Zinc sulfate improved the unbalanced T cell profiles in Der p‐allergic asthma: An ex vivo study

Introduction In the pathogenesis of asthma, an imbalance between helper T (Th) 1/Th2 and Th17/Treg cells is believed to play a key role in asthmatic inflammatory responses. Some studies indicated that zinc deficiency increases inflammatory factor production and worsens asthma. However, the effects o...

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Veröffentlicht in:The clinical respiratory journal 2018-02, Vol.12 (2), p.563-571
Hauptverfasser: Tsai, Yu Lin, Ko, Wang‐Sheng, Hsiao, Jung‐Lung, Pan, Hsin‐Hung, Chiou, Ya‐Ling
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Sprache:eng
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Zusammenfassung:Introduction In the pathogenesis of asthma, an imbalance between helper T (Th) 1/Th2 and Th17/Treg cells is believed to play a key role in asthmatic inflammatory responses. Some studies indicated that zinc deficiency increases inflammatory factor production and worsens asthma. However, the effects of zinc on T cell profiles to reduce inflammatory response remain unclear. Objectives We investigated the beneficial effects of zinc on isolated cell populations and cytokine levels from patients with asthma. Methods Thirty‐six individuals Dermatophagoides pteronyssinus (Der p)‐allergic and 31 healthy subjects were enrolled in the study, and peripheral blood mononuclear cells (PBMCs) were collected. Harvested PBMCs were stimulated with recombinant Der p antigen in the presence or absence of zinc sulfate (25 μM or 50 μM) for 48 h. Cell surface markers and intracellular cytokine levels were examined by flow cytometry. The pro‐inflammatory factors in plasma and culture supernatants were measured by commercial enzyme‐linked immunosorbent assay. Results Zinc sulfate dramatically reduced the proportions of Th2 and Th17 cells, but increased that of Th1 and Treg cells. Zinc sulfate also markedly reduced the levels of interleukin (IL)‐4 and IL‐17, but increased the levels of IFN‐γ. Conclusions Zinc ameliorates the imbalance in T cell profiles and could be a potential adjuvant therapy for Der p‐induced allergic hypersensitivity.
ISSN:1752-6981
1752-699X
DOI:10.1111/crj.12563