Innate Immunity最新文献_第3页

Retraction notice. 撤稿通知。

IF 3.2 4区医学

Innate Immunity Pub Date : 2024-02-01 Epub Date: 2024-03-21 DOI: 10.1177/17534259231224147

引用次数: 0

Nasal mucosal fibroblasts produce IL-4 to induce Th2 response. 鼻粘膜成纤维细胞产生 IL-4 以诱导 Th2 反应。

IF 2.8 4区医学

Innate Immunity Pub Date : 2024-02-01 Epub Date: 2024-05-09 DOI: 10.1177/17534259241254623

Xianhai Zeng, Juanjuan Li, Jiangqi Liu, Lihua Mo, Yu Liu, Aizhi Zhang, Pingchang Yang, Hui Kong

{"title":"Nasal mucosal fibroblasts produce IL-4 to induce Th2 response.","authors":"Xianhai Zeng, Juanjuan Li, Jiangqi Liu, Lihua Mo, Yu Liu, Aizhi Zhang, Pingchang Yang, Hui Kong","doi":"10.1177/17534259241254623","DOIUrl":"10.1177/17534259241254623","url":null,"abstract":"Th2 polarization is essential for the pathogenesis of allergic rhinitis (AR). Th2 polarization's mechanism requires further understanding. IL-4 is the primary cytokine involved in Th2 response. Fibroblasts play a role in immune regulation. This study aims to elucidate the role of nasal mucosal fibroblast-derived IL-4 in the induction of Th2 responses. Nasal mucosal tissues were obtained from surgically removed samples from patients with nasal polyps, whether with or without AR. Fibroblasts were isolated from the tissues by flow cytometry cell sorting, and analyzed by RNA sequencing (RNAseq). The data from RNAseq showed that nasal fibroblasts expressed genes of GATA3, CD80, CD83, CD86, STAT6, IL2, IL4, IL5, IL6, IL13 and costimulatory factor. The data were verified by RT-qPCR. The level of gene activity was positively correlated with those of AR-related cytokines present in nasal secretions. Nasal fibroblasts release IL-4 upon activation. Nasal fibroblasts had the ability to transform naive CD4+ T cells into Th2 cells, which can be eliminated by inhibiting IL-4 receptor or CD28 in CD4+ T cells. To sum up, nasal mucosal fibroblasts produce IL-4, which can induce Th2 cell development. The data implicate that nasal fibroblasts are involved in the pathogenesis of nasal allergy.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":"55-65"},"PeriodicalIF":2.8,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11165659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140897971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction notice. 撤稿通知。

IF 3.2 4区医学

Innate Immunity Pub Date : 2024-02-01 Epub Date: 2024-02-29 DOI: 10.1177/17534259231224146

引用次数: 0

Mechanical gated ion channel Piezo1: Function, and role in macrophage inflammatory response. 机械门控离子通道 Piezo1：功能以及在巨噬细胞炎症反应中的作用

IF 2.8 4区医学

Innate Immunity Pub Date : 2024-02-01 Epub Date: 2024-05-06 DOI: 10.1177/17534259241249287

Yafei Xie, Lihua Hang

引用次数: 0

CRISPR activation as a platform to identify interferon stimulated genes with anti-viral function. 将 CRISPR 激活作为识别具有抗病毒功能的干扰素刺激基因的平台。

IF 2.8 4区医学

Innate Immunity Pub Date : 2024-02-01 Epub Date: 2024-01-23 DOI: 10.1177/17534259231225611

Emily N Kirby, Xavier B Montin, Timothy P Allen, Jaslan Densumite, Brooke N Trowbridge, Michael R Beard

{"title":"CRISPR activation as a platform to identify interferon stimulated genes with anti-viral function.","authors":"Emily N Kirby, Xavier B Montin, Timothy P Allen, Jaslan Densumite, Brooke N Trowbridge, Michael R Beard","doi":"10.1177/17534259231225611","DOIUrl":"10.1177/17534259231225611","url":null,"abstract":"Interferon Stimulated Gene (ISG) expression plays a key role in the control of viral replication and development of a robust adaptive response. Understanding this dynamic relationship between the pathogen and host is critical to our understanding of viral life-cycles and development of potential novel anti-viral strategies. Traditionally, plasmid based exogenous prompter driven expression of ISGs has been used to investigate anti-viral ISG function, however there are deficiencies in this approach. To overcome this, we investigated the utility of CRISPR activation (CRISPRa), which allows for targeted transcriptional activation of a gene from its endogenous promoter. Using the CRISPRa-SAM system to induce targeted expression of a panel of anti-viral ISGs we showed robust induction of mRNA and protein expression. We then employed our CRISPRa-SAM ISG panel in several antiviral screen formats to test for the ability of ISGs to prevent viral induced cytopathic cell death (CPE) and replication of Dengue Virus (DENV), Zika Virus (ZIKV), West Nile Virus Kunjin (WNVKUN), Hepatitis A Virus (HAV) and Human Coronavirus 229E (HCoV-229E). Our CRISPRa approach confirmed the anti-viral activity of ISGs like IFI6, IFNβ and IFNλ2 that prevented viral induced CPE, which was supported by high-content immunofluorescence imaging analysis. This work highlights CRISPRa as a rapid, agile, and powerful methodology to identify and characterise ISGs and viral restriction factors.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":"40-54"},"PeriodicalIF":2.8,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11165661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139520557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acacetin protects against sepsis-induced acute lung injury by facilitating M2 macrophage polarization via TRAF6/NF-κB/COX2 axis. Acacetin通过TRAF6/NF-κB/COX2轴促进M2巨噬细胞极化，保护脓毒症诱导的急性肺损伤。

