NLRP3 Knockout Enhances Immune Infiltration and Inflammatory Responses and Improves Survival in a Burn‐Sepsis Model

Immunology ◽  
2021 ◽  
Author(s):  
Mile Stanojcic ◽  
Roohi Vinaik ◽  
Abdikarim Abdullahi ◽  
Peter Chen ◽  
Marc G Jeschke
Keyword(s):  
Inflammatory Responses ◽  
Immune Infiltration ◽  
Sepsis Model

scholarly journals Astaxanthin Provides Antioxidant Protection in LPS-Induced Dendritic Cells for Inflammatory Control

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 534
Author(s):  
Yinyan Yin ◽  
Nuo Xu ◽  
Tao Qin ◽  
Bangyue Zhou ◽  
Yi Shi ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Responses ◽  
Reduced Glutathione ◽  
Bioactive Compound ◽  
Heme Oxygenase 1 ◽  
No Production ◽  
Related Factor ◽  
Oxygen Species ◽  
Sepsis Model ◽  
Antioxidant Characteristics

Astaxanthin, originating from marine organisms, is a natural bioactive compound with powerful antioxidant activity. Here, we evaluated the antioxidant ability of astaxanthin on dendritic cells (DCs), a key target of immune regulation, for inflammatory control in a sepsis model. Our results showed that astaxanthin suppressed nitric oxide (NO) production, reactive oxygen species (ROS) production, and lipid peroxidation activities in LPS-induced DCs and LPS-challenged mice. Moreover, the reduced glutathione (GSH) levels and the GSH/GSSG ratio were increased, suggesting that astaxanthin elevated the level of cellular reductive status. Meanwhile, the activities of antioxidant enzymes, including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD), were significantly upregulated. Astaxanthin also inhibited the LPS-induced secretions of IL-1β, IL-17, and TGF-β cytokines. Finally, we found that the expressions of heme oxygenase 1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) were significantly upregulated by astaxanthin in LPS-induced DCs, suggesting that the HO-1/Nrf2 pathway plays a significant role in the suppression of oxidative stress. These results suggested that astaxanthin possesses strong antioxidant characteristics in DC-related inflammatory responses, which is expected to have potential as a method of sepsis treatment.

scholarly journals A New Approach to Monitoring and Evaluation of Cecal Ligation and Puncture Sepsis Model

2021 ◽  
Vol 3 (2) ◽  
pp. 97-106
Author(s):  
Arezou Khosrojerdi ◽  
◽  
Sara Soudi ◽  
Ahmad Zavaran Hosseini ◽  
Seyed Mahmoud Hashemi ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Clinical Chemistry ◽  
Cecal Ligation ◽  
Serum Levels ◽  
Cecal Ligation And Puncture ◽  
Inflammatory Status ◽  
Sepsis Model ◽  
Tnf Α ◽  
Systemic Inflammatory Disease ◽  
Tgf Β1

Background: Sepsis is a systemic inflammatory disease in response to the pathogens that leads to vital organ failures the failure of vital organs. Appropriate animal models should be developed to measure the effectiveness of therapeutic methods. Cecal Ligation and Puncture (CLP) is the most widely used methods of creating the sepsis model. Some variables interfere in the creation of the CLP model which terminated to result in an unrepeatable dynamic of the inflammatory responses. The current research, suggests presents the simultaneous study of inflammatory responses in serum and liver as a criterion for determining the inflammatory status of the CLP model. Materials and Methods: CLP model was induced in 15 female C57bl/6 mice. IL-6, TNF-α, IL-10, and TGF-β1 cytokines levels were measured at 24, 48, and 72 hours after CLP induction in both serum and liver tissue by ELISA method. Serum levels of liver enzymes were analyzed by the clinical chemistry analyzer. All studies were performed in healthy mice as well. The results were reported as Mean±SD. Results: The levels of IL-10 and TGF- β1 in the liver is were significantly (P≤0.05) higher than serum. The production of IL-10 and TGF- β1 in the serum and liver reaches its maximum at peaked 24 and 72 hours after CLP induction. The level of TNF-α in the liver is was significantly (P≤0.05) higher than serum with a maximum production 24 hours after CLP induction. Conclusion: Serum is not a good representative of the inflammatory condition in sepsis. Therefore, it is suggested that local inflammatory responses be considered in evaluating the model, and the determination of drug efficacy.

