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Sepsis is defined as a kind of life-threatening organ dysfunction due to a dysregulated host immune response to infection and is a leading cause of mortality in the intensive care unit. Sepsis-induced myocardial dysfunction, also called septic cardiomyopathy, is a common and serious complication in patients with sepsis, which may indicate a bad prognosis. Although efforts have been made to uncover the pathophysiology of septic cardiomyopathy, a number of uncertainties remain. This article sought to review available literature to summarize the existing knowledge on current diagnostic tools and biomarkers, pathogenesis, and treatments for septic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Interleukin-10 (IL-10) promotes the formation and development of malignant pleural effusion (MPE). Previous studies have elucidated the pathogenesis from the view of the immune-regulation function of CD4+ T-cells. However, the underlying mechanism is still not fully understood. In this study, our results showed that IL-10 deficiency reduced the percentage of macrophages in mouse MPE and regulated M1/M2 polarization in vivo and in vitro. The migration capacity of tumor cells was suppressed, and apoptosis was promoted when tumor cells were cocultured with MPE macrophages in the absence of IL-10. Messenger RNA sequencing of MPE macrophages showed that S100A9 was downregulated in IL-10−/− mice. Bone marrow-derived macrophages obtained from wild-type mice transfected with S100A9-specific small interfering RNAs (siRNAs) also showed less M2 and more M1 polarization than those from the siRNA control group. Furthermore, downregulation of S100A9 using S100A9-specific siRNA suppressed MPE development, decreased macrophages, and modulated macrophage polarization in MPE in vivo. In conclusion, S100A9 plays a vital role in the process of IL-10 deficiency-mediated MPE suppression by regulating M1/M2 polarization, thus influencing the tumor-migration capacity and apoptosis. This could result in clinically applicable strategies to inhibit the formation of MPE by regulating the polarization of MPE macrophages. [ABSTRACT FROM AUTHOR]

Abnormal function of immune cells is one of the key mechanisms leading to severe clinical symptoms in coronavirus disease 2019 patients, and metabolic pathways can destroy the function of the immune system by affecting innate and adaptive immune responses. However, the metabolic characteristics of the immune cells of the SARS-CoV-2 infected organs in situ remaining elusive. We reanalyzed the metabolic-related gene profiles in single-cell RNA sequencing data, drew the metabolic landscape in bronchoalveolar lavage fluid immune cells, and elucidated the metabolic remodeling mechanism that might lead to the progression of COVID-19 and the cytokine storm. Enhanced glycolysis is the most important common metabolic feature of all immune cells in COVID-19 patients. CCL2+ T cells, Group 2 macrophages with high SPP1 expression and myeloid dendritic cells are among the main contributors to the cytokine storm produced by infected lung tissue. Two metabolic analysis methods, including Compass, showed that glycolysis, fatty acid metabolism, bile acid synthesis and purine and pyrimidine metabolism levels of CCL2+ T cells, Group 2 macrophages and myeloid dendritic cells were upregulated and correlated with cytokine storms of COVID-19 patients. This might be the key metabolic regulatory factor for immune cells to produce large quantities of cytokines. [ABSTRACT FROM AUTHOR]

The role of IL‐10 in malignant pleural effusion (MPE) remains unknown. By using murine MPE models, we observed that an increase in pleural IL‐10 was a significant predictor of increased risk of death. We noted that TH1‐ and TH17‐cell content in MPE was higher in IL‐10–/– mice than in WT mice, and IL‐10 deficiency promoted differentiation into TH1 but not into TH17 cells. A higher fraction of TH1 and TH17 cells in the MPE of IL‐10–/– mice expressed CXCR3 compared with WT mice. We also demonstrated that Lewis lung cancer and colon adenocarcinoma cells secreted large amounts of CXCL10, a ligand of CXCR3, which induced the migration of TH1 and TH17 cells into the MPE, and IFN‐γ could promote this signaling cascade. Furthermore, intrapleural injection of mice with CXCL10‐deficient tumor cells led to decreased TH1‐ and TH17‐cell content in MPE, increased MPE volume, and reduced survival of MPE‐bearing mice. Taken together, we demonstrated that IL‐10 deficiency promoted T‐cell differentiation into TH1 cells and upregulated the CXCR3‐CXCL10 signaling pathway that recruits TH1 and TH17 cells into MPE, ultimately resulting in decreased MPE formation and longer survival time of mice‐bearing MPE. IL‐10 promoted the development of malignant pleural effusion by suppressing the differentiation of naïve CD4+ T cells into TH1 cells and by suppressing the CXCR3‐CXCL10 signal that traffics TH1 and TH17 cells into the pleural space. [ABSTRACT FROM AUTHOR]