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http://purl.uniprot.org/citations/27456484http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27456484http://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/27456484http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1600528"xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/author"Chen K."xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/author"Kolls J.K."xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/author"Trevejo-Nunez G."xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/author"Elsegeiny W."xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/author"Conboy P."xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/pages"1877-1883"xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/title"Critical Role of IL-22/IL22-RA1 Signaling in Pneumococcal Pneumonia."xsd:string
http://purl.uniprot.org/citations/27456484http://purl.uniprot.org/core/volume"197"xsd:string
http://purl.uniprot.org/citations/27456484http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27456484
http://purl.uniprot.org/citations/27456484http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27456484
http://purl.uniprot.org/uniprot/#_A0A7R8GV04-mappedCitation-27456484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/#_Q3TS18-mappedCitation-27456484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/#_Q80XZ4-mappedCitation-27456484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/#_Q3SXE1-mappedCitation-27456484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/#_Q9JJY9-mappedCitation-27456484http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/Q3TS18http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/A0A7R8GV04http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/Q80XZ4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/Q3SXE1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27456484
http://purl.uniprot.org/uniprot/Q9JJY9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/27456484