Abstract
Infants are exposed to a wide range of potential pathogens in the first months of life. Although maternal antibodies acquired transplacentally protect full-term neonates from many systemic pathogens, infections at mucosal surfaces still occur with great frequency, causing significant morbidity and mortality. At least part of this elevated risk is attributable to the neonatal immune system that tends to favor T regulatory and Th2 type responses when microbes are first encountered. Early-life infection with respiratory viruses is of particular interest because such exposures can disrupt normal lung development and increase the risk of chronic respiratory conditions, such as asthma. The immunologic mechanisms that underlie neonatal host–virus interactions that contribute to the subsequent development of asthma have not yet been fully defined. The goals of this review are (1) to outline the differences between the neonatal and adult immune systems and (2) to present murine and human data that support the hypothesis that early-life interactions between the immune system and respiratory viruses can create a lung environment conducive to the development of asthma.
Highlights
The young of any species face microbial threats similar to those faced by adults
The precise mechanisms by which respiratory syncytial virus (RSV) infection induces alternatively activated macrophages (M2) polarization are still unknown, it seems likely that production of thymic stromal lymphopoietin (TSLP), IL-25, and/or IL-33 by RSV-infected or -exposed respiratory epithelial cells contributes to both M2 differentiation and long-term maintenance of a Th2biased macrophage population in the lung [123, 130, 163, 164]
The only factors known to increase susceptibility to RSV-induced asthma are family history of atopy, premature birth, and certain host genetic polymorphisms that are linked with severe disease [111]
Summary
The young of any species face microbial threats similar to those faced by adults. the developing mammalian immune system does not mount “adult-type” immune responses to most pathogens. The neonatal immune system must first and foremost distinguish between self and nonself, and rapidly proceed to distinguish between benign or even “helpful” non-self (e.g., the commensal microbiome) and potential pathogens During this period of immune education, the developing immune system has to strike a delicate and pathogenspecific balance between the induction of potentially damaging, pro-inflammatory responses mediated by T helper (Th) cell 1-type (Th1) and some Th17-type cells, less damaging inflammatory responses (e.g., Th2-type) or even suppressive responses mediated by regulatory T cells (Treg). Because RSV, influenza, and RVs cause a large proportion of respiratorytract infections in neonates, we will focus primarily on these three pathogens as models to better understand how early-life infection and antiviral immune responses might contribute to the subsequent development of asthma
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