Additionally, when examining downstream targets of NF-κB signaling, we observed a notable significant increased protein expression of IL-1β (cleaved IL-1β expression against pro-IL-1β) and IL-17A (IL-17A expression normalized against β-actin) in the GWI+AB group compared to GWI mice (Figure 1A,C,D; for IL-1β- p = 0.02 and for IL-17A- p = 0.001 between the GWI+ AB and GWI group), suggesting that the exposure to antibiotics for a prolonged period might not be effective in mitigating the inflammatory response associated with GWI but plays a role in exacerbating renal inflammation. The gene discussed is IL1B; the disease is inflammation.