2.50
Hdl Handle:
http://hdl.handle.net/10033/620540
Title:
Lung epithelium and myeloid cells cooperate to clear acute pneumococcal infection.
Authors:
Dudek, M; Puttur, F; Arnold-Schrauf, C; Kühl, A A; Holzmann, B; Henriques-Normark, B; Berod, L; Sparwasser, T
Abstract:
The Gram-positive bacterium Streptococcus pneumoniae causes life-threatening infections, especially among immunocompromised patients. The host's immune system senses S. pneumoniae via different families of pattern recognition receptors, in particular the Toll-like receptor (TLR) family that promotes immune cell activation. Yet, while single TLRs are dispensable for initiating inflammatory responses against S. pneumoniae, the central TLR adapter protein myeloid differentiation factor 88 (MyD88) is of vital importance, as MyD88-deficient mice succumb rapidly to infection. Since MyD88 is ubiquitously expressed in hematopoietic and non-hematopoietic cells, the extent to which MyD88 signaling is required in different cell types to control S. pneumoniae is unknown. Therefore, we used novel conditional knockin mice to investigate the necessity of MyD88 signaling in distinct lung-resident myeloid and epithelial cells for the initiation of a protective immune response against S. pneumoniae. Here, we show that MyD88 signaling in lysozyme M (LysM)- and CD11c-expressing myeloid cells, as well as in pulmonary epithelial cells, is critical to restore inflammatory cytokine and antimicrobial peptide production, leading to efficient neutrophil recruitment and enhanced bacterial clearance. Overall, we show a novel synergistic requirement of compartment-specific MyD88 signaling in S. pneumoniae immunity.
Affiliation:
Twincore
Citation:
Lung epithelium and myeloid cells cooperate to clear acute pneumococcal infection. 2016, 9 (5):1288-302 Mucosal Immunol
Journal:
Mucosal immunology
Issue Date:
Sep-2016
URI:
http://hdl.handle.net/10033/620540
DOI:
10.1038/mi.2015.128
PubMed ID:
26627460
Type:
Article
Language:
en
ISSN:
1935-3456
Appears in Collections:
publications of the research group biomarker in infection and immunity [[TC] BIOM)

Full metadata record

DC FieldValue Language
dc.contributor.authorDudek, Men
dc.contributor.authorPuttur, Fen
dc.contributor.authorArnold-Schrauf, Cen
dc.contributor.authorKühl, A Aen
dc.contributor.authorHolzmann, Ben
dc.contributor.authorHenriques-Normark, Ben
dc.contributor.authorBerod, Len
dc.contributor.authorSparwasser, Ten
dc.date.accessioned2016-09-29T09:03:26Z-
dc.date.available2016-09-29T09:03:26Z-
dc.date.issued2016-09-
dc.identifier.citationLung epithelium and myeloid cells cooperate to clear acute pneumococcal infection. 2016, 9 (5):1288-302 Mucosal Immunolen
dc.identifier.issn1935-3456-
dc.identifier.pmid26627460-
dc.identifier.doi10.1038/mi.2015.128-
dc.identifier.urihttp://hdl.handle.net/10033/620540-
dc.description.abstractThe Gram-positive bacterium Streptococcus pneumoniae causes life-threatening infections, especially among immunocompromised patients. The host's immune system senses S. pneumoniae via different families of pattern recognition receptors, in particular the Toll-like receptor (TLR) family that promotes immune cell activation. Yet, while single TLRs are dispensable for initiating inflammatory responses against S. pneumoniae, the central TLR adapter protein myeloid differentiation factor 88 (MyD88) is of vital importance, as MyD88-deficient mice succumb rapidly to infection. Since MyD88 is ubiquitously expressed in hematopoietic and non-hematopoietic cells, the extent to which MyD88 signaling is required in different cell types to control S. pneumoniae is unknown. Therefore, we used novel conditional knockin mice to investigate the necessity of MyD88 signaling in distinct lung-resident myeloid and epithelial cells for the initiation of a protective immune response against S. pneumoniae. Here, we show that MyD88 signaling in lysozyme M (LysM)- and CD11c-expressing myeloid cells, as well as in pulmonary epithelial cells, is critical to restore inflammatory cytokine and antimicrobial peptide production, leading to efficient neutrophil recruitment and enhanced bacterial clearance. Overall, we show a novel synergistic requirement of compartment-specific MyD88 signaling in S. pneumoniae immunity.en
dc.language.isoenen
dc.titleLung epithelium and myeloid cells cooperate to clear acute pneumococcal infection.en
dc.typeArticleen
dc.contributor.departmentTwincoreen
dc.identifier.journalMucosal immunologyen

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