IF 2.8 4区医学

Innate Immunity Pub Date : 2024-01-01 Epub Date: 2023-12-03 DOI: 10.1177/17534259231216852

Binbin Chang, Zhang Wang, Hui Cheng, Tingyuan Xu, Jieyu Chen, Wan Wu, Yizhi Li, Yong Zhang

{"title":"Acacetin protects against sepsis-induced acute lung injury by facilitating M2 macrophage polarization via TRAF6/NF-κB/COX2 axis.","authors":"Binbin Chang, Zhang Wang, Hui Cheng, Tingyuan Xu, Jieyu Chen, Wan Wu, Yizhi Li, Yong Zhang","doi":"10.1177/17534259231216852","DOIUrl":"10.1177/17534259231216852","url":null,"abstract":"Acute lung injury (ALI) is the leading cause of death in patients with sepsis syndrome and without effective protective or therapeutic treatments. Acacetin, a natural dietary flavonoid, reportedly exerts several biological effects, such as anti-tumor, anti-inflammatory, and anti-oxidative effects. However, acacetin's effect and underlying mechanism on sepsis-induced ALI remain unclear. Here, the mouse model was established to explore the impact of acacetin on sepsis-induced ALI. Acacetin significantly increased ALI murine survival and attenuated lung injury in histological examinations. Additionally, acacetin down-regulated myeloperoxidase activity, protein concentration, and number of neutrophils and macrophages in bronchoalveolar lavage fluid. Subsequently, inflammatory cytokines, including TNF-α, IL-1β, and IL-6, were examined. Results showed that acacetin dramatically suppressed the production of TNF-α, IL-1β, and IL-6. These above results indicated that acacetin attenuated sepsis-induced ALI by inhibiting the inflammatory response. Moreover, acacetin inhibited the expression of markers for M1-type (iNOS, CD86) macrophages and promoted the expression of markers for M2-type (CD206, Arg1) macrophages by western blot. In addition, acacetin down-regulated the expression TRAF6, NF-κB, and Cyclooxygenase-2 (COX2) by western blot. The high concentration of acacetin had a better effect than the low concentration. Besides, over-expression of TRAF6 up-regulated the expression of COX2, CD86, and iNOS, and the ratio of p-NF-κB to NF-κB increased the mRNA levels of TNF-α, IL-1β, and IL-6, down-regulated the expression of CD206 and Arg1. The effects of TRAF6 were the opposite of acacetin. And TRAF6 could offset the impact of acacetin. This study demonstrated that acacetin could prevent sepsis-induced ALI by facilitating M2 macrophage polarization via TRAF6/NF-κB/COX2 axis.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":"11-20"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10720600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138477606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Knockdown of DAPK1 inhibits IL-1β-induced inflammation and cartilage degradation in human chondrocytes by modulating the PEDF-mediated NF-κB and NLRP3 inflammasome pathway. 通过调节PEDF介导的NF-κB和NLRP3炎性体通路，敲除DAPK1可抑制IL-1β诱导的人软骨细胞炎症和软骨降解。

IF 2.8 4区医学

Innate Immunity Pub Date : 2024-01-01 Epub Date: 2022-11-21 DOI: 10.1177/17534259221086837

Zhongyuan Zhao, Wei Liu, Gong Cheng, Shengjie Dong, Yuchi Zhao, Hao Wu, Zhilin Cao