scholarly journals Identification of Key Genes Related to Immune Infiltration of Cirrhosis via Bioinformatics Analysis

2022 ◽  
Author(s):  
Tong-Yue Du ◽  
Yi-Shan Zheng
Keyword(s):  
Immune Responses ◽  
Molecular Mechanism ◽  
Immune Cells ◽  
Bioinformatics Analysis ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Enrichment Analysis ◽  
Immune Infiltration ◽  
Tight Connection ◽  
Enrichment Function

Abstract BackgroundAccumulating researches have indicated that cirrhosis is a vital risk factor for morbidity and mortality worldwide. Nevertheless, the underlying immune-related molecular mechanism remains indistinct.MethodsGene expression profiles of GSE89377 and GSE139602 were investigated to identify differentially expressed genes (DEGs) related to cirrhosis. Enrichment analysis for DEGs was explored. CIBERSORT algorithm was used for evaluating DEGs immune infiltration. The String and Cytoscape database were utilized for analyses hub DEGs with a high tight connection, and the association between hub DEGs and immune cells infiltration was analyzed by Spearman method. Finally, the underlying molecular mechanism of the key DEGs was predicted via KEGG pathway analysis.ResultsIn all, 299 DEGs were attained among them 136 and 163 were up and down-regulated respectively. Then Enrichment function of DEGs and CIBERSORT algorithm showed that they are significant in immune and inflammatory responses. Four hub DEGs (ACTB, TAGLN, VIM, SOX9) were identified. Subsequently, the immune infiltration findings indicated that, the hub DEGs highly related immune cells. Finally, KEGGs pathways were predicted related with ACTB. ConclusionsThis study revealed key DEGs may implement inflammatory immune responses with cirrhosis, which could be used as biomarkers or therapeutic targets.

scholarly journals CXCL2/10/12/14 are prognostic biomarkers and correlated with immune infiltration in hepatocellular carcinoma

2021 ◽  
Author(s):  
Tong Lin ◽  
E Zhang ◽  
Pei-pei Mai ◽  
Ying-zhao Zhang ◽  
Xiang Chen ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Functional Enrichment ◽  
Immune Infiltration ◽  
Normal Tissues ◽  
Cancer Immunity ◽  
Chemokine Ligands ◽  
Treatment Responses ◽  
Necrosis Factor

Background: C-x-C motif chemokine ligands (CXCLs) are critical regulators of cancer immunity and angiogenesis, which affect disease progression and treatment responses. The character of each CXCL in the prognosis and immune infiltration of HCC patients is unclear yet. Methods: Differentially expressed CXCLs between HCC and normal control were screened by Oncomine and GEPIA2. Genetic alternations of CXCLs in HCC were analyzed by cBioPortal. Clinicopathological relevance of CXCLs in HCC patients was analyzed using UALCAN. The prognostic value of CXCLs was evaluated using univariate and multivariate analyses. Correlations of CXCLs’ expression with immune infiltration, chemokines and their receptors were assessed integrating TIMER, TISIDB, and GEPIA2. The co-expressed genes of CXCLs were discovered, and functional enrichment analysis was performed for them. Results: CXCL9/10 was significantly higher expressed while CXCL2/12/14 was lower expressed in HCC than normal tissues, but they didn’t show significant clinicopathological relevance in HCC patients. High-expression of CXCL2/10/12/14 indicated favorable outcomes of HCC patients. The expression of CXCL9/10/12/14 was significantly positively correlated with the infiltration and biomarkers’ expression of various tumor-infiltrating immune cells, also the abundance of chemokines and their receptors. The co-expressed genes of the five CXCLs were extracellular components and regulated immune or inflammatory responses, and signaling pathways of chemokine, Toll-like receptor, tumor necrosis factor might be involved. Conclusion: This study proposed CXCL2/10/12/14 might predict outcomes of HCC patients and were extensively related with the immune microenvironment in HCC. It would be a prospective therapeutic strategy for HCC to enhance effective immunity surveillance through intervening in these CXCLs.

