IL-33 Induces a Protective Response against Irritant-induced Airway Inflammation and Dysfunction.
Utako Fujii1,2, Tomotaka Nishizawa1,2, Yumiko Ishii1,2
1Meakins-Christie Laboratories, McGill University Health Centre Research Institute, Montreal, Quebec, Canada; and.
Summary
Interleukin-33 (IL-33) activates innate lymphoid cells (ILCs) to protect against airway dysfunction and inflammation caused by chlorine gas inhalation, involving IL-13 and macrophages.
Area of Science:
- Immunology
- Respiratory Medicine
- Toxicology
Background:
- Interleukin-33 (IL-33) and innate lymphoid cells (ILCs) are implicated in Type 2 (T2)-high asthma.
- The role of IL-33 and ILCs in irritant-induced airway dysfunction remains unclear.
Purpose of the Study:
- To investigate the effects of chlorine (Cl2) inhalation on IL-33 release, pulmonary ILCs, airway inflammation, and airway hyperresponsiveness (AHR).
Main Methods:
- Mice were exposed to Cl2, and IL-33 release, ILC populations, airway inflammation, and AHR were assessed.
- Studies involved IL-33 receptor inhibition, ILC depletion, and administration of recombinant IL-33, IL-13, or clodronate liposomes.
Main Results:
- Cl2 exposure increased IL-33 release and ILC2s in mouse airways.
- IL-33 administration inhibited Cl2-induced neutrophilia and AHR, an effect dependent on ILCs.
- IL-33 promoted IL-13 production by ILC2s, biased macrophages to M2 phenotype, and IL-13 mediated protective effects against AHR.
Conclusions:
- IL-33-driven expansion of ILC2s activates a protective pathway involving IL-13 and macrophages against Cl2-induced airway dysfunction and inflammation.
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