategies. Macrophage polarization modulation is a future potential strategy for cardiac repair and the treatment of cardiac disease.

Conclusion

Targeting macrophage polarization to restore balance and homeostasis is a promising strategy for supporting cardiac regeneration and the treatment of inflammatory cardiac disease.

背景：巨噬细胞是先天免疫的重要组成部分，并通过其极化状态调节心脏表型。经典的M1巨噬细胞被促炎刺激激活，而M2巨噬细胞被抗炎刺激激活。M1和M2极化之间的平衡是维持组织稳态的重要和严格控制。目的：本综述旨在解释人类和斑马鱼再生能力的多样性，免疫系统在心脏再生中的作用，以及巨噬细胞在正常状态和疾病中的功能。研究还探讨了年龄对巨噬细胞功能的影响以及在心脏损伤治疗中操纵巨噬细胞极化的治疗策略。方法：系统回顾巨噬细胞极化、心脏再生机制、免疫调节治疗等方面的文献。结果：巨噬细胞M1-M2极化失衡与炎症和心脏病有关。巨噬细胞在不同状态和不同物种中的功能机制有助于深入理解新的治疗策略。巨噬细胞极化调节是未来心脏修复和心脏疾病治疗的潜在策略。结论：靶向巨噬细胞极化恢复平衡和内稳态是支持心脏再生和治疗炎症性心脏病的一种有前景的策略。

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引用次数: 0

Lipoic Acid Ameliorates Lipopolysaccharide-Induced Inflammation via Inhibition of Glycolysis in RAW264.7 Macrophages 硫辛酸通过抑制RAW264.7巨噬细胞糖酵解改善脂多糖诱导的炎症。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-08 DOI: 10.1002/iid3.70313

Liduo Yue, Kai Wang, Rongyuan Wang, Linbei Lu, Lihong Fan

<div> <section> <h3> Background</h3> <p>Sustained pulmonary inflammation contributes significantly to lung carcinogenesis. Macrophages play a pivotal role in perpetuating inflammatory responses, undergoing a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis upon activation. The interplay between metabolic reprogramming and macrophage polarization remains poorly defined. The objective of this study is to examines the anti-inflammatory mechanism of lipoic acid (LA), focusing on its ability to modulate immunometabolism in activated macrophages.</p> </section> <section> <h3> Methods</h3> <p>We utilized lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and a murine acute lung injury (ALI) model to evaluate the anti-inflammatory effects of LA. Inflammatory cytokine expression was assessed by qPCR, ELISA, and Western blot. Metabolic profiling was performed using Seahorse XF technology to measure oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), evaluating glycolytic and oxidative metabolic functions.</p> </section> <section> <h3> Results</h3> <p>This study systematically elucidates the molecular mechanism by which LA modulates macrophage inflammatory responses through targeting the HIF1α/glycolysis axis. The main findings are as follows: (1) In LPS-induced RAW264.7 macrophages, LA treatment significantly inhibited the expression of M1 macrophage markers (iNOS, CD86) and the secretion of proinflammatory cytokines (IL-1β, IL-6, etc.). (2) LA effectively reduced the expression of GSDMD, the key executor of pyroptosis, demonstrating its inhibitory effect on macrophage pyroptosis. (3) Metabolic analysis revealed that LA reversed LPS-induced metabolic reprogramming by decreasing the ECAR and increasing the OCR, thereby suppressing glycolysis. (4) Mechanistic studies showed that siRNA-mediated knockdown of HIF1α replicated both the anti-inflammatory and metabolic regulatory effects of LA, confirming HIF1α as the key target in this pathway. (5) In an ALI mouse model, LA treatment significantly reduced HIF1α expression in lung tissues and effectively alleviated inflammatory responses, further validating the proposed mechanism.</p> </section> <section> <h3> Conclusion</h3> <p>LA exerts potent anti-inflammatory effects by targeting HIF1α-mediated metabolic reprogramming in macrophages. Our results highlight the therapeutic potential of targeting immunometabolic pathways in inflammatory lung diseases, providing new insights into the mechanism by which LA ameliorates pulmonary inflammation.</p> </secti

