Bacterial presence was further confirmed by the colocalization of LPS and LTA with TNF-α and IL-23a via double IIF, in line with the transcriptomic upregulation of Tnfa, Il17f, Il23a, and Il33. This pattern resembles findings in other tissues, where bacterial dysbiosis drives inflammation without infection, such as in the central nervous system [96], lungs [97], bladder [98], and gut [99]. The gene discussed is IL33; the disease is infection.