The human body consists of protective mechanisms that safeguard it against harm. This is known as immunity which can be either innate or acquired. The immune system is the body’s way of preventing harmful infections and diseases. One of the important factors is inflammasome. These are protein complexes of the innate immune system responsible for triggering inflammatory reactions. They are part of the innate immune system receptors that control caspase-1 expression and trigger inflammation in reaction to infectious agents and compounds made of host proteins.
Inflammasome participation in the onset or progression of diseases with major public health effects, such as metabolic disorders and neurodegenerative diseases, is further supported by mounting evidence from mice models and human data. Recently, a study was carried out by Paudel et al to investigate the role NLRP3 plays in urinary tract infection(UTI) caused by methicillin-resistant Staphylococcus aureus(MRSA).
NLRP3 might have a limited effect
Some findings have suggested that NLRP3 inflammasomes are not that important in UTIs caused by MRSA. This study was carried out to approve this school of thought.
Laboratory-bred mice were used as subjects during the study, some had a targeted genetic mutation in the NLRP3 gene. A strain of MRSA and reagents were used. The mice were kept at the University of Louisiana’s biology department mouse station. The strain used was MRSA 1369 which was cultivated overnight at a temperature of 37°C and was spun at a rate of 200rpm in tryptic soy broth (TSB). Mice were inoculated via transurethral catheterization, and MRSA 1369 inoculum was delivered for the mouse model of catheter-associated UTI (CAUTI) just after implanting a 4- to 5-mm silicone catheter. Tissues were collected and prepared for histopathology, flow cytometry, and ELISA. Next, NLRP3 inhibitor was administered to some of the subjects while DMSO vehicle was administered to the others, 4hrs after the inoculation.
On results analysis, it was observed that MRSA caused an increase in pro-inflammatory cytokines and chemokines and granulocyte formation in the bladder and kidneys before administration of the NLRP3 inhibitor. In addition, the genetic deletion on NLