RGD Reference Report - Genetic polymorphisms in immunoresponse genes TNFA, IL6, IL10, and TLR4 are associated with recurrent acute otitis media. - Rat Genome Database

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Genetic polymorphisms in immunoresponse genes TNFA, IL6, IL10, and TLR4 are associated with recurrent acute otitis media.

Authors: Emonts, M  Veenhoven, RH  Wiertsema, SP  Houwing-Duistermaat, JJ  Walraven, V  De Groot, R  Hermans, PW  Sanders, EA 
Citation: Emonts M, etal., Pediatrics. 2007 Oct;120(4):814-23.
RGD ID: 7365054
Pubmed: PMID:17908769   (View Abstract at PubMed)
DOI: DOI:10.1542/peds.2007-0524   (Journal Full-text)

OBJECTIVE: Cytokines and other inflammatory mediators are involved in the pathogenesis of otitis media. We hypothesized that polymorphisms in inflammatory response genes contribute to the increased susceptibility to acute otitis media in otitis-prone children. PATIENTS AND METHODS: DNA samples from 348 children with > or = 2 acute otitis media episodes, who were participating in a randomized, controlled vaccination trial, and 463 healthy adult controls were included. Polymorphisms in TNFA, IL1B, IL4, IL6, IL10, IL8, NOS2A, C1INH, PARP, TLR2, and TLR4 were genotyped. Genotype distributions in children with recurrent acute otitis media were compared with those in controls. Within the patient group, the number of acute otitis media episodes before vaccination and the clinical and immunologic response to pneumococcal conjugate vaccinations were analyzed. RESULTS: The IL6-174 G/G genotype was overrepresented in children with acute otitis media when compared with controls. In the patient group, TNFA promoter genotypes -238 G/G and -376 G/G and the TLR4 299 A/A genotype were associated with an otitis-prone condition. Furthermore, lower specific anticapsular antibody production after complete vaccination was observed in patients with the TNFA-238 G/G genotype or TNFA-863 A allele carriage. Finally, the IL10-1082 A/A genotype contributed to protection from the recurrence of acute otitis media after pneumococcal vaccination. CONCLUSIONS: Variation in innate immunoresponse genes such as TNFA-863A, TNFA-376G, TNFA-238G, IL10-1082 A, and IL6-174G alleles in the promoter sequences may result in altered cytokine production that leads to altered inflammatory responses and, hence, contributes to an otitis-prone condition.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL10Humanotitis media susceptibilityIAGP DNA:SNP:promoter:-1082G>A (human)RGD 
IL6Humanotitis media susceptibilityIAGP DNA:polymorphism:promoter:-174G>C(human)RGD 
Il10Ratotitis media susceptibilityISOIL10 (Homo sapiens)DNA:SNP:promoter:-1082G>A (human)RGD 
Il10Mouseotitis media susceptibilityISOIL10 (Homo sapiens)DNA:SNP:promoter:-1082G>A (human)RGD 
Il6Ratotitis media susceptibilityISOIL6 (Homo sapiens)DNA:polymorphism:promoter:-174G>C(human)RGD 
Il6Mouseotitis media susceptibilityISOIL6 (Homo sapiens)DNA:polymorphism:promoter:-174G>C(human)RGD 

Phenotype Annotations    Click to see Annotation Detail View

Manual Human Phenotype Annotations - RGD

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL10HumanOtitis media susceptibilityIAGP DNA:SNP:promoter:-1082G>ARGD 
Objects Annotated

Genes (Rattus norvegicus)
Il10  (interleukin 10)
Il6  (interleukin 6)

Genes (Mus musculus)
Il10  (interleukin 10)
Il6  (interleukin 6)

Genes (Homo sapiens)
IL10  (interleukin 10)
IL6  (interleukin 6)


Additional Information