Abstract
Abstract The hygiene hypothesis states that the lack of early childhood exposure to infectious agents, which promotes type 1 immunity, results in increased incidents of allergy and asthma, which are predominantly type 2 immune responses. Recently identified group 2 innate lymphoid cells (ILC2s) are essential for the development of protease allergen induced type 2 lung inflammation. To better understand how type 2 immunity is regulated, we tested the effect of LPS-induced type 1 inflammation on ILC2s and type 2 lung inflammation. Intranasal LPS pretreatment of mice suppressed both papain- and IL-33-induced ILC2 activation and eosinophilic lung inflammation. Specifically, the number of activated ILC2s that express IL-5 and IL-13 was decreased with LPS treatment. The LPS effect on ILC2s was dose and time dependent. The in vivo findings were reproduced in vitro. Pretreatment with LPS inhibited the production of type 2 cytokines IL-5 and IL-13 by ILC2s cultured in the presence of IL-33 and TSLP. These results indicate that LPS triggers an ILC2 inhibitory signal, which leads to the suppression of ILC2 activation and type 2 inflammation in the lung upon allergen exposure.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call