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http://purl.uniprot.org/citations/27456484 | http://www.w3.org/2000/01/rdf-schema#comment | "IL-22-IL-22R signaling plays a crucial role in regulating host defenses against extracellular pathogens, particularly in the intestine, through the induction of antimicrobial peptides and chemotactic genes. However, the role of IL-22-IL-22R is understudied in Streptococcus pneumoniae lung infection, a prevalent pathogen of pneumonia. This paper presents the findings of IL-22 signaling during a murine model of pneumococcal pneumonia and improvement of bacterial burden upon IL-22 administration. IL-22 was rapidly induced in the lung during pneumococcal infection in wild-type mice, and Il22(-/-) mice had higher pneumococcal burdens compared with controls. Additionally, mice with hepatic-specific deletion of Il22ra1 also had higher bacterial burdens in lungs compared with littermate controls after intrapulmonary pneumococcal infection, suggesting that IL-22 signaling in the liver is important to control pneumococcal pneumonia. Thus, we hypothesized that enhancement of IL-22 signaling would control pneumococcal burden in lung tissues in an experimental pneumonia model. Administration of rIL-22 systemically to infected wild-type mice decreased bacterial burden in lung and liver at 24 h postinfection. Our in vitro studies also showed that mice treated with IL-22 had increased C3 expression in the liver compared with the isotype control group. Furthermore, serum from mice treated with IL-22 had improved opsonic capacity by increasing C3 binding on S. pneumoniae Taken together, endogenous IL-22 and hepatic IL-22R signaling play critical roles in controlling pneumococcal lung burden, and systemic IL-22 decreases bacterial burden in the lungs and peripheral organs by potentiating C3 opsonization on bacterial surfaces, through the increase of hepatic C3 expression."xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1600528"xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/author | "Chen K."xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/author | "Kolls J.K."xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/author | "Trevejo-Nunez G."xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/author | "Elsegeiny W."xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/author | "Conboy P."xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/pages | "1877-1883"xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/title | "Critical Role of IL-22/IL22-RA1 Signaling in Pneumococcal Pneumonia."xsd:string |
http://purl.uniprot.org/citations/27456484 | http://purl.uniprot.org/core/volume | "197"xsd:string |
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