Eosinophils Promote Effector Functions of Lung Group 2 Innate Lymphoid Cells in Allergic Airway Inflammation in Mice

Authors

William E LeSuer
Melanie Kienzl
Sergei I Ochkur
Rudolf Schicho
Alfred D Doyle
Benjamin L Wright
Matthew A Rank
Alexander S Krupnick
Hirohito Kita
Elizabeth A Jacobsen

Publication Date

8-1-2023

Journal

The Journal of Allergy and Clinical Immunology

Abstract

BACKGROUND: Group 2 innate lymphoid cells (ILC2s) are critical mediators of type 2 respiratory inflammation, releasing IL-5 and IL-13 and promoting the pulmonary eosinophilia associated with allergen provocation. Although ILC2s have been shown to promote eosinophil activities, the role of eosinophils in group 2 innate lymphoid cell (ILC2) responses is less well defined.

OBJECTIVE: We sought to investigate the role of eosinophils in activation of ILC2s in models of allergic asthma and in vitro.

METHODS: Inducible eosinophil-deficient mice were exposed to allergic respiratory inflammation models of asthma, such as ovalbumin or house dust mite challenge, or to innate models of type 2 airway inflammation, such as inhalation of IL-33. Eosinophil-specific IL-4/13-deficient mice were used to address the specific roles for eosinophil-derived cytokines. Direct cell interactions between ILC2s and eosinophils were assessed by in vitro culture experiments.

RESULTS: Targeted depletion of eosinophils resulted in significant reductions of total and IL-5

CONCLUSION: These studies demonstrate that eosinophils play a reciprocal role in ILC2 effector functions as part of both adaptive and innate type 2 pulmonary inflammatory events.

Keywords

Mice, Animals, Immunity, Innate, Eosinophils, Interleukin-33, Interleukin-13, Interleukin-5, Interleukin-4, Lymphocytes, Lung, Cytokines, Asthma, Inflammation, Allergens

Comments

Supplementary Materials

PMID: 37028525