In infection models, the expression of sRNA102 suppressed the expression of the anti-inflammatory cytokine interleukin-10 (IL-10) (downregulated by approximately 50% in the sRNA102-overexpressing infection group), while promoting the expression of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) and the immunomodulatory marker arginase 1 (Arg1), ultimately leading to increased bacterial colonization in the mouse peritoneal cavity. The gene discussed is TNF; the disease is infection.