Several microscopic pathways have been identified, including the intracellular bacterial community, QIR, LPS, multimicrobial infection, and urothelial mucosal remodelling. These mechanisms allow uropathogens to persist in the bladder and survive antibiotic therapy and host immune response. Furthermore, immunological defences show some abnormalities in UTI-prone women, such as increased levels of IL-12, absence of T-cell response, less VEGF, lower level of monocyte chemotactic protein 1, the upregulation of immediate-early (IE) genes, such Nur77. This evidence concerns the gene CCL2 and bacterial urinary tract infection.