Nancy A. Melville

May 31, 2012

May 31, 2012 (Thessaloniki, Greece) — Infants carrying a particular allele of the anti-inflammatory cytokine interleukin 10 (IL10) gene are significantly less likely to develop asthma after acute bronchiolitis than infants carrying other alleles, researchers reported here at the European Society for Paediatric Infectious Diseases 30th Annual Meeting.

Infants are commonly hospitalized with acute bronchiolitis, and up to 40% go on to develop asthma symptoms later in childhood.

In a previous study, Petri Koponen, MD, from the Paediatric Research Centre at Tampere University Hospital in Finland, and colleagues found that infants who lack a G allele at position 1082 of the IL10 gene are at greater risk for rhinovirus infection and, possibly, asthma in early life. The results of their new study support the association with asthma risk, Dr. Koponen told Medscape Medical News.

"There has been conflicting evidence of the association between the interleukin 10 polymorphism and asthma development after early bronchiolitis," Dr. Koponen said. "We found that those who are 'low producers' of IL-10 are more likely to be future asthmatics."

For this study, the researchers used the same cohort as they had used in their rhinovirus study, this time focusing on the potential association between preschool asthma and the polymorphism of IL10-1082 G/A, as well as other cytokines, such as IL18-137 G/C, TLR4-896 A/G, and IFNG-874 T/A, after bronchiolitis in early infancy.

The study involved 205 infants 6 months of age or younger who were hospitalized for bronchiolitis. The children were enrolled during viral outbreaks that occurred in 2001 and 2004. The rate of viral infection in the infants was greater than 95%.

At follow-up in 2008 and 2009, 166 children (mean age, 6.4 years) were available for reevaluation, which included comprehensive interviews for asthma symptoms, blood samples, and skin prick tests. In total, 135 frozen whole-blood samples were available for IL10 genotyping.

Overall, 17 children (12.6%) had asthma, 47 (34.8%) had atopic eczema, and 36 (26.7%) had allergic rhinitis.

However, in children who were homozygous carriers of allele G at position 1082 of IL10, only 1 of 32 (3.1%) had asthma at 5 to 7 years of age (P = .04).

Moreover, in preschool aged children, up to 21% of non-G allele carriers of IL10 had asthma, compared with just 10% of allele G carriers.

"We found 3 different genotypes in the patients. Those with allele G had a very low prevalence of asthma (only 3.1%), whereas in the general population, the prevalence is around 5% to 6 %," Dr. Koponen said.

"Meanwhile, those with the genotype A/A of IL10 had almost a 7-fold increase in asthma prevalence following bronchiolitis," he explained.

"All groups had quite a high prevalence of atopy, which was kind of surprising with genotype G/G, since those patients had the low prevalence of asthma," he added.

Such findings could be essential in the identification of children most at risk of developing asthma, Dr. Koponen noted.

"Diagnosing asthma in small children is often quite difficult and is based only on the parents' report of symptoms; lung function cannot be measured reliably in children younger than 3 to 4 years," he said.

"Therefore, it is important that we develop new risk-assessment tools to help us make more accurate diagnoses and allow us to identify the children who may benefit most from early asthma medication."

Genotyping could be one of those tools, he said.

"In the future, it may be that we will be able to use single DNA polymorphisms and/or haplotypes in clinical work to make more accurate diagnoses."

Dr. Koponen is currently employed by GSK, but reports that this study was conducted entirely at Tampere University Hospital prior to his employment with GSK.

European Society for Paediatric Infectious Diseases (ESPID) 30th Annual Meeting: Abstract 489. Presented May 11, 2012.

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