Innate Immunity最新文献_第9页

Does chronic dietary exposure to the mycotoxin deoxynivalenol affect the porcine hepatic transcriptome when an acute-phase response is initiated through first or second-pass LPS challenge of the liver? 当通过肝脏的第一次或第二次LPS刺激引发急性期反应时，慢性饮食暴露于真菌毒素脱氧雪腐镰刀菌醇是否会影响猪肝脏转录组?

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-07-01 Epub Date: 2021-07-31 DOI: 10.1177/17534259211030563

Sven Dänicke, Ann-Katrin Heymann, Michael Oster, Klaus Wimmers, Tanja Tesch, Erik Bannert, Susanne Bühler, Susanne Kersten, Jana Frahm, Jeannette Kluess, Stefan Kahlert, Hermann-Josef Rothkötter, Fabian Billenkamp

{"title":"Does chronic dietary exposure to the mycotoxin deoxynivalenol affect the porcine hepatic transcriptome when an acute-phase response is initiated through first or second-pass LPS challenge of the liver?","authors":"Sven Dänicke, Ann-Katrin Heymann, Michael Oster, Klaus Wimmers, Tanja Tesch, Erik Bannert, Susanne Bühler, Susanne Kersten, Jana Frahm, Jeannette Kluess, Stefan Kahlert, Hermann-Josef Rothkötter, Fabian Billenkamp","doi":"10.1177/17534259211030563","DOIUrl":"https://doi.org/10.1177/17534259211030563","url":null,"abstract":"The sensitivity of pigs to deoxynivalenol (DON) might be increased by systemic inflammation (SI), which also has consequences for hepatic integrity. Liver lesions and a dys-regulated gene network might hamper hepatic handling and elimination of DON whereby the way of initiation of hepatic inflammation might play an additional role. First and second-pass exposure of the liver with LPS for triggering a SI was achieved by LPS infusion via pre- or post-hepatic venous route, respectively. Each infusion group was pre-conditioned either with a control diet (0.12 mg DON/kg diet) or with a DON-contaminated diet (4.59 mg DON/kg diet) for 4 wk. Liver transcriptome was evaluated at 195 min after starting infusions. DON exposure alone failed to modulate the mRNA expression significantly. However, pre- and post-hepatic LPS challenges prompted transcriptional responses in immune and metabolic levels. The mRNAs for B-cell lymphoma 2-like protein 11 as a key factor in apoptosis and IFN-γ released by T cells were clearly up-regulated in DON-fed group infused with LPS post-hepatically. On the other hand, mRNAs for nucleotide binding oligomerization domain containing 2, IFN-α and eukaryotic translation initiation factor 2α kinase 3 as ribosomal stress sensors were exclusively up-regulated in control pigs with pre-hepatic LPS infusion. These diverse effects were traced back to differences in TLR4 signalling.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 5","pages":"388-408"},"PeriodicalIF":3.2,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a2/3b/10.1177_17534259211030563.PMC8419296.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39267456","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

Synergistic effect of genetic polymorphisms in TLR6 and TLR10 genes on the risk of pulmonary tuberculosis in a Moldavian population. TLR6和TLR10基因遗传多态性对摩尔多瓦人群肺结核风险的协同作用

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-07-01 Epub Date: 2021-07-18 DOI: 10.1177/17534259211029996

Alexander Varzari, Igor V Deyneko, Elena Tudor, Harald Grallert, Thomas Illig

{"title":"Synergistic effect of genetic polymorphisms in TLR6 and TLR10 genes on the risk of pulmonary tuberculosis in a Moldavian population.","authors":"Alexander Varzari, Igor V Deyneko, Elena Tudor, Harald Grallert, Thomas Illig","doi":"10.1177/17534259211029996","DOIUrl":"https://doi.org/10.1177/17534259211029996","url":null,"abstract":"Polymorphisms in genes that control immune function and regulation may influence susceptibility to pulmonary tuberculosis (TB). In this study, 14 polymorphisms in 12 key genes involved in the immune response (VDR, MR1, TLR1, TLR2, TLR10, SLC11A1, IL1B, IL10, IFNG, TNF, IRAK1, and FOXP3) were tested for their association with pulmonary TB in 271 patients with TB and 251 community-matched controls from the Republic of Moldova. In addition, gene-gene interactions involved in TB susceptibility were analyzed for a total of 43 genetic loci. Single nucleotide polymorphism (SNP) analysis revealed a nominal association between TNF rs1800629 and pulmonary TB (Fisher exact test P = 0.01843). In the pairwise interaction analysis, the combination of the genotypes TLR6 rs5743810 GA and TLR10 rs11096957 GT was significantly associated with an increased genetic risk of pulmonary TB (OR = 2.48, 95% CI = 1.62-3.85; Fisher exact test P value = 1.5 × 10-5, significant after Bonferroni correction). In conclusion, the TLR6 rs5743810 and TLR10 rs11096957 two-locus interaction confers a significantly higher risk for pulmonary TB; due to its high frequency in the population, this SNP combination may serve as a novel biomarker for predicting TB susceptibility.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 5","pages":"365-376"},"PeriodicalIF":3.2,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211029996","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39195722","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: 4

