In:
Immunology, Wiley, Vol. 143, No. 3 ( 2014-11), p. 447-461
Abstract:
Bacterial meningitis is, despite progress in research and the development of new treatment strategies, still a cause of severe neuronal sequelae. The brain is protected from penetrating pathogens by both the blood–brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G ‐protein coupled formyl peptide receptors ( FPR s), which are expressed by immune cells of the central nervous system. The expression of FPR s is up‐regulated during bacterial meningitis, but the consequence on the progression of inflammation and impact on mortality are far from clear. Therefore, we used mFPR 1 and mFPR2‐deficient mice to investigate the effects on inflammation, bacterial growth and mortality in a mouse model of pneumococcal meningitis. Our results revealed increased bacterial burden, increased neutrophil infiltration and higher mortality in mFPR 1/2‐deficient mice in comparison to wild‐type mice. The mFPR 1‐ or m FPR 2‐deficient mice also showed significantly increased glial cell density, whereas the immune responses including the expression of anti‐inflammatory cytokines and antimicrobial peptides were decreased in bacterial meningitis. Taken together, the results suggest that FPR 1 and FPR 2 play an important role in the innate immune responses against S treptococcus pneumoniae within the central nervous system and the lack of the receptors leads to a dysregulation of the inflammatory response compared with wild‐type mice.
Type of Medium:
Online Resource
ISSN:
0019-2805
,
1365-2567
DOI:
10.1111/imm.2014.143.issue-3
Language:
English
Publisher:
Wiley
Publication Date:
2014
detail.hit.zdb_id:
2006481-0
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