Vitamin A supplement after neonatal Streptococcus pneumoniae pneumonia inhibits the progression of experimental asthma by altering CD4+T cell subsets

Abstract

Studies demonstrated that pneumonia can decrease vitamin A productions and vitamin A reduction/ deficiency may promote asthma development. Our previous study showed that neonatal Streptococcus pneumoniae (S. pneumoniae) infection promoted asthma development. Whether neonatal S. pneumoniae pneumonia induced asthma was associated with vitamin A levels remains unclear. The aim of this study was to investigate the effects of neonatal S. pneumoniae pneumonia on vitamin A expressions, to explore the effects of vitamin A supplement after neonatal S. pneumoniae pneumonia on adulthood asthma development. Non-lethal S. pneumoniae pneumonia was established by intranasal inoculation of neonatal (1-week-old) female BALB/c mice with D39. S. pneumoniae pneumonia mice were supplemented with or without all-trans retinoic acid 24 hours after infection. Vitamin A concentrations in lung, serum and liver were measured post pneumonia until early adulthood. Four weeks after pneumonia, mice were sensitized and challenged with OVA to induce allergic airway disease (AAD). Twenty-four hours after the final challenge, the lungs and bronchoalveolar lavage fluid (BALF) were collected to assess AAD. We stated that serum vitamin A levels in neonatal S. pneumoniae pneumonia mice were lower than 0.7µmol/L from day 2-7 post infection, while pulmonary vitamin A productions were significantly lower than those in the control mice from day 7-28 post infection. Vitamin A supplement after neonatal S. pneumoniae pneumonia significantly promoted Foxp3 + treg and Th1 productions, decreased Th2 and Th17 cells expressions, alleviated airway hyperresponsiveness (AHR) and inflammatory cells infiltration during AAD. Our data suggest that neonatal S. pneumoniae pneumonia induce serum vitamin A deficiency and long-time lung vitamin A reduction, vitamin A supplement after neonatal S. pneumoniae pneumonia inhibit the progression of asthma by altering CD4 + T cell subsets. Asthma is a heterogeneous disease characterized by airway chronic inflammation together with airway hyperresponsiveness 1. Asthma is more common in childhood, and most adult asthma originate from childhood, which suggesting childhood events play an important role in the pathogenesis of asthma 2-4. Childhood is a pivotal period for the immune system maturation. Specific pathogen may play a critical role in the allergic airway diseases (AAD) pathogenesis by affecting the immune system 5. Epidemiological studies show that neonates colonized with S. pneumoniae, Haemophilus influenzae or Moraxella catarrhalis significantly increases the risk of asthma in the first 5 years of life 6,7. S. pneumoniae is the most common bacterial pathogen of community acquired pneumonia in childhood. Our previous study suggested that neonatal S. pneumoniae infection promoted OVA-induced

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