Long non-coding RNA ZFAS1 alleviates sepsis-induced myocardial injury via target miR-34b-5p/SIRT1. 长链非编码RNA ZFAS1通过靶miR-34b-5p/SIRT1减轻败血症诱导的心肌损伤。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-07-01 Epub Date: 2021-08-02 DOI: 10.1177/17534259211034221

Dan-Dan Chen, Hong-Wu Wang, Xing-Jun Cai

{"title":"Long non-coding RNA ZFAS1 alleviates sepsis-induced myocardial injury via target miR-34b-5p/SIRT1.","authors":"Dan-Dan Chen, Hong-Wu Wang, Xing-Jun Cai","doi":"10.1177/17534259211034221","DOIUrl":"https://doi.org/10.1177/17534259211034221","url":null,"abstract":"Long non-coding RNA ZFAS1 is down-regulated in sepsis. However, whether ZFAS1 participates in sepsis-induced cardiomyopathy (SIC) remains largely unknown. LPS injection to rats was used to establish an in vivo sepsis model, while LPS stimulation with H9C2 cell was used to mimic an in vitro sepsis-induced myocardial injury model. Western blots and quantitative RT-PCR were performed to evaluate protein and mRNA levels, respectively. ELISA was conducted to determine cytokine levels in supernatant. Flow cytometry was used to test apoptosis. Dual-luciferase assay was performed to validate binding between ZFAS1 and miR-34b-5p, miR-34b-5p and SIRT1. Our data revealed that ZFAS1 and SIRT1 were down-regulated, while miR-34b-5p was up-regulated in LPS-induced H9C2 cells. Inhibition of miR-34b-5p or overexpression of ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells. A mechanism study revealed that ZFAS1 sponged miR-34b-5p and thus elevated expression of SIRT1, which was prohibited by miR-34b-5p. ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells via the miR-34b-5p/SIRT1 axis, providing novel potential therapeutic targets for SIC.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 5","pages":"377-387"},"PeriodicalIF":3.2,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211034221","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39269232","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: 5

Effects of fatty acid nitroalkanes on signal transduction pathways and airway macrophage activation. 脂肪酸硝基烷烃对信号转导通路和气道巨噬细胞活化的影响。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-07-01 Epub Date: 2021-08-10 DOI: 10.1177/17534259211015330

Melissa L Wilkinson, Andrew J Gow

{"title":"Effects of fatty acid nitroalkanes on signal transduction pathways and airway macrophage activation.","authors":"Melissa L Wilkinson, Andrew J Gow","doi":"10.1177/17534259211015330","DOIUrl":"10.1177/17534259211015330","url":null,"abstract":"Fatty acid nitroalkenes are reversibly-reactive electrophiles that are endogenously detectable at nM concentrations and display anti-inflammatory, pro-survival actions. These actions are elicited through the alteration of signal transduction proteins via a Michael addition on nucleophilic cysteine thiols. Nitrated fatty acids (NO2-FAs), like 9- or 10-nitro-octadec-9-enolic acid, will act on signal transduction proteins directly or on key regulatory proteins to cause an up-regulation or down-regulation of the protein's expression, yielding an anti-inflammatory response. These responses have been characterized in many organ systems, such as the cardiovascular system, with the pulmonary system less well defined. Macrophages are one of the most abundant immune cells in the lung and are essential in maintaining lung homeostasis. Despite this, macrophages can play a role in both acute and chronic lung injury due to up-regulation of anti-inflammatory signal transduction pathways and down-regulation of pro-inflammatory pathways. Through their propensity to alter signal transduction pathways, NO2-FAs may be able to reduce macrophage activation during pulmonary injury. This review will focus on the implications of NO2-FAs on macrophage activation in the lung and the signal transduction pathways that may be altered, leading to reduced pulmonary injury.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 5","pages":"353-364"},"PeriodicalIF":3.2,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fa/17/10.1177_17534259211015330.PMC8419298.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39297143","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: 1

