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obesity ; contact hypersensitivity ; NK cells
Abstract:
This project sheds light on a poorly explored subject such as the influence of DIO on the course of NK cell-mediated CHS reaction in mice and the role of natural gut microbiota phenomenon.The presented data show that mice fed HFD for 8 weeks developed aggravated CHS reaction determined by ear swelling measurement when compared to animals kept on normal diet (ND). Analysis of cells infiltrating the auricle and the auricular ear-draining lymph nodes showed higher number of inflammatory cells in HFD-fed mice.DIO also exacerbates liver inflam1nation by affecting the profile of cytokine production in liver mononuclear cells (LMNC) and by shifting the phenotype of these cells towards pro-inflammatory. Adoptive cell transfer showed that the transfer of LMNC cells from the obese mice to syngeneic naive recipients with normal weight transfer the CHS reaction, but does not aggravate it. Obtained data may suggest that the obesity-induced metainflammation plays an important role in shaping NK cell activity and is necessary in both induction and effector phases of CHS reaction. Further analysis of gut sample showed that 8 week HFD treatment leads to a decrease in the number of anti-inflammatory bacteria in the gut microbiota and induces inflammation in the intestines.In summary, current results suggest that the DIO and the subsequent changes in intestinal microbiota significantly modulate ; the local and systemie inflarnmatory respo11se, contributing to exacerbation of the CHS response mediated by liver NK cells.