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Review
. 2017:2017:8734504.
doi: 10.1155/2017/8734504. Epub 2017 Nov 9.

Pulmonary Susceptibility of Neonates to Respiratory Syncytial Virus Infection: A Problem of Innate Immunity?

Carole Drajac  1 , Daphné Laubreton  1 , Sabine Riffault  1 , Delphyne Descamps  1
Affiliations
Review

Pulmonary Susceptibility of Neonates to Respiratory Syncytial Virus Infection: A Problem of Innate Immunity?

Carole Drajac et al. J Immunol Res. 2017.

Abstract

Human respiratory syncytial virus (RSV) is a common and highly contagious viral agent responsible for acute lower respiratory infection in infants. This pathology characterized by mucus hypersecretion and a disturbed T cell immune response is one of the major causes of infant hospitalization for severe bronchiolitis. Although different risk factors are associated with acute RSV bronchiolitis, the immunological factors contributing to the susceptibility of RSV infection in infants are not clearly elucidated. Epidemiological studies have established that the age at initial infection plays a central role in the severity of the disease. Thus, neonatal susceptibility is intrinsically linked to the immunological characteristics of the young pulmonary mucosa. Early life is a critical period for the lung development with the first expositions to external environmental stimuli and microbiota colonization. Furthermore, neonates display a lung immune system that profoundly differs to those from adults, with the predominance of type 2 immune cells. In this review, we discuss the latest information about the lung immune environment in the early period of life at a steady state and upon RSV infection and how we can modulate neonatal susceptibility to RSV infection.

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Figures

Figure 1
Figure 1
Immune cell colonization of the lungs during the postnatal period (schematization of cellular frequencies in CD45+ lung cells). Adapted from [25, 27, 30, 38] and personal unpublished data.
Figure 2
Figure 2
Immediate immune responses of pulmonary resident cells to RSV infection in neonates. Servier Medical Art has provided images. Neonatal RSV exposure leads to an early IL-33 secretion by respiratory epithelial cells [96]. IL-33 signals through its receptor ST2 localized at the membrane of ILC2. This alarmin supports the increase in the ILC2 number and IL-13 production in the lungs of RSV-infected neonatal mice [74]. ILC2 can promote a switch towards a type 2 phenotype for AMs or lung DCs at a steady state or in a house dust mite-induced asthma model [27, 30]. Concerning the IFN-I pathway, neonatal pDCs display a poor pulmonary mobilization and a weak activation of the IFN-I pathway following RSV infection [29]. AMs are the main source of IFN-I in RSV-infected adult lungs, but the question remains open during the neonatal period [54]. Therefore, it is strongly suspected that ILC2 cells are indirectly responsible for the inability of neonatal mice to mount an effective IFN-I response to counteract RSV infection. In addition, IL-10-secreting nBregs may constitute another cellular subset contributing to the type 2 immunity induced by RSV infection in neonates [40, 99].
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