Innate lymphoid cells contribute to allergic airway disease exacerbation by obesity

Everaere L. et al., J Allergy Clin Immunol. 138(5):1309-1318. (2016)

Speaker: Chia-Ying Cheng (鄭嘉瑩)                                    Time:13:10~ 14:00, Mar. 29, 2017

Commentator: Prof. Yu-Hsiang Hsu (許育祥 助理教授)   Place: Room 601

Abstract:

Obesity is a condition in which excess fat has accumulated in the body, which can have an adverse effect on health. Epidemiologic and clinical observations showed that obesity is an important risk factor for asthma exacerbation, but the underlying mechanisms remain poorly understood. Innate lymphoid cells (ILCs) act as early orchestrators of immunity, responding to epithelium derived signals by expressing cytokines and cell surface receptors. Previous research showed that ILC2s regulated visceral adipose tissue (VAT) eosinophils and allogeneic macrophages. Furthermore, IL-17-producing ILC3s have been recently associated with obesity-induced AHR but no evidence was shown regarding allergen-induced asthma. In this study, the authors aimed to know whether ILCs contribute to obesity-driven exacerbation of allergen-induced asthma. Obesity was induced by high fat diet (HFD) feeding, and allergic airway inflammation was induced by intranasal sensitization and stimulation with house dust mite (HDM) extract in wild type mice and RAG2-deficient mice. In results, they first found that HFD-induced obesity exacerbates HDM-induced airway disease and lung Th2- and Th17-type profiles. Second, HFD-induced obesity increased lung ILC2s and ILC3s infiltration and decreased ILC markers in VAT in HDM-induced airway inflammation. Third, they depleted ILCs with anti-CD90.2, and found reduced HDM-induced airway disease and lung Th2 and Th17 infiltration predominantly in HFD-induced obesity. Taken together, these results showed that ILC2s and ILC3s functionally contribute to obesity-mediated allergic airway inflammation and affect Th2 and Th17 lymphocytes infiltration in lung. This research indicated that HFD-induced obesity may exacerbate allergic airway inflammation through mechanisms involving ILC2s and ILC3s.

References：

1.     Molofsky AB, Nussbaum JC, Liang HE, Van Dyken SJ, Cheng LE, Mohapatra A, et al. Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages. J Exp Med 2013;210:535-49.

2.     Kim HY, Lee HJ, Chang YJ, Pichavant M, Shore SA, Fitzgerald KA, et al. Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity. Nat Med 2014; 20:54-61.