背景：持续的肺部炎症对肺癌的发生有重要作用。巨噬细胞在持续炎症反应中发挥关键作用，经历从氧化磷酸化（OXPHOS）到糖酵解的代谢转变。代谢重编程和巨噬细胞极化之间的相互作用仍不清楚。本研究的目的是探讨硫辛酸（LA）的抗炎机制，重点研究其在活化巨噬细胞中调节免疫代谢的能力。方法：采用脂多糖（LPS）刺激的RAW264.7巨噬细胞和小鼠急性肺损伤（ALI）模型来评价LA的抗炎作用。采用qPCR、ELISA和Western blot检测炎症细胞因子的表达。使用Seahorse XF技术进行代谢分析，测量氧气消耗率（OCR）和细胞外酸化率（ECAR），评估糖酵解和氧化代谢功能。结果：本研究系统阐明了LA通过靶向HIF1α/糖酵解轴调控巨噬细胞炎症反应的分子机制。主要发现如下：(1)在lps诱导的RAW264.7巨噬细胞中，LA处理显著抑制了M1巨噬细胞标志物（iNOS、CD86）的表达和促炎细胞因子（IL-1β、IL-6等）的分泌。(2) LA有效降低了巨噬细胞焦亡的关键执行者GSDMD的表达，显示了其对巨噬细胞焦亡的抑制作用。(3)代谢分析表明，LA通过降低ECAR和增加OCR来逆转lps诱导的代谢重编程，从而抑制糖酵解。(4)机制研究表明，sirna介导的HIF1α下调可复制LA的抗炎和代谢调节作用，证实HIF1α是该途径的关键靶点。(5)在ALI小鼠模型中，LA治疗显著降低肺组织中HIF1α的表达，有效减轻炎症反应，进一步验证了上述机制。结论：LA通过靶向hif1 α介导的巨噬细胞代谢重编程，具有较强的抗炎作用。我们的研究结果强调了靶向免疫代谢途径在炎症性肺部疾病中的治疗潜力，为LA改善肺部炎症的机制提供了新的见解。

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引用次数: 0

Liver Cirrhosis Caused by Food-Borne Zoonotic Fasciola gigantica in Cattle in Bangladesh: Pathology and Immunological Orchestra 孟加拉牛食源性人畜共患病巨片吸虫引起肝硬化：病理学和免疫学

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-08 DOI: 10.1002/iid3.70320

Md. Haydar Ali, Joydeep Paul, Romana Parvin, Md. Shahadat Hossain, Sharmin Shahid Labony, Nusrat Nowrin Shohana, Md. Mahmudul Alam, Umme Razia Islam, Anita Rani Dey, Md. Abu Hadi Noor Ali Khan, Md. Abdul Alim, Anisuzzaman

Background

Fasciolosis is a food-borne parasitic zoonotic disease caused by widespread liver flukes that affect ruminants and humans, and is responsible for non-resolving hepatic damage. Although fasciolosis occurs in both acute and chronic forms, chronic fasciolosis is more common.

Objectives

This study investigates the pathological changes and immunological cascade in the livers of Fasciola gigantica infected cattle, both at the transcriptional and translational levels.

Methods

Normal and suspected liver samples from cattle were collected and examined. Affected tissues were subjected to routine histological and immunohistochemical analysis. Transcription factors and interleukins (IL) were measured by sqRT-PCR and ELISA.

Results

In chronic fasciolosis, liver became atrophied, marked with whitish fibrotic patches, calcification and bile duct hyperplasia filled with blackish-brown sandy contents. Histopathological examinations showed massive loss of hepatocytes, fibrous proliferation, and infiltration of mononuclear cells and eosinophils. In addition, a huge deposition of amyloid was noticed in severely affected livers. T-bet (T-box expressed in T cells protein) remained at the basal level, whereas expression of GATA-3 (GATA-binding protein 3) was dramatically increased in severe fasciolosis. Also, there was a noticeable increase in the GATA-3 positive cells, while T-bet positive cells were largely absent, displaying a drift towards Th2 type immune response. In severe infection, mRNAs of IL-4, IL-5, IL-6, IL-10 and IL-13 highly expressed compared to the non-infected control, but the interferon- (INF)-γ expression remained unaltered. Similarly, we detected significant (p < 0.01) elevation of IL-4, IL-5, IL-6 and IL-13 in severely affected liver lysate. To further validate the notion, bovine peripheral blood mononuclear cells (bPBMCs) were treated with F. gigantica-culture milieu (FCM). FCM treatment elevated IL-4, IL-5, IL-6 and IL-13 in a time dependent manner, confirming liver fluke-induced Th2-biased immune response.

