Dectin-2-dependent host defense in mice infected with serotype 3 Streptococcus pneumoniae. (December 2016)
- Record Type:
- Journal Article
- Title:
- Dectin-2-dependent host defense in mice infected with serotype 3 Streptococcus pneumoniae. (December 2016)
- Main Title:
- Dectin-2-dependent host defense in mice infected with serotype 3 Streptococcus pneumoniae
- Authors:
- Akahori, Yukiko
Miyasaka, Tomomitsu
Toyama, Masahiko
Matsumoto, Ikumi
Miyahara, Anna
Zong, Tong
Ishii, Keiko
Kinjo, Yuki
Miyazaki, Yoshitsugu
Saijo, Shinobu
Iwakura, Yoichiro
Kawakami, Kazuyoshi - Abstract:
- Abstract Background Streptococcus pneumoniae, a major causative bacterial pathogen of community-acquired pneumonia, possesses a thick polysaccharide capsule. Host defense against this bacterium is mediated by activation of innate immune cells that sense bacterial components. Recently, C-type lectin receptors (CLRs) have garnered much attention in elucidating the recognition mechanism of pathogen-derived polysaccharides. Methods In the present study, we first compared the clinical course and neutrophil accumulation in the lungs of Dectin-2 knock-out (KO) and wild type (WT) mice. Mice were infected intratracheally with a serotype 3 strain ofS. pneumoniae, andS. pneumoniae bacterial engulfment by neutrophils and inflammatory cytokine and anti-pneumococcal polysaccharide-specific IgG levels were evaluated in bronchoalveolar lavage fluid (BALF). We also examined the effect of Dectin-2 deficiency on interleukin (IL)-12 production by bone marrow-derived dendritic cells (BM-DCs) stimulated with the bacterial components. Results S. pneumonia- infected Dectin-2KO mice had a shorter survival time, larger bacterial burden and lower interferon gamma (IFN-γ) production in the lungs than WT mice. Although neutrophilic infiltration in the lungs was equivalent between Dectin-2KO mice and WT mice, S. pneumonia engulfment by neutrophils was attenuated in Dectin-2KO mice compared to WT mice. The anti-pneumococcal polysaccharide-specific IgG and IgG3 levels in BALF were lower in Dectin-2KO miceAbstract Background Streptococcus pneumoniae, a major causative bacterial pathogen of community-acquired pneumonia, possesses a thick polysaccharide capsule. Host defense against this bacterium is mediated by activation of innate immune cells that sense bacterial components. Recently, C-type lectin receptors (CLRs) have garnered much attention in elucidating the recognition mechanism of pathogen-derived polysaccharides. Methods In the present study, we first compared the clinical course and neutrophil accumulation in the lungs of Dectin-2 knock-out (KO) and wild type (WT) mice. Mice were infected intratracheally with a serotype 3 strain ofS. pneumoniae, andS. pneumoniae bacterial engulfment by neutrophils and inflammatory cytokine and anti-pneumococcal polysaccharide-specific IgG levels were evaluated in bronchoalveolar lavage fluid (BALF). We also examined the effect of Dectin-2 deficiency on interleukin (IL)-12 production by bone marrow-derived dendritic cells (BM-DCs) stimulated with the bacterial components. Results S. pneumonia- infected Dectin-2KO mice had a shorter survival time, larger bacterial burden and lower interferon gamma (IFN-γ) production in the lungs than WT mice. Although neutrophilic infiltration in the lungs was equivalent between Dectin-2KO mice and WT mice, S. pneumonia engulfment by neutrophils was attenuated in Dectin-2KO mice compared to WT mice. The anti-pneumococcal polysaccharide-specific IgG and IgG3 levels in BALF were lower in Dectin-2KO mice than in WT mice. When BM-DCs were stimulated withS. pneumoniae culture supernatant or its Concanavalin A (ConA)-bound fraction, IL-12 production was abrogated in Dectin-2KO mice compared to WT mice. Conclusions We demonstrated that Dectin-2 is intimately involved in the host defense against infection with a serotype 3 strain ofS. pneumoniae . Dectin-2-dependent IL-12 production may contribute to IFN-γ synthesis and subsequent production of serotype-specific anti-capsular polysaccharide IgG afterS. pneumoniae infection, which may promoteS. pneumoniae bacterial opsonization for engulfment. … (more)
- Is Part Of:
- BMC immunology. Volume 17:Number 1(2016)
- Journal:
- BMC immunology
- Issue:
- Volume 17:Number 1(2016)
- Issue Display:
- Volume 17, Issue 1 (2016)
- Year:
- 2016
- Volume:
- 17
- Issue:
- 1
- Issue Sort Value:
- 2016-0017-0001-0000
- Page Start:
- 1
- Page End:
- 11
- Publication Date:
- 2016-12
- Subjects:
- Streptococcus pneumonia -- Dectin-2 -- Neutrophils -- Anti-capsular polysaccharide IgG -- IFN-γ
Immunology -- Periodicals
Immune System -- Periodicals
Immunity -- Periodicals
Immune System Diseases -- Periodicals
Immunologic Techniques -- Periodicals
616.07905 - Journal URLs:
- http://www.biomedcentral.com/bmcimmunol/ ↗
http://www.pubmedcentral.nih.gov/tocrender.fcgi?journal=35 ↗
http://link.springer.com/ ↗ - DOI:
- 10.1186/s12865-015-0139-3 ↗
- Languages:
- English
- ISSNs:
- 1471-2172
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
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- British Library DSC - BLDSS-3PM
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