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Obesity

The number and function of T regulatory cells in obese atopic female asthmatics

, MD Msc (QIPS), FACP, FCCP, FCCM, , BM, , DNP, NP-C & , MD, PhD
Pages 303-310 | Received 20 Dec 2017, Accepted 11 Mar 2018, Published online: 11 Apr 2018
 

ABSTRACT

Background: Mechanisms underlying the association between asthma and obesity remain poorly understood. Obesity appears to be a risk factor for asthma, and obese asthmatics fare poorly compared to lean asthmatics. Objectives: To explore the possibility that reduced regulatory T cell (Treg) number and function contribute to the obesity-asthma association. We concentrated on obese females with childhood-onset asthma, since Treg may be involved in this phenotype. Methods: We recruited 64 women (ages 18–50) into four groups: lean (BMI 18–25 kg/m2) controls (n = 17) and asthmatics (n = 13), and obese (BMI ≥ 35 kg/m2) controls (n = 17) and asthmatics (n = 17). Asthmatics had atopy and childhood-diagnosed asthma. We assessed lung function, asthma control and quality of life. Peripheral blood CD4+/CD25+/FoxP3+ Treg cells were identified and counted by flow cytometry and expressed as % total CD4+ T cells. We assessed Treg cell function by the ability of CD4+/CD25+ Treg cells to suppress autologous CD4+/CD25- responder T cell (Tresp) proliferation and measured as % suppression of Tresp cell proliferation. Results: Obese asthmatics had worse lung function, asthma control, and quality of life compared to lean asthmatics. Compared to lean or obese control groups, the number of Treg cells in the obese asthmatics was approximately 1.58- or 1.73-fold higher. The ability of Treg cells from obese-asthmatics to suppress Tresp cell proliferation was reduced. Conclusions: Obese, atopic women with childhood diagnosed asthma demonstrate increased Treg cell number and mildly decreased Treg cell function. Our data do not support the view that reduced Treg cell number contributes to this obese-asthma phenotype.

Declarations of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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