Respiratory syncytial virus (RSV) preferentially infects airway epithelial cells,which might be responsible for susceptibility to asthma; however, the underlying mechanism is not clear. This study determined the activation of lymphocytes and drift of helper T (Th) subsets induced by RSV-infected human bronchial epithelial cells (HBECs) in vitro. HBECs had prolonged infection with RSV, and lymphocytes isolated from human peripheral blood were co-cultured with RSV-infected HBECs. Four groups were established, as follows: lymphocytes (group L); lymphocytes infected with RSV (group RL); co-culture of lymphocytes with non-infected HBECs (group HL); and co-culture of lymphocytes with infected HBECs (group HRL). After co-culture with HBECs for 24 hours, lymphocytes were collected and the following were determined in the 4 groups: cell cycle status; apoptosis rate; and concentrations of IL-4, IFN-γ, and IL-17 in the supernatants. Cell cycle analysis for lymphocytes showed a significant increase in S phase cells, a decrease in G1 phase cells, and a higher apoptosis rate in group HRL compared with the other three groups. In group HRL, the levels of IL-4, IFN-γ, and IL-17 in supernatants were also higher than the other three groups. For further study, lymphocytes were individually treated with supernatants from non-infected and RSV-infected HBECs for 24 h. We showed that supernatants from RSV-infected HBECs induced the differentiation of Th2 and Th17 subsets, and suppressed the differentiation of Treg subsets. Our results showed that HBECs with prolonged RSV infection can induce lymphocyte proliferation and apoptosis, and enhance the release of cytokines by lymphocytes. Moreover, subset drift might be caused by RSV-infected HBECs.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
BackgroundAdrenal neuroendocrine plays an important role in asthma. The activity of the
sympathoadrenal system could be altered by early life events. The effects of
maternal asthma during pregnancy on the adrenal medulla of offspring remain
unknown.Methodology/Principal FindingsThis study aims to explore the influence of maternal asthma during pregnancy
on the development and function of adrenal medulla in offspring from
postnatal day 3 (P3) to postnatal day 60 (P60). Asthmatic pregnant rats
(AP), nerve growth factor (NGF)-treated pregnant rats (NP) and NGF
antibody-treated pregnant rats (ANP) were sensitized and challenged with
ovalbumin (OVA); NP and ANP were treated with NGF and NGF antibody
respectively. Offspring rats from the maternal group were divided into four
groups: offspring from control pregnant rats (OCP), offspring from AP (OAP),
offspring from NP (ONP), and offspring from ANP (OANP). The expressions of
phenylethanolamine N-methyltransferase (PNMT) protein in adrenal medulla
were analyzed. The concentrations of epinephrine (EPI), corticosterone and
NGF in serum were measured. Adrenal medulla chromaffin cells (AMCC) were
prone to differentiate into sympathetic nerve cells in OAP and ONP. Both EPI
and PNMT were decreased in OAP from P3 to P14, and then reached normal level
gradually from P30 to P60, which were lower from birth to adulthood in ONP.
Corticosterone concentration increased significantly in OAP and ONP.Conclusion/SignificanceAsthma pregnancy may promote AMCC to differentiate into sympathetic neurons
in offspring rats and inhibit the synthesis of EPI, resulting in dysfunction
of bronchial relaxation.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.