The TNF-α (-238 G/A) polymorphism could protect against development of severe sepsis. TNF-α（-238 G/A）多态性可预防严重败血症的发生。

IF 2.8 4区医学

Innate Immunity Pub Date : 2021-07-01 DOI: 10.1177/17534259211036186

A Hugo Montes, Eulalia Valle-Garay, Guadalupe Martin, Julio Collazos, Victoria Alvarez, Alvaro Meana, Laura Pérez-Is, José A Carton, Francisco Taboada, Víctor Asensi

{"title":"The TNF-α (-238 G/A) polymorphism could protect against development of severe sepsis.","authors":"A Hugo Montes, Eulalia Valle-Garay, Guadalupe Martin, Julio Collazos, Victoria Alvarez, Alvaro Meana, Laura Pérez-Is, José A Carton, Francisco Taboada, Víctor Asensi","doi":"10.1177/17534259211036186","DOIUrl":"10.1177/17534259211036186","url":null,"abstract":"Primary responses in sepsis-mediated inflammation are regulated by pro-inflammatory cytokines. Variations in the cytokine genes might modify their transcription or expression, plasma cytokines levels and response to sepsis. Activation protein-1 (AP-1) and NF-κB regulate cytokines gene expression in sepsis. A total of 90 severely septic and 91 non-infected patients were prospectively studied. IL-1α (-889 C/T), IL-1β (+3954 C/T), IL-6 (-174 G/C), TNF-α (-238 G/A), TNF-α (-308G/A), IL-8 (-251A/T) and IL-10 (-1082 G/A) SNPs, plasma IL-1β, IL-4, IL-6, IL-8, IL-10, IL-13, IFN-γ, TNF-α and monocyte chemoattractant protein 1 (MCP-1) levels, and AP-1 and NF-κB gene expression by neutrophils were assessed. A allele carriers of TNF-α (-238 G/A) SNP were less frequent among septic patients. IL-6, IL-8, IL-10, TNF-α and MCP-1 levels were higher, and AP-1 and NF-κB gene expressions lower in septic patients. Sepsis was independently associated with higher fibrinogen, neutrophils counts and IL-8 levels, lower prothrombin, absence of the variant A allele of the TNF-α (-238 G/A) SNP, and haemodynamic failure. Death was independently associated with a higher APACHE II score, higher IL-8 levels, and the diagnosis of sepsis. TNF-a (-238 G/A) SNP could protect against sepsis development. Higher IL-8 levels are predictive of sepsis and mortality.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 5","pages":"409-420"},"PeriodicalIF":2.8,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9e/06/10.1177_17534259211036186.PMC8419297.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39376818","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

miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response. miR-150和SRPK1调节AKT3表达参与lps诱导的炎症反应。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 DOI: 10.1177/17534259211018800

Yanfen Yao, Hong Wang, Xueqin Xi, Wei Sun, Junke Ge, Pibao Li

{"title":"miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response.","authors":"Yanfen Yao, Hong Wang, Xueqin Xi, Wei Sun, Junke Ge, Pibao Li","doi":"10.1177/17534259211018800","DOIUrl":"https://doi.org/10.1177/17534259211018800","url":null,"abstract":"miR-150 was found to target the 3'-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significantly reduced, while the expression of AKT3 and SRPK1 were markedly increased in LPS-treated A549, THP-1 and RAW 264.7 cells. miR-150 significantly decreased levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α, reduced the expression of AKT3, but had no impact on SRPK1 expression compared with the control group in LPS-treated A549, THP-1 and RAW 264.7 cells. AKT3 silencing only reduced the production of pro-inflammatory cytokines and showed no effect on miR-150 and SRPK1 expression. Finally, we observed that miR-150 mimics and/or silencing of SRPK1 decreased the expression of AKT3 mRNA. Besides, over-expression of miR-150 or silencing of SRPK1 also reduced the expression of AKT3 protein, which exhibited the lowest level in the miR-150 mimics plus si-SRPK1 group. However, si-SRPK1 had no effect on miR-150 level. In conclusion, miR-150 and SRPK1 separately and cooperatively participate into inflammatory responses in ALI through regulating AKT3 pathway. Increased miR-150 and silenced SRPK1 may be a novel potential factor for preventing and treating more inflammatory lung diseases.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"343-350"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211018800","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38997301","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: 5

