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Lautz, K.* ; Damm, A.* ; Menning, M.* ; Wenger, J.* ; Adam, A.C.* ; Zigrino, P.* ; Kremmer, E. ; Kufer, T.A.*

NLRP10 enhances Shigella-induced pro-inflammatory responses.

Cell. Microbiol. 14, 1568-1583 (2012)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Members of the NLR family evolved as intracellular sensors for bacterial and viral infection. However, our knowledge on the implication of most of the human NLR proteins in innate immune responses still remains fragmentary. Here we characterized the role of human NLRP10 in bacterial infection. Our data revealed that NLRP10 is a cytoplasmic localized protein that positively contributes to innate immune responses induced by the invasive bacterial pathogen Shigella flexneri. SiRNA-mediated knock-down studies showed that NLRP10 contributes to pro-inflammatory cytokine release triggered by Shigella in epithelial cells and primary dermal fibroblasts, by influencing p38 and NF-κB activation. This effect is dependent on the ATPase activity of NLRP10 and its PYD domain. Mechanistically, NLRP10 interacts with NOD1, a NLR that is pivotally involved in sensing of invasive microbes, and both proteins are recruited to the bacterial entry point at the plasma membrane. Moreover, NLRP10 physically interacts with downstream components of the NOD1 signalling pathway, such as RIP2, TAK1 and NEMO. Taken together, our data revealed a novel role of NLRP10 in innate immune responses towards bacterial infection and suggest that NLRP10 functions as a scaffold for the formation of the NOD1-Nodosome.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords NOD-LIKE RECEPTOR; NF-KAPPA-B; MURAMYL DIPEPTIDE RECOGNITION; CELL-DEATH; CONTAINING PROTEIN; EPITHELIAL-CELLS; GENE-EXPRESSION; III SECRETION; ACTIVATION; FLEXNERI
ISSN (print) / ISBN 1462-5814
e-ISSN 1462-5822
Journal Cellular Microbiology
Quellenangaben Volume: 14, Issue: 10, Pages: 1568-1583 Article Number: , Supplement: ,
Publisher Wiley
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Molecular Immunology (IMI)