Abstract
Epidemiologic studies have demonstrated that some bacteria colonization or infections in early-life increased the risk for subsequent asthma development. However, little is known about the mechanisms by which early-life bacterial infection increases this risk. The aim of this study was to investigate the effect of neonatal Streptococcus pneumoniae infection on the development of adulthood asthma, and to explore the possible mechanism. A non-lethal S. pneumoniae lung infection was established by intranasal inoculation of neonatal (1-week-old) female mice with D39. Mice were sensitized and challenged with ovalbumin in adulthood to induce allergic airways disease (AAD). Twenty-four hours later, the lungs and bronchoalveolar lavage fluid (BALF) were collected to assess AAD. Neonatal S. pneumoniae infection exacerbated adulthood hallmark features of AAD, with enhanced airway hyperresponsiveness and increased neutrophil recruitment into the airways, increased Th17 cells and interleukin (IL)-17A productions. Depletion of IL-17A by i.p. injection of a neutralizing monoclonal antibody reduced neutrophil recruitment into the airways, alleviated airway inflammation and decreased airway hyperresponsiveness. Furthermore, IL-17A depletion partially restored levels of inteferon-γ, but had no effect on the release of IL-5 or IL-13. Our data suggest that neonatal S. pneumoniae infection may promote the development of adulthood asthma in association with increased IL-17A production.
Highlights
Asthma is a common disease in children and the origin of the majority of adult cases, indicating that childhood events have an important role in asthma pathogenesis [1,2,3]
Neonates colonized with Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, or a combination of these three, have an increased risk for recurrent wheezing and asthma [12], and these bacteria are consistently associated with exacerbations of asthma in children [13]
We investigated the effect of neonatal S. pneumoniae infection on airways disease (AAD) in an adult mouse model with or without IL-17A depletion
Summary
Asthma is a common disease in children and the origin of the majority of adult cases, indicating that childhood events have an important role in asthma pathogenesis [1,2,3]. Neonatal S. pneumoniae Infection May Promote OVA-Induced AAD alter immunologic programming, which plays a critical role in the progression of allergic airways disease (AAD) in adulthood. Studies have demonstrated that viral infections in childhood promote subsequent development of asthma [4,5,6,7]. Recent studies suggest some bacterial infection may have an important role in asthma pathogenesis [8,9]. Some young children with acute episodes of wheezing have bacterial infections that are closely associated [11]. Whether S. pneumoniae infection in neonatal mice can induce different immune responses is unclear
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