Implication of Toll/IL-1 receptor domain containing adapters in Porphyromonas gingivalis-induced inflammation. Toll/IL-1受体结构域在牙龈卟啉单胞菌诱导炎症中的意义。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-21 DOI: 10.1177/17534259211013087

Isaac M Bugueno, Nadia Benkirane-Jessel, Olivier Huck

{"title":"Implication of Toll/IL-1 receptor domain containing adapters in Porphyromonas gingivalis-induced inflammation.","authors":"Isaac M Bugueno, Nadia Benkirane-Jessel, Olivier Huck","doi":"10.1177/17534259211013087","DOIUrl":"https://doi.org/10.1177/17534259211013087","url":null,"abstract":"Periodontitis is induced by periodontal dysbiosis characterized by the predominance of anaerobic species. TLRs constitute the classical pathway for cell activation by infection. Interestingly, the Toll/IL-1 receptor homology domain adapters initiate signaling events, leading to the activation of the expression of the genes involved in the host immune response. The aim of this study was to evaluate the effects of Porphyromonas gingivalis on the expression and protein-protein interactions among five TIR adapters (MAL, MyD88, TRIF, TRAM and SARM) in gingival epithelial cells and endothelial cells. It was observed that P. gingivalis is able to modulate the signaling cascades activated through its recognition by TLR4/2 in gingival epithelial cells and endothelial cells. Indeed, MAL-MyD88 protein-protein interactions associated with TLR4 was the main pathway activated by P. gingivalis infection. When transient siRNA inhibition was performed, cell viability, inflammation, and cell death induced by infection decreased and such deleterious effects were almost absent when MAL or TRAM were targeted. This study emphasizes the role of such TIR adapter proteins in P. gingivalis elicited inflammation and the precise evaluation of TIR adapter protein interactions may pave the way for future therapeutics in both periodontitis and systemic disease with a P. gingivalis involvement, such as atherothrombosis.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"324-342"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211013087","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38923187","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: 1

Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression. 黄芩苷通过增加miR-200b-3p表达，减弱FSTL1信号通路，从而减轻lps诱导的肺泡II型上皮细胞A549损伤。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-18 DOI: 10.1177/17534259211013887

Xin-Ya Duan, Yang Sun, Zhu-Feng Zhao, Yao-Qing Shi, Xun-Yan Ma, Li Tao, Ming-Wei Liu

{"title":"Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression.","authors":"Xin-Ya Duan, Yang Sun, Zhu-Feng Zhao, Yao-Qing Shi, Xun-Yan Ma, Li Tao, Ming-Wei Liu","doi":"10.1177/17534259211013887","DOIUrl":"https://doi.org/10.1177/17534259211013887","url":null,"abstract":"In China, baicalin is the main active component of Scutellaria baicalensis, which has been used in the treatment of inflammation-related diseases, such as inflammation-induced acute lung injury. However, its specific mechanism remains unclear. This study examined the protective effect of baicalin on LPS-induced inflammation injury of alveolar epithelial cell line A549 and explored its protective mechanism. Compared with the LPS-induced group, the proliferation inhibition rates of alveolar type II epithelial cell line A549 intervened by different concentrations of baicalin decreased significantly, as did the levels of inflammatory factors IL-6, IL-1β, prostaglandin 2 and TNF-α in the supernatant. The expression levels of inflammatory proteins inducible NO synthase (iNOS), NF-κB65, phosphorylated ERK (p-ERK1/2), and phosphorylated c-Jun N-terminal kinase (p-JNK1) significantly decreased, as did the protein expression of follistatin-like protein 1 (FSTL1). In contrast, expression of miR-200b-3p significantly increased in a dose-dependent manner. These results suggested that baicalin could significantly inhibit the expression of inflammation-related proteins and improve LPS-induced inflammatory injury in alveolar type II epithelial cells. The mechanism may be related to the inhibition of ERK/JNK inflammatory pathway activation by increasing the expression of miR-200b-3p. Thus, FSTL1 is the regulatory target of miR-200b-3p.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"294-312"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211013887","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38992137","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: 9

