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One of the common illnesses that affect women's physical and mental health is urinary tract infection (UTI). The disappointing results of empirical anti-infective treatment and the lengthy time required for urine bacterial culture are two issues. Antibiotic misuse is common, especially in females who experience recurrent UTI (rUTI). This leads to a higher prevalence of antibiotic resistance in the microorganisms that cause the infection. Antibiotic therapy will face major challenges in the future, prompting clinicians to update their practices. New testing techniques are making the potential association between the urogenital microbiota and UTIs increasingly apparent. Monitoring changes in female urinary tract (UT) microbiota, as well as metabolites, may be useful in exploring newer preventive treatments for UTIs. This review focuses on advances in urogenital microbiology and organismal metabolites relevant to the identification and handling of UTIs in an attempt to provide novel methods for the identification and management of infections of the UT. Particular attention is paid to the microbiota and metabolites in the patient's urine in relation to their role in supporting host health. [ABSTRACT FROM AUTHOR]

Pasteurella multocida (P. multocida) is a significant zoonotic pathogen that has the ability to infect various animals. The inflammatory response caused by P. multocida and the negative regulatory mechanism are not completely understood. NOD-like receptor family CARD-containing 3 (NLRC3), an intracellular member of the NLR family, has been reported as a negative regulator in human. In this study, we aimed to explore the role of rabbit NLRC3 (rNLRC3) in P. multocida infection. Our findings revealed a negative correlation between the expression of rNLRC3 and inflammatory cytokines during P. multocida infection. The expression of rNLRC3 was reduced at the initial stage of P. multocida infection and then recovered. Furthermore, rNLRC3 significantly inhibited the activation of NF-κB by reducing phosphorylation and nuclear import of p65 in response to P. multocida infection. Additionally, overexpression of rNLRC3 attenuated the expression of pro-inflammatory cytokines IL-1β , IL-6 , IL-8 , and TNF-α. Moreover, we demonstrated that rNLRC3 diminished NF-κB activation by interacting with rTRAF4 and rTRAF6. Overexpression of rNLRC3 promoted P. multocida proliferation, while P. multocida proliferation decreased after knockdown of rNLRC3. We also found that the NACHT-LRR domain is a functional domain of rNLRC3 that regulates the NF-κB pathway. Our study suggests that rNLRC3 negatively regulates P. multocida -induced NF-κB signaling in rabbits. It can serve as a checkpoint to prevent dysfunctional inflammation. • rNLRC3 inhibit P. multocida -induced NF-κB. • NOD-LRR is functional domain. • rNLRC3 diminish NF-κB by interacting with rTRAF4 and 6. [ABSTRACT FROM AUTHOR]