A1 Refereed original research article in a scientific journal

Polymorphisms of Mannose-Binding Lectin and Toll-Like Receptors 2, 3, 4, 7, and 8 and the Risk of Respiratory Infections and Acute Otitis Media in Children




AuthorsToivonen L, Vuononvirta J, Mertsola J, Waris M, He Q, Peltola V

Publication year2017

JournalPediatric Infectious Disease Journal

Volume36

Issue5

First page e114

Last pagee122

DOIhttps://doi.org/10.1097/INF.0000000000001479


Abstract
BACKGROUND: 

Mannose-binding lectin (MBL) and toll-like receptors (TLR) are important components of the innate immune system. We assessed the susceptibility of children with genetic variants in these factors to respiratory infections, rhinovirus infections, and acute otitis media.

METHODS: 

In a prospective cohort study, blood samples from 381 Finnish children were analyzed for polymorphisms in MBL2 at codons 52, 54, and 57, TLR2 Arg753Gln, TLR3 Leu412Phe, TLR4 Asp299Gly, TLR7 Gln11Leu, and TLR8 Leu651Leu. Children were followed for respiratory infections until 24 months of age with daily diaries. PCR and antigen tests were used for detection of respiratory viruses from nasal swabs.

RESULTS: 

Children with MBL variant genotype had a mean of 59 days with symptoms of respiratory infection per year, compared with 49 days in those with wild-type (P = 0.01). TLR8 polymorphisms were associated with an increased risk and TLR7 polymorphisms with a decreased risk of recurrent rhinovirus infections (P = 0.02 for both). TLR2 polymorphisms were associated with recurrent acute otitis media (P = 0.02). MBL polymorphisms were associated with an increased and TLR7 polymorphisms with a decreased risk of rhinovirus-associated acute otitis media (P = 0.03 and P = 0.006, respectively).

CONCLUSIONS: 

Genetic polymorphisms in MBL and TLRs promote susceptibility to, or protection against respiratory infections. In addition to environmental factors, genetic variations may explain why some children are more prone to respiratory infections.



Last updated on 2024-26-11 at 11:50