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Activation of NLRP3...
Activation of NLRP3 by uropathogenic Escherichia coli is associated with IL-1β release and regulation of antimicrobial properties in human neutrophils
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- Demirel, Isak, 1987- (author)
- Örebro universitet,Institutionen för medicinska vetenskaper,iRiSC - Inflammatory Response and Infection Susceptibility Centre
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- Persson, Alexander, 1978- (author)
- Örebro universitet,Institutionen för medicinska vetenskaper,iRiSC - Inflammatory Response and Infection Susceptibility Centre
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- Brauner, Annelie (author)
- Karolinska Institutet
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- Särndahl, Eva, 1963- (author)
- Örebro universitet,Institutionen för medicinska vetenskaper,iRiSC - Inflammatory Response and Infection Susceptibility Centre
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- Kruse, Robert, 1972- (author)
- Örebro universitet,Institutionen för medicinska vetenskaper,Department of Clinical Research Laboratory,iRiSC - Inflammatory Response and Infection Susceptibility Centre
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- Persson, Katarina, 1962- (author)
- Örebro universitet,Institutionen för medicinska vetenskaper,iRiSC - Inflammatory Response and Infection Susceptibility Centre
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(creator_code:org_t)
- 2020-12-14
- 2020
- English.
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In: Scientific Reports. - : Nature Publishing Group. - 2045-2322. ; 10:1
- Related links:
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https://doi.org/10.1...
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https://www.nature.c...
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https://urn.kb.se/re...
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Abstract
Subject headings
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- The NLRP3 inflammasome and IL-1β have recently been linked to the severity of uropathogenic Escherichia coli (UPEC)-mediated urinary tract infection (UTI). However, not much is known about the contribution of NLRP3 to the antimicrobial properties of neutrophils and the release of IL-1β during UPEC infection. The purpose of this study was to elucidate the mechanisms behind UPEC-induced IL-1β release from human neutrophils, and to investigate the contribution of the NLRP3 inflammasome in neutrophil-mediated inhibition of UPEC growth. We found that the UPEC strain CFT073 increased the expression of NLRP3 and increased caspase-1 activation and IL-1β release from human neutrophils. The IL-1β release was mediated by the NLRP3 inflammasome and by serine proteases in an NF-κB-and cathepsin B-dependent manner. The UPEC virulence factors α-hemolysin, type-1 fimbriae and p-fimbriae were all shown to contribute to UPEC mediated IL-1β release from neutrophils. Furthermore, inhibition of caspase-1 and NLRP3 activation increased neutrophil ROS-production, phagocytosis and the ability of neutrophils to suppress UPEC growth. In conclusion, this study demonstrates that UPEC can induce NLRP3 and serine protease-dependent release of IL-1β from human neutrophils and that NLRP3 and caspase-1 can regulate the antimicrobial activity of human neutrophils against UPEC.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Microbiology in the medical area (hsv//eng)
Publication and Content Type
- ref (subject category)
- art (subject category)
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