2017
DOI: 10.1128/iai.00806-16
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Flagellin-Mediated Protection against Intestinal Yersinia pseudotuberculosis Infection Does Not Require Interleukin-22

Abstract: Signaling through Toll-like receptors (TLRs), the main receptors in innate immunity, is essential for the defense of mucosal surfaces. It was previously shown that systemic TLR5 stimulation by bacterial flagellin induces an immediate, transient interleukin-22 (IL-22)-dependent antimicrobial response to bacterial or viral infections of the mucosa. This process was dependent on the activation of type 3 innate lymphoid cells (ILCs). The objective of the present study was to analyze the effects of flagellin treatm… Show more

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Cited by 6 publications
(3 citation statements)
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“…In this study, we employed a recombinant flagellin, FliC Δ174–40 , that lacks its antigenic domain. This molecule has a lower intrinsic antigenicity than native flagellin, and it has been demonstrated to be safe and effective against different pathogens after several flagellin administrations ( 7 ). Flagellin stimulation has been shown to provide protection in several disease backgrounds (e.g., Salmonella spp., Burkholderia cepacia , and Yersinia pseudotuberculosis ) ( 35 ).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In this study, we employed a recombinant flagellin, FliC Δ174–40 , that lacks its antigenic domain. This molecule has a lower intrinsic antigenicity than native flagellin, and it has been demonstrated to be safe and effective against different pathogens after several flagellin administrations ( 7 ). Flagellin stimulation has been shown to provide protection in several disease backgrounds (e.g., Salmonella spp., Burkholderia cepacia , and Yersinia pseudotuberculosis ) ( 35 ).…”
Section: Discussionmentioning
confidence: 99%
“…This process is required to trigger a signaling cascade that activates NF-κB and the MAPK (mitogen-activated protein kinases) ( 6 ), thus releasing proinflammatory cytokines. This proinflammatory signaling at the mucosal interfaces promotes the recruitment and maturation of immune cells, orchestrating an enhanced protection against pathogens ( 4 , 7 ). The flagellin-mediated proinflammatory response is believed to be short-lived because of the strong regulatory mechanisms that involve transcriptional and posttranscriptional regulators such as TNFAIP3, IκBα, or IκBε ( 8 ).…”
mentioning
confidence: 99%
“…We are the first to demonstrate that treatment with FliC is also efficient against NTHi whereas its interest has been shown in infection with other bacteria including S. pneumoniae in non-CS-exposed mice [28][29][30]. Since the pathophysiology of COPD exacerbation episodes implicated a defect in IL-22 production and a deleterious effect of neutrophils on lung function, we choose to treat our mice by intraperitoneal route rather than a local administration which promotes a strong neutrophil recruitment in the airways.…”
Section: Plos Onementioning
confidence: 99%