About: Genetic dissection of host immune response in pneumonia development and progression

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About: Genetic dissection of host immune response in pneumonia development and progression Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Genetic dissection of host immune response in pneumonia development and progression
Creator	Belopolskaya, Olesya Golubev, Arkadiy Kuzovlev, Artem Moroz, Viktor Pabalan, Noel Smelaya, Tamara Smirnova, Svetlana Lyubov, & Salnikova, E
Source	Medline; PMC
abstract	The role of host genetic variation in pneumonia development and outcome is poorly understood. We studied common polymorphisms in the genes of proinflammatory cytokines (IL6 rs1800795, IL8 rs4073, IL1B rs16944), anti-inflammatory cytokines (IL10 rs1800896, IL4 rs2243250, IL13 rs20541) and toll-like receptors (TLR2 rs5743708 and rs4696480, TLR4 rs4986791, TLR9 rs352139, rs5743836 and rs187084) in patients with community-acquired pneumonia (CAP) (390 cases, 203 controls) and nosocomial pneumonia (355 cases, 216 controls). Experimental data were included in a series of 11 meta-analyses and eight subset analyses related to pneumonia susceptibility and outcome. TLR2 rs5743708 minor genotype appeared to be associated with CAP/Legionnaires’ disease/pneumococcal disease. In CAP patients, the IL6 rs1800795-C allele was associated with severe sepsis/septic shock/severe systemic inflammatory response, while the IL10 rs1800896-A allele protected against the development of these critical conditions. To contribute to deciphering of the above results, we performed an in silico analysis and a qualitative synthesis of literature data addressing basal and stimulated genotype-specific expression level. This data together with database information on transcription factors’ affinity changes caused by SNPs in putative promoter regions, the results of linkage disequilibrium analysis along with SNPs functional annotations supported assumptions about the complexity underlying the revealed associations.
has issue date	2016-10-11(xsd:dateTime)
bibo:doi	10.1038/srep35021
bibo:pmid	27725770
has license	cc-by
sha1sum (hex)	58a21f91c8d3c79e8be084088092f29dec2fc4d3
schema:url	https://doi.org/10.1038/srep35021
resource representing a document's title	Genetic dissection of host immune response in pneumonia development and progression
has PubMed Central identifier	PMC5057148
has PubMed identifier	27725770
schema:publication	Sci Rep
resource representing a document's body	covid:58a21f91c8d3c79e8be084088092f29dec2fc4d3#body_text
is schema:about of	named entity 'HOST IMMUNE RESPONSE' named entity 'GENETIC' named entity 'IL8' named entity 'controls' named entity 'complexity' named entity 'TLR2' named entity 'addressing' named entity 'IL10' named entity 'CAP' named entity 'conditions' named entity 'host' named entity 'patients' named entity 'development' named entity 'IL1B' named entity 'CONTRIBUTE ' named entity 'COMMUNITY-ACQUIRED PNEUMONIA' named entity 'DATABASE' named entity 'NOSOCOMIAL PNEUMONIA' named entity 'ASSOCIATED WITH' named entity 'CAP' named entity 'GENOTYPE' named entity 'IL13' named entity 'IL10' named entity 'PROINFLAMMATORY CYTOKINES' named entity 'MINOR' named entity 'ALLELE' named entity 'REVEALED' named entity 'ANNOTATIONS' named entity 'ROLE' named entity 'SPECIFIC' named entity 'GENETIC VARIATION' named entity 'CONDITIONS' named entity 'THESE' named entity 'UNDERSTOOD' named entity 'COMMON' named entity 'DEVELOPMENT' named entity 'LINKAGE DISEQUILIBRIUM' named entity 'IL8' named entity 'PERFORMED' named entity 'EXPRESSION LEVEL' named entity 'DISEASE' named entity 'CASES' named entity 'ANTI-INFLAMMATORY' named entity '216' named entity 'STIMULATED' named entity 'ABOUT' named entity 'FUNCTIONAL' named entity 'META-ANALYSES' named entity 'SYSTEMIC' named entity 'QUALITATIVE SYNTHESIS' named entity 'UNDERLYING' named entity 'RELATED' named entity 'SUPPORTED' named entity 'RESULTS' named entity 'PNEUMONIA' named entity 'POORLY' named entity 'BASAL' named entity 'GENES' named entity 'IN SILICO ANALYSIS' named entity 'SHOCK' named entity 'POLYMORPHISMS' named entity 'TLR9' named entity 'EXPERIMENTAL DATA' named entity 'PATIENTS' named entity 'DEVELOPMENT' named entity 'PROGRESSION' named entity 'PNEUMONIA' named entity 'OPEN' named entity 'DISSECTION' named entity 'AFFINITY' named entity 'IL4' named entity 'DATA' named entity 'OUTCOME'

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