{"title":"Knockdown of DAPK1 inhibits IL-1β-induced inflammation and cartilage degradation in human chondrocytes by modulating the PEDF-mediated NF-κB and NLRP3 inflammasome pathway.","authors":"Zhongyuan Zhao, Wei Liu, Gong Cheng, Shengjie Dong, Yuchi Zhao, Hao Wu, Zhilin Cao","doi":"10.1177/17534259221086837","DOIUrl":"10.1177/17534259221086837","url":null,"abstract":"Osteoarthritis (OA) is a common joint disease that is characterized by inflammation and cartilage degradation. Death-associated protein kinase 1 (DAPK1) is a multi-domain serine/threonine kinase and has been reported to be involved in the progression of OA. However, its role and mechanism in OA remain unclear. Here, we found the expression of DAPK1 in OA cartilage tissues was higher than that in normal cartilage tissues. The expression of DAPK1 in chondrocytes was up-regulated by IL-1β. Knockdown of DAPK1 promoted cell viability and anti-apoptotic protein expression, while it inhibited the apoptosis rate and pro-apoptotic protein expressions in IL-1β-induced chondrocytes. In addition, DAPK1 inhibition reduced the levels of inflammatory cytokines and expressions of matrix metalloproteinases (MMPs), and increased the expressions of collagen II and aggrecan. The data of mechanistic investigation indicated that the expression of pigment epithelium-derived factor (PEDF) was positively regulated by DAPK1. Overexpression of PEDF attenuated the effects of DAPK1 knockdown on IL-1β-induced cell viability, apoptosis, inflammation, and cartilage degradation. Furthermore, PEDF overexpression restored the activity of the NF-κB pathway and NLRP3 inflammasome after DAPK1 knockdown. Collectively, down-regulation of DAPK1 inhibited IL-1β-induced inflammation and cartilage degradation via the PEDF-mediated NF-κB and NLRP3 inflammasome pathways.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":"21-30"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10720599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40480841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immunomodulatory actions of myeloid-derived suppressor cells in the context of innate immunity. 先天免疫背景下髓源性抑制细胞的免疫调节作用。

IF 2.8 4区医学

Innate Immunity Pub Date : 2024-01-01 Epub Date: 2023-11-28 DOI: 10.1177/17534259231215581

Nikoleta Bizymi, Andreas M Matthaiou, Irene Mavroudi, Aristea Batsali, Helen A Papadaki

引用次数: 0

Obesity Alters cytokine signaling and gut microbiome in septic mice. 肥胖改变脓毒症小鼠的细胞因子信号传导和肠道微生物组。

IF 2.8 4区医学

Innate Immunity Pub Date : 2023-11-01 Epub Date: 2023-10-06 DOI: 10.1177/17534259231205959

Lauren Bodilly, Lauren Williamson, Patrick Lahni, Matthew N Alder, David B Haslam, Jennifer M Kaplan

{"title":"Obesity Alters cytokine signaling and gut microbiome in septic mice.","authors":"Lauren Bodilly, Lauren Williamson, Patrick Lahni, Matthew N Alder, David B Haslam, Jennifer M Kaplan","doi":"10.1177/17534259231205959","DOIUrl":"10.1177/17534259231205959","url":null,"abstract":"Sepsis is a leading cause of mortality. Plasma cytokine levels may identify those at increased risk of mortality from sepsis. Our aim was to understand how obesity alters cytokine levels during early sepsis and its correlation with survival. Six-week-old C57BL/6 male mice were randomized to control (non-obese) or high fat diet (obese) for 5-7 weeks. Sepsis was induced by cecal ligation and perforation (CLP). Cytokine levels were measured from cheek bleeds 8 h after CLP, and mice were monitored for survival. Other cohorts were sacrificed 1 h after CLP for plasma and tissue. Septic obese mice had higher survival. At 8 h after sepsis, obese mice had higher adiponectin, leptin, and resistin but lower TNFα and IL-6 compared to non-obese mice. When stratified by 24-h survival, adipokines were not significantly different in obese and non-obese mice. TNFα and IL-6 were higher in non-obese, compared to obese, mice that died within 24 h of sepsis. Diet and to sepsis significantly impacted the cecal microbiome. IL-6 is a prognostic biomarker during early sepsis in non-obese and obese mice. A plausible mechanism for the survival difference in non-obese and obese mice may be the difference in gut microbiome and its evolution during sepsis.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":"161-170"},"PeriodicalIF":2.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10621470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41096068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Synthesis and validation of click-modified NOD1/2 agonists. 点击修饰NOD1/2激动剂的合成和验证。

IF 2.8 4区医学

Innate Immunity Pub Date : 2023-11-01 Epub Date: 2023-10-13 DOI: 10.1177/17534259231207198

Ravi Bharadwaj, Madison V Anonick, Swati Jaiswal, Siavash Mashayekh, Ashley Brown, Kimberly A Wodzanowski, Kendi Okuda, Neal Silverman, Catherine L Grimes

引用次数: 0