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Neisseria meningitidis-Induced Caspase-1 Activation in Human Innate Immune Cells Is LOS-Dependent
Örebro University, School of Medical Sciences. iRiSC-Inflammatory Response and Infection Susceptibility Centre.
iRiSC-Inflammatory Response and Infection Susceptibility Centre, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Karolinska University Hospital, Solna, Stockholm, Sweden.
Örebro University, School of Medical Sciences. Örebro University Hospital. iRiSC-Inflammatory Response and Infection Susceptibility Centre.
Örebro University, School of Medical Sciences. iRiSC-Inflammatory Response and Infection Susceptibility Centre.
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2019 (English)In: Journal of Immunology Research, ISSN 2314-8861, E-ISSN 2314-7156, article id 6193186Article in journal (Refereed) Published
Abstract [en]

Meningococcal disease such as sepsis and meningitidis is hallmarked by an excessive inflammatory response. The causative agent, Neisseria meningitidis, expresses the endotoxin lipooligosaccharide (LOS) that is responsible for activation of immune cells and the release of proinflammatory cytokines. One of the most potent proinflammatory cytokines, interleukin-1 (IL-1), is activated following caspase-1 activity in the intracellular multiprotein complex called inflammasome. Inflammasomes are activated by a number of microbial factors as well as danger molecules by a two-step mechanismpriming and licensing of inflammasome activationbut there are no data available regarding a role for inflammasome activation in meningococcal disease. The aim of this study was to investigate if N. meningitidis activates the inflammasome and, if so, the role of bacterial LOS in this activation. Cells were subjected to N. meningitidis, both wild-type (FAM20) and its LOS-deficient mutant (lpxA), and priming as well as licensing of inflammasome activation was investigated. The wild-type LOS-expressing parental FAM20 serogroup C N. meningitidis (FAM20) strain significantly enhanced the caspase-1 activity in human neutrophils and monocytes, whereas lpxA was unable to induce caspase-1 activity as well as to induce IL-1 release. While the lpxA mutant induced a priming response, measured as increased expression of NLRP3 and IL1B, the LOS-expressing FAM20 further increased this priming. We conclude that although non-LOS components of N. meningitidis contribute to the priming of the inflammasome activity, LOS per se is to be considered as the central component of N. meningitidis virulence, responsible for both priming and licensing of inflammasome activation.

Place, publisher, year, edition, pages
Hindawi Publishing Corporation, 2019. article id 6193186
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Immunology in the medical area
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URN: urn:nbn:se:oru:diva-74647DOI: 10.1155/2019/6193186ISI: 000468500900001OAI: oai:DiVA.org:oru-74647DiVA, id: diva2:1321954
Available from: 2019-06-10 Created: 2019-06-10 Last updated: 2019-06-10Bibliographically approved

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Asfaw Idosa, BerhaneJacobsson, SusanneDemirel, IsakSärndahl, EvaPersson, Alexander

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