Acetylcholine producing innate type 2 and 3 lymphoid cells promote protease driven allergic lung inflammation - 09/03/22

Doi : 10.1016/j.rmr.2022.02.003

E. Culerier ¹, D. Togbe ¹, I. Maillet ¹, M. LeBert ¹, M. Selkirk ², W. Horsnell ², V. Quesniaux ¹, B. Ryffel ^1,^⁎
¹ Laboratory of Molecular and Experimental Immunology and Neurogenetics, UMR 7355, CNRS and University of Orleans, France
² Institute of Infectious Disease and Molecular Medicine, University of Cape Town, South Africa

^⁎Corresponding author.

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Resumen

Introduction

Protease induced disruption of the epithelial barrier activates a type 2 innate immune lung response. Here we show that activation of the airway epithelium by papain or A. Alternata is regulated by lymphocyte-derived acetylcholine (Ach).

Methods

Proteases were administered for three days by intranasal instillation in Ach Transferase (ChAT) reporter, Rag-gc KO and newly created RoRgt^CreChAT^loxp mice. The cell recruitment and inflammatory lung response was analyzed 24h later.

Results

Using ChAT reporter mice, we observe a rapid increase of ACh production by type 2 and 3 innate lymphoid cells (ILC) following papain challenge. To ascertain that the ACh⁺ILC3 subpopulation contributes to the response, we generated RoRgt^CreChAT^loxp mice. We find decreased eosinophil recruitment, epithelial injury and airway hyperreactivity in ACh⁺ILC3 deficient mice upon acute papain or A. Alternata challenge.

Conclusions

These findings identify that in addition of ILC2, ILC3-derived ACh as a significant contributor to papain induced allergic asthma.

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Keywords : Asthma, Acetylcholine, Innate lymphoid cells

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Vol 39 - N° 2

P. 108-109 - février 2022 Regresar al número

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