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Diet‐induced obesity aggravates NK cell–mediated contact hypersensitivity reaction in Rag1 −/− mice
Author(s) -
Kowalczyk Paulina,
MajewskaSzczepanik Monika,
Strzępa Anna,
Biała Dominika,
Szczepanik Marian
Publication year - 2021
Publication title -
contact dermatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.524
H-Index - 96
eISSN - 1600-0536
pISSN - 0105-1873
DOI - 10.1111/cod.13871
Subject(s) - immunology , inflammation , sensitization , flow cytometry , chemistry , population , recombination activating gene , peripheral blood mononuclear cell , t cell , endocrinology , medicine , immune system , in vitro , biochemistry , recombination , gene , environmental health
Background Previous studies showed that natural killer (NK) cells mediate contact hypersensitivity (CHS) reaction. Many reports are showing that obesity promotes several inflammatory diseases. It was shown that diet‐induced obesity (DIO) aggravates classical T cell–mediated CHS in mice. Objectives To determine whether the high‐fat diet (HFD)–induced obesity modulates antigen‐specific NK cell–mediated response. Methods We evaluated the effect of DIO on NK cell–mediated CHS reaction using a model of dinitrofluorobenzene (DNFB)–induced CHS in Rag1 −/− mice. Results Rag1 −/− mice fed HFD for 8 but not for 4 weeks developed aggravated CHS reaction determined by ear swelling measurement when compared to animals kept on normal diet (ND) prior to DNFB sensitization. The obese Rag1 −/− mice presented the adipose tissue inflammation. Furthermore, in vitro analysis showed that feeding with HFD significantly increases interferon γ (IFN‐γ) and interleukin (IL)‐12p70 and decreases adiponectin concentration in liver mononuclear cell (LMNC) culture supernatants. The flow cytometry analysis of LMNC revealed that HFD treatment prior to DNFB sensitization increases the percentage of NK1.1 + IFN‐γ + cell population and affects the development and maturation of NK1.1 + cells. Conclusions In summary, current results suggest that the DIO significantly modulates the local and systemic inflammatory response, contributing to exacerbation of the CHS response mediated by liver NK cells.