Lower interleukin-8 levels in airway aspirates from breastfed infants with acute bronchiolitis.

Breastfeeding during the first 12 months of life confers demonstrable immunologic benefit against infective pathogens, including those of the respiratory tract. However, the mechanism by which the ingestion of human milk modifies immunologic defense against such pathogens remains elusive. Bronchiolitis, caused predominantly by respiratory syncytial virus, is the most common clinical presentation of severe upper respiratory illness requiring hospitalization in infants and remains one of the developed world's leading causes of infant mortality and morbidity over both the short and long term. The mechanism by which an early, severe case of bronchiolitis can result in the development of recurrent childhood wheeze or asthma is unclear; however, mucosal inflammation and pulmonary neutrophilia are believed to play a significant role. The aim of this study was to examine the immune response of breastfed infants hospitalized with severe bronchiolitis, compared with formula-fed controls. Nasopharyngeal aspirates (NPA) were collected from 18 infants (aged <or=12 months), seven breastfed and 11 formula fed and assayed by enzyme immunoassays for chemokines interleukin (IL)-8 and monocyte chemotactic protein (MCP)-1. NPA cellular component was quantified by light microscopy. Breastfed infants had lower levels of the chemokine IL-8 in their nasal airways with a concurrent decrease in cellular infiltrate (p <or= 0.04). NPA cell number correlated with lactoferrin concentration (p = 0.02) but not with myeloperoxidase, suggesting the predominance of mature, secondary granule laden neutrophils. These findings indicate a potential mechanism of protective immune regulation during bronchiolitis in the breastfed infant.