Anti-HMGB1 auto-Abs influence fatigue in patients with Crohn's disease. 抗hmgb1自身抗体对克罗恩病患者疲劳的影响

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-03 DOI: 10.1177/17534259211014252

Ingeborg Kvivik, Tore Grimstad, Grete Jonsson, Jan T Kvaløy, Roald Omdal

{"title":"Anti-HMGB1 auto-Abs influence fatigue in patients with Crohn's disease.","authors":"Ingeborg Kvivik, Tore Grimstad, Grete Jonsson, Jan T Kvaløy, Roald Omdal","doi":"10.1177/17534259211014252","DOIUrl":"https://doi.org/10.1177/17534259211014252","url":null,"abstract":"Fatigue is common in all chronic inflammatory and autoimmune diseases. A conceptual model for understanding the biological basis of fatigue describes it as being a part of the sickness behaviour response generated by pro-inflammatory cytokines and other mediators. We hypothesised that the pro-inflammatory high mobility group box 1 (HMGB1) protein is a fatigue-inducing molecule and that auto-Abs against HMGB1 reduce fatigue. We measured Abs against disulphide (ds) HMGB1 and fully reduced (fr) HMGB1 in plasma from 57 patients with Crohn's disease. Fatigue was rated using the fatigue visual analogue scale (fVAS) and disease activity with faecal calprotectin, C-reactive protein and the Simple Endoscopic Score for Crohn's disease. Multivariable regression models identified anti-dsHMGB1 and anti-frHMGB1 Abs as the strongest contributing factors for fVAS scores (B = -29.10 (P = 0.01), R2 = 0.17, and B = -17.77 (P = 0.01), R2 = 0.17, respectively). Results indicate that anti-HMGB1 auto-Abs alleviate fatigue possibly by down-regulating HMGB1-induced sickness behaviour.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"286-293"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211014252","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38864353","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: 4

Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization. 旋毛虫重组53-kDa蛋白通过促进M2巨噬细胞极化减轻肺焦亡对小鼠急性肺损伤的保护作用。

IF 3.2 4区医学

Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-20 DOI: 10.1177/17534259211013397

Ling-Yu Wei, An-Qi Jiang, Ren Jiang, Si-Ying Duan, Xue Xu, Ze-da-Zhong Su, Jia Xu

{"title":"Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization.","authors":"Ling-Yu Wei, An-Qi Jiang, Ren Jiang, Si-Ying Duan, Xue Xu, Ze-da-Zhong Su, Jia Xu","doi":"10.1177/17534259211013397","DOIUrl":"https://doi.org/10.1177/17534259211013397","url":null,"abstract":"Trichinella spiralis represents an effective treatment for autoimmune and inflammatory diseases. The effects of recombinant T. spiralis (TS) 53-kDa protein (rTsP53) on acute lung injury (ALI) remain unclear. Here, mice were divided randomly into a control group, LPS group, and rTsP53 + LPS group. ALI was induced in BALB/c mice by LPS (10 mg/kg) injected via the tail vein. rTsP53 (200 µl; 0.4 μg/μl) was injected subcutaneously three times at an interval of 5 d before inducing ALI in the rTsP53+LPS group. Lung pathological score, the ratio and markers of classic activated macrophages (M1) and alternatively activated macrophages (M2), cytokine profiles in alveolar lavage fluid, and pyroptosis protein expression in lung tissue were investigated. RTsP53 decreased lung pathological score. Furthermore, rTsP53 suppressed inflammation by increasing IL-4, IL-10, and IL-13. There was an increase in alveolar M2 macrophage numbers, with an increase in CD206 and arginase-1-positive cells and a decrease in alveolar M1 markers such as CD197 and iNOS. In addition, the polarization of M2 macrophages induced by rTsP53 treatment could alleviate ALI by suppressing lung pyroptosis. RTsP53 was identified as a potential agent for treating LPS-induced ALI via alleviating lung pyroptosis by promoting M2 macrophage polarization.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"27 4","pages":"313-323"},"PeriodicalIF":3.2,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/17534259211013397","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38930803","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: 8