Anti-β2 Glycoprotein I Antibodies Cause Inflammation and Recruit Dendritic Cells in Platelet Clearance

2001 ◽  
Vol 86 (11) ◽  
pp. 1257-1263 ◽  
Author(s):  
Attilio Bondanza ◽  
Angelo Manfredi ◽  
Valérie Zimmermann ◽  
Matteo Iannacone ◽  
Angela Tincani ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Responses ◽  
Glycoprotein I ◽  
Activated Platelets ◽  
Tnf Α ◽  
Per Se ◽  
Antigen Presenting ◽  
Antiinflammatory Cytokine

SummaryScavenger phagocytes are mostly responsible for the in vivo clearance of activated or senescent platelets. In contrast to other particulate substrates, the phagocytosis of platelets does not incite pro-inflammatory responses in vivo. This study assessed the contribution of macrophages and dendritic cells (DCs) to the clearance of activated platelets. Furthermore, we verified whether antibodies against the β2 Glycoprotein I (β2GPI), which bind to activated platelets, influence the phenomenon. DCs did not per se internalise activated platelets. In contrast, macrophages efficiently phagocytosed platelets. In agreement with the uneventful nature of the clearance of platelets in vivo, phagocytosing macrophages did not release IL-1β, TNF-α or IL-10. β2GPI bound to activated platelets and was required for their recognition by anti-ββ2GPI antibodies. DCs internalised platelets opsonised by anti-ββ2GPI antibodies. The phagocytosis of opsonised platelets determined the release of TNF-α and IL-1β by DCs and macrophages. Phagocytosing macrophages, but not DCs, secreted the antiinflammatory cytokine IL-1β0. We conclude that anti-ββ2GPI antibodies cause inflammation during platelet clearance and shuttle platelet antigens to antigen presenting DCs.

Oxidative Stress and Atherosclerosis: Its Relationship to Growth Factors, Thrombus Formation and Therapeutic Approaches

1999 ◽  
Vol 82 (S 01) ◽  
pp. 32-37 ◽  
Author(s):  
Karlheinz Peter ◽  
Wolfgang Kübler ◽  
Johannes Ruef ◽  
Thomas K. Nordt ◽  
Marschall S. Runge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factors ◽  
Vessel Wall ◽  
Inflammatory Responses ◽  
Plaque Rupture ◽  
Thrombus Formation ◽  
Vascular Lesion ◽  
Coagulation System ◽  
Therapeutic Approaches ◽  
Causative Relationship

SummaryThe initiating event of atherogenesis is thought to be an injury to the vessel wall resulting in endothelial dysfunction. This is followed by key features of atherosclerotic plaque formation such as inflammatory responses, cell proliferation and remodeling of the vasculature, finally leading to vascular lesion formation, plaque rupture, thrombosis and tissue infarction. A causative relationship exists between these events and oxidative stress in the vessel wall. Besides leukocytes, vascular cells are a potent source of oxygen-derived free radicals. Oxidants exert mitogenic effects that are partially mediated through generation of growth factors. Mitogens, on the other hand, are potent stimulators of oxidant generation, indicating a putative self-perpetuating mechanism of atherogenesis. Oxidants influence the balance of the coagulation system towards platelet aggregation and thrombus formation. Therapeutic approaches by means of antioxidants are promising in both experimental and clinical designs. However, additional clinical trials are necessary to assess the role of antioxidants in cardiovascular disease.

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