دورية أكاديمية

Flagellar motility is a key determinant of the magnitude of the inflammasome response to Pseudomonas aeruginosa.

التفاصيل البيبلوغرافية
العنوان: Flagellar motility is a key determinant of the magnitude of the inflammasome response to Pseudomonas aeruginosa.
المؤلفون: Patankar YR; Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, New Hampshire, USA., Lovewell RR, Poynter ME, Jyot J, Kazmierczak BI, Berwin B
المصدر: Infection and immunity [Infect Immun] 2013 Jun; Vol. 81 (6), pp. 2043-52. Date of Electronic Publication: 2013 Mar 25.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Society For Microbiology Country of Publication: United States NLM ID: 0246127 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1098-5522 (Electronic) Linking ISSN: 00199567 NLM ISO Abbreviation: Infect Immun Subsets: MEDLINE
أسماء مطبوعة: Publication: Washington, DC : American Society For Microbiology
Original Publication: [Bethesda, Md.] American Society for Microbiology.
مواضيع طبية MeSH: Flagella/*physiology , Inflammasomes/*metabolism , Movement/*physiology , Pseudomonas Infections/*microbiology , Pseudomonas aeruginosa/*metabolism, Animals ; Apoptosis Regulatory Proteins ; CARD Signaling Adaptor Proteins ; Caspase 1/genetics ; Caspase 1/metabolism ; Cell Death ; Cytoskeletal Proteins/genetics ; Cytoskeletal Proteins/metabolism ; Dendritic Cells/metabolism ; Gene Expression Regulation/immunology ; Inflammasomes/genetics ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Macrophages, Peritoneal/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phagocytosis ; Pseudomonas Infections/immunology ; Pseudomonas aeruginosa/cytology ; Pseudomonas aeruginosa/immunology
مستخلص: We previously demonstrated that bacterial flagellar motility is a fundamental mechanism by which host phagocytes bind and ingest bacteria. Correspondingly, loss of bacterial motility, consistently observed in clinical isolates from chronic Pseudomonas aeruginosa infections, enables bacteria to evade association and ingestion of P. aeruginosa by phagocytes both in vitro and in vivo. Since bacterial interactions with the phagocyte cell surface are required for type three secretion system-dependent NLRC4 inflammasome activation by P. aeruginosa, we hypothesized that reduced bacterial association with phagocytes due to loss of bacterial motility, independent of flagellar expression, will lead to reduced inflammasome activation. Here we report that inflammasome activation is reduced in response to nonmotile P. aeruginosa. Nonmotile P. aeruginosa elicits reduced IL-1β production as well as caspase-1 activation by peritoneal macrophages and bone marrow-derived dendritic cells in vitro. Importantly, nonmotile P. aeruginosa also elicits reduced IL-1β levels in vivo in comparison to those elicited by wild-type P. aeruginosa. This is the first demonstration that loss of bacterial motility results in reduced inflammasome activation and antibacterial IL-1β host response. These results provide a critical insight into how the innate immune system responds to bacterial motility and, correspondingly, how pathogens have evolved mechanisms to evade the innate immune system.
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معلومات مُعتمدة: P20 RR016437 United States RR NCRR NIH HHS; R01 AI067405 United States AI NIAID NIH HHS; T32 GM008704 United States GM NIGMS NIH HHS; R01 HL107291 United States HL NHLBI NIH HHS; GM008704 United States GM NIGMS NIH HHS; AI0073634 United States AI NIAID NIH HHS; P30 CA023108 United States CA NCI NIH HHS; P20RR016437 United States RR NCRR NIH HHS
المشرفين على المادة: 0 (Apoptosis Regulatory Proteins)
0 (CARD Signaling Adaptor Proteins)
0 (Cytoskeletal Proteins)
0 (Inflammasomes)
0 (Interleukin-1beta)
0 (Pycard protein, mouse)
EC 3.4.22.36 (Caspase 1)
تواريخ الأحداث: Date Created: 20130327 Date Completed: 20130808 Latest Revision: 20211021
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3676033
DOI: 10.1128/IAI.00054-13
PMID: 23529619
قاعدة البيانات: MEDLINE
الوصف
تدمد:1098-5522
DOI:10.1128/IAI.00054-13