Rescue of T-cell function during persistent pulmonary adenoviral infection by Toll-like receptor 9 activation

Abstract

21 ] i may in turn activate TRPA 1 leading to a greater rise in [Ca 21 ] i . We also recognize that these studies were performed in vitro, which may not fully recapitulate what occurs in vivo. Finally, studies using primary bronchial epithelial cells from deceased donors are intrinsically limited by the availability of donor cells, especially in the pediatric age group. Additionally, history of atopic status and lung function is frequently not available, as well as comorbidities and cause of death. Thus, it is possible that the age effect could be explained by other factors and future studies will need to be done using cells from identified samples from patients with documented asthma status and severity.In conclusion, the results of this study show for the first time that lower airway epithelium from asthmatic children displays elevated basal TRPV 1 activity when compared with that of nonasthmatic controls. We have also shown that RSV infection of epithelial cells from asthmatic children-but not from adults-leads to an increase in overall TRPV 1 activation. Pharmacological inhibition of TRPV 1 may lead in the future to strategies that might reduce the impact of RSV infections in both asthmatic and nonasthmatic children.

Monocyte-derived macrophages aggravate pulmonary vasculitis via cGAS/STING/IFN-mediated nucleic acid sensing

“…Pulmonary vasculitis was induced by intratracheal (i.t.) application of 50 µl PBS containing 10 µg LPS (Serotype 026:B6, Sigma) and 10 µg fMLP (Sigma) with the help of a small-animal laryngoscope and mechanical ventilation (Harvard Apparatus) for 1 minute at 250 µl air/stroke and 250 strokes/minute as previously described (Holland et al 2017), followed by intraperitoneal (i.p.) injection of 1 mg anti-MPO (clones 6D1 and 6G4, 0.5 mg of each clone) in 200 µl PBS.…”