Background: Chronic stress (CS) due to prolonged exposure to negative life events increases the risk of psychiatric illnesses and significantly affects physiological processes. CS has also been linked to sustained systemic inflammation, resulting in dysregulated immune responses and organ function. We hypothesized that CS would lead to kidney inflammation and tested this in mice. Methods: Male C57BL/6J mice were subjected to CS by pair-housing them with CD-1 retired breeder mice. Kidney immune cells were isolated and evaluated by spectral flow cytometry. Cytokines were measured using a multiplex assay in kidney tissue and serum. Serum creatinine, cystatin C, and neutrophil gelatinase-associated lipocalin (NGAL) levels were measured. Results: Mice subjected to CS exhibited greater weight gain than the control group and had reduced fur quality. CS led to a decrease in the percentage of CD4 + T cells (54.26 ± 0.89% vs. 59.88 ± 1.25%, P < 0.001) and an increase in T helper 17 (Th17) (2.3 ± 0.3% vs. 0.83 ± 0.15%, P < 0.001) and regulatory T cells (Tregs) (3.42 ± 0.45% vs. 1.53 ± 0.21%, P < 0.001). There was an increase in the macrophage percentage in CS mice (88.33 ± 1.16% vs. 84.26 ± 0.73%, P < 0.01). TNF-α levels were higher in the kidney of stressed mice (8.53 ± 1.18 vs. 3.15 ± 1.29 pg/mL, P < 0.01). CS led to elevated levels of cystatin C (515.9 ± 16.88 vs. 456.6 ± 14.79 ng/mL, P < 0.05) and NGAL (833.1 ± 282.4 vs. 90.58 ± 5.57 ng/mL, P < 0.0001). Conclusions: CS in mice led to kidney inflammation and immunologic changes. These could predispose to acute and chronic kidney diseases in which inflammation plays a pathogenic role.
Rastegar et al. (Thu,) studied this question.