Document Detail


NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNA.
MedLine Citation:
PMID:  22184724     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Group B streptococci, a major cause of sepsis, induce inflammatory cytokines in strict dependence on bacterial ssRNA and the host molecules MyD88 and UNC-93B. In this study, we show that NO plays an important role in Group B streptococci-induced transcriptional activation of cytokine genes. Phagocytosis induced NO in a MyD88-dependent fashion. In turn, NO propagated the acidification of phagosomes and the processing of phagosomal bacterial nucleic acids and was required for potent transcriptional activation of cytokine genes by streptococci. This NO-dependent amplification loop has important mechanistic implications for the anti-streptococcal macrophage response and sepsis pathogenesis.
Authors:
Sachin D Deshmukh; Sabrina Müller; Katrin Hese; Katharina S Rauch; Julia Wennekamp; Osamu Takeuchi; Shizuo Akira; Douglas T Golenbock; Philipp Henneke
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-12-19
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  188     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-06     Completed Date:  2012-02-21     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  774-80     Citation Subset:  AIM; IM    
Affiliation:
Center of Chronic Immunodeficiency, University of Freiburg, 79106 Freiburg, Germany. Sachin.Deshmukh@uniklinik-freiburg.de
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line, Transformed
Cytokines / biosynthesis*
Humans
Infant, Newborn
Macrophages / immunology*,  metabolism,  microbiology*
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Myeloid Differentiation Factor 88 / deficiency,  physiology
Nitric Oxide / biosynthesis,  physiology*
Nitric Oxide Synthase Type II / deficiency,  genetics
Phagocytosis / immunology
Phagosomes / immunology,  microbiology
RNA Processing, Post-Transcriptional / immunology*
RNA, Bacterial / metabolism*
Streptococcus agalactiae / genetics,  immunology*
Grant Support
ID/Acronym/Agency:
R01 AI052455-10/AI/NIAID NIH HHS; R0I AI052455-06A1/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/Myd88 protein, mouse; 0/Myeloid Differentiation Factor 88; 0/RNA, Bacterial; 10102-43-9/Nitric Oxide; EC 1.14.13.39/Nitric Oxide Synthase Type II
Comments/Corrections

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