Conclusion

This study reveals distinct pathology and dysregulation of transcription factors and cytokines profiles in F. gigantica infected cattle.

片形吸虫病是一种食源性寄生虫性人畜共患疾病，由广泛存在的反刍动物和人类肝吸虫引起，可导致非解决性肝损伤。虽然筋膜吸虫病有急性和慢性两种形式，但慢性筋膜吸虫病更为常见。目的研究巨片吸虫感染牛肝脏的病理变化和免疫级联反应，并从转录和翻译两个方面进行研究。方法采集牛正常肝脏和疑似肝脏标本进行检测。对受累组织进行常规组织学和免疫组织化学分析。采用sqRT-PCR和ELISA检测转录因子和白细胞介素（IL）。结果慢性片形吸虫病患者肝脏萎缩，呈白色纤维化斑块、钙化、胆管增生，充满黑褐色砂质内容物。组织病理学检查显示肝细胞大量丢失，纤维增生，单核细胞和嗜酸性粒细胞浸润。此外，严重病变的肝脏中可见大量淀粉样蛋白沉积。T-bet （T细胞中表达的T-box蛋白）保持在基础水平，而GATA-3 （gata结合蛋白3）的表达在严重的片形虫病中显著增加。同时，GATA-3阳性细胞明显增多，而T-bet阳性细胞基本缺失，表现出向Th2型免疫反应的漂移。在严重感染时，与未感染对照组相比，IL-4、IL-5、IL-6、IL-10和IL-13 mrna高表达，但干扰素- (INF)-γ的表达保持不变。同样，我们在严重感染的肝裂解液中检测到IL-4、IL-5、IL-6和IL-13的显著升高（p < 0.01）。为了进一步验证这一概念，牛外周血单个核细胞（bPBMCs）用F. gigantica培养环境（FCM）处理。FCM处理后，IL-4、IL-5、IL-6和IL-13呈时间依赖性升高，证实了肝吸虫诱导的th2偏向性免疫应答。结论本研究揭示了牛巨型牛瘟菌感染后不同的病理和转录因子及细胞因子谱的失调。

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引用次数: 0

Kaempferitrin Attenuates Lipopolysaccharide-Induced Cardiac Dysfunction Through Suppression of the NF-κB/NLRP3 Signaling Pathway. 山奈素通过抑制NF-κB/NLRP3信号通路减轻脂多糖诱导的心功能障碍。

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2026-01-01 DOI: 10.1002/iid3.70323

Hongyu Kuang, Qiang Li, Min Chen, Huaan Du

Purpose: The inflammatory activation and metabolic disorders of cardiomyocytes are essential mechanisms in sepsis-related cardiac dysfunction. Kaempferitrin (Kae), a flavonoid compound, possesses various properties including anti-inflammatory and anti-glycation effects. Hence, the current study is conducted to investigate the protective effects of Kae against sepsis-induced cardiac dysfunction.

Methods: C57BL/6 J mice were treated with Kae for 2 h, followed by lipopolysaccharide (LPS) treatment. After 12 h, the echocardiographic measurements were conducted. Serum test, pathological analysis, transcriptomics, western blotting, and RT-PCR were used for exploring mechanisms. Additionally, in vitro, H9c2 and AC16 cardiomyocyte cell lines were pretreated with Kae (10 μM) for 2 h, followed by LPS stimulation (1 μg/mL).

Results: In vivo, pretreatment with Kae mitigates LPS-induced cardiac dysfunction. Kae suppresses the levels of IL-6, TNF-α, IL-1β, and IL-18 in the cardiac tissue of mice mediated by LPS. Additionally, serological and histological assessments demonstrate that Kae exhibits protective effects against LPS-induced cardiomyocyte injury and apoptosis. Transcriptomic analysis reveals that the nuclear factor kappa-B (NF-κB)/NLRP3 signaling pathway may be a crucial mechanism. Meanwhile, it proved that LPS significantly activates NF-κB/NLRP3 to induce cardiomyocyte pyroptosis, which is attenuated by Kae. In vitro, H9c2 and AC16 cardiomyocyte cell lines were pretreated with Kae followed by LPS stimulation, showing an inhibition of NF-κB/NLRP3 pathway, with a decreased mRNA levels of Il-6, Tnf-α, Il-1β. The NLRP3-knock out (Nlrp3 ^-/- ) mice have verified that Kae ameliorating LPS-induced spetic cardiomyopathy by inhibiting NLRP3.

Conclusions: This study confirms that Kae alleviates LPS-induced left ventricular remodeling and cardiac dysfunction by suppressing the NF-κB/NLRP3/pyroptosis pathway.

目的：心肌细胞的炎症激活和代谢紊乱是脓毒症相关心功能障碍的重要机制。山柰素（Kae）是一种类黄酮化合物，具有抗炎和抗糖化作用等多种特性。因此，本研究旨在探讨Kae对败血症性心功能障碍的保护作用。方法：C57BL/ 6j小鼠经Kae处理2 h后，再进行脂多糖（LPS）处理。12 h后进行超声心动图测量。采用血清试验、病理分析、转录组学、western blotting、RT-PCR等方法探讨其发病机制。另外，在体外用Kae （10 μM）预处理H9c2和AC16心肌细胞2 h，然后用LPS （1 μg/mL）刺激。结果：在体内，Kae预处理可减轻lps诱导的心功能障碍。Kae可抑制LPS介导小鼠心脏组织中IL-6、TNF-α、IL-1β和IL-18的水平。此外，血清学和组织学评估表明，Kae对lps诱导的心肌细胞损伤和凋亡具有保护作用。转录组学分析显示，核因子κ b (NF-κB)/NLRP3信号通路可能是其重要机制。同时证明LPS可显著激活NF-κB/NLRP3诱导心肌细胞焦亡，而Kae可减轻心肌细胞焦亡。体外对H9c2和AC16心肌细胞进行Kae预处理后再进行LPS刺激，可抑制NF-κB/NLRP3通路，降低Il-6、Tnf-α、Il-1β mRNA水平。Nlrp3敲除（Nlrp3 -/-）小鼠证实，Kae通过抑制Nlrp3改善lps诱导的特异性心肌病。结论：本研究证实Kae可通过抑制NF-κB/NLRP3/焦亡通路减轻lps诱导的左室重构和心功能障碍。

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引用次数: 0

Targeting P4HA1 Inhibits Colorectal Cancer Growth, Metastasis, and Tumor-Associated Macrophage Infiltration via P4HA2-PI3K-AKT Pathway 靶向P4HA1通过P4HA2-PI3K-AKT通路抑制结直肠癌生长、转移和肿瘤相关巨噬细胞浸润

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2025-12-30 DOI: 10.1002/iid3.70315

Nanlin Cao, Yuan Li, Zhijie Chen, Zuliang Deng, Yangzhi Hu

Background

Colorectal cancer (CRC) is a leading cause of cancer-related mortality, which necessitates the exploration of novel therapeutic targets.

Objective

This study aims to investigate the effects of Prolyl 4-hydroxylase subunit alpha-1 (P4HA1) inhibition on CRC tumor growth, metastasis, and tumor-associated macrophage (TAM) infiltration.

Methods

The association between P4HA1 expression and CRC progression as well as tumor immune infiltration was analyzed. In vitro experiments were performed to evaluate the effect of targeting P4HA1 on CRC cell proliferation and migration. The secretion of CCL2, CCL4, and CCL7 and recruitment of TAMs were detected after P4HA1 knockdown. Mechanistic studies were conducted to explore the interaction between P4HA1 and P4HA2 and its regulation on the PI3K-AKT signaling pathway. In vivo experiments were also carried out to verify the effect of P4HA1 knockdown on CRC tumor growth, metastasis, and TAM infiltration polarization.

Results

P4HA1 expression was found to be associated with CRC progression and tumor immune infiltration. Targeting P4HA1 significantly suppressed CRC cell proliferation and migration in vitro. Moreover, P4HA1 knockdown reduced the secretion of CCL2, CCL4, CCL7 and the recruitment of TAMs. Mechanistically, P4HA1 interacted with P4HA2, thereby disrupting the PI3K-AKT signaling pathway which is crucial for CRC progression and TAMs recruitment. In vivo experiments confirmed that P4HA1 knockdown inhibited CRC tumor growth, metastasis, and TAM infiltration polarization.

Conclusion

Our findings elucidate the importance of the P4HA1-P4HA2-PI3K-AKT axis in CRC and identify P4HA1 as a promising therapeutic target to impede CRC growth and metastasis while altering the tumor immune landscape. This research provides a foundation for further investigations into P4HA1-targeted therapies, which may improve clinical outcomes for patients with CRC.

背景：结直肠癌（Colorectal cancer， CRC）是癌症相关死亡的主要原因之一，因此需要探索新的治疗靶点。目的：探讨脯氨酸4-羟化酶亚基α -1 （P4HA1）抑制对结直肠癌肿瘤生长、转移及肿瘤相关巨噬细胞（TAM）浸润的影响。方法：分析P4HA1表达与结直肠癌进展及肿瘤免疫浸润的关系。体外实验评估靶向P4HA1对结直肠癌细胞增殖和迁移的影响。P4HA1敲除后检测CCL2、CCL4、CCL7的分泌和tam的募集。通过机制研究，探讨P4HA1与P4HA2的相互作用及其对PI3K-AKT信号通路的调控作用。体内实验也验证了P4HA1敲低对结直肠癌肿瘤生长、转移和TAM浸润极化的影响。结果：P4HA1表达与结直肠癌的进展和肿瘤免疫浸润有关。靶向P4HA1可显著抑制CRC细胞的体外增殖和迁移。此外，P4HA1敲低可减少CCL2、CCL4、CCL7的分泌和tam的募集。从机制上讲，P4HA1与P4HA2相互作用，从而破坏了PI3K-AKT信号通路，而PI3K-AKT信号通路对于结直肠癌的进展和tam的募集至关重要。体内实验证实P4HA1敲低抑制CRC肿瘤生长、转移和TAM浸润极化。结论：我们的研究结果阐明了P4HA1- p4ha2 - pi3k - akt轴在结直肠癌中的重要性，并确定P4HA1是一个有希望的治疗靶点，可以在改变肿瘤免疫景观的同时阻止结直肠癌的生长和转移。本研究为进一步研究p4ha1靶向治疗提供了基础，可能改善结直肠癌患者的临床预后。

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引用次数: 0

EXPRESSION OF CONCERN: Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β 关注表达：丹酚酸B通过下调TLR4、p-p38MAPK、p-JNK、NF-κB和IL-1β对小鼠脑缺血再灌注损伤的神经保护机制

IF 2.7 4区医学 Q3 IMMUNOLOGY

Immunity, Inflammation and Disease

Pub Date : 2025-12-30 DOI: 10.1002/iid3.70314

EXPRESSION OF CONCERN: X. Zheng, X. Zhang, L. Dong, J. Zhao, C. Zhang and R. Chen, “Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β,” Immunity, Inflammation and Disease 11, no. 10 (2023): e1030, https://doi.org/10.1002/iid3.1030.

This Expression of Concern is for the above article, published online on 04 October 2023 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley & Sons Ltd. The Expression of Concern has been agreed upon due to inconsistencies and discrepancies identified in Figure 2. Although the authors provided some raw data corresponding to the study, the data supplied was incomplete. Additionally, the authors were unable to provide documentation of ethics approval granted prior to the commencement of the study, as required. Instead, retrospective approval was obtained. The journal is issuing this expression of concern to alert readers.

关注表达：郑霞，张霞，董莉，赵军，张超，陈仁，“丹参酚酸B通过下调TLR4、p-p38MAPK、p-JNK、NF-κB和IL-1β对小鼠脑缺血再灌注损伤的神经保护机制”，《免疫与炎症杂志》，第11期，no。10 (2023): e1030, https://doi.org/10.1002/iid3.1030.This对上述文章表示关注，该文章已于2023年10月4日在线发表在Wiley在线图书馆（wileyonlinelibrary.com）上，并已由期刊主编Marc Veldhoen；及约翰威利父子有限公司。由于图2中确定的不一致和差异，关注表达已经达成一致。虽然作者提供了一些与该研究相对应的原始数据，但所提供的数据并不完整。此外，作者无法按要求提供在研究开始前获得伦理批准的文件。相反，获得了回顾性批准。《华尔街日报》发表这篇文章是为了提醒警惕的读者。

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引用次数: 0