| Literature DB >> 24107312 |
Paul Lemire1, Cynthia Calzas, Mariela Segura.
Abstract
Group B Streptococcus (GBS) capsular type III is an important agent of life-threatening invasive infections. It has been previously shown that encapsulated GBS is easily internalized by dendritic cells (DCs) and this internalization has an impact on cytokine production. The intracellular receptors or pathways underlying this response are not well understood. In this work, we investigated the role of NOD2 in the pathogenesis of GBS using a mouse model of infection. NOD2(-/-) mice showed similar levels of survival and bacteremia than control mice. Interestingly, ex vivo analysis of total spleen cells from infected animals showed that the absence of NOD2 results in reduced production of inflammatory cytokines. However this abridged inflammatory response does not seem to improve mouse survival. In conclusion, we demonstrated that NOD2 is not a crucial receptor to fight GBS infection and only partially contributes to the inflammatory response.Entities:
Keywords: CPS; DCs; GBS; Group B Streptococcus; Inflammatory cytokines; NLR family pyrin domain-containing protein 3; NLRP3; NLRs; NOD1; NOD2; Pathogenesis; TLR; capsular polysaccharide; dendritic cells; nod-like receptors; nucleotide-binding oligomerization domain-containing protein 1; nucleotide-binding oligomerization domain-containing protein 2; toll-like receptor
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Year: 2013 PMID： 24107312 DOI： 10.1016/j.micpath.2013.09.006
Source DB: PubMed Journal: Microb Pathog ISSN： 0882-4010 Impact factor: 3.738