Host defense against pulmonary infection in neonates

Abstract

It is well known that neonatal immune function is immature compared to adults and that ontogeny of the immune system continues for some time postnatally. This renders infants particularly susceptible to pulmonary bacterial and viral infections often associated with childhood. Innate immune responses are less intense and delayed compared to adults. Antigen presentation is immature in that antigen presenting cells are slow in upregulating costimulatory molecules. This results in reduced T-cell responses including T-cell help and cytotoxic lymphocytes (CTL) function. B-cell responses suffer from the lack of T-cell help. The maturation process of immune mediators in newborns corresponds with postnatal development of the lungs and may be a mechanism that keeps inflammation from causing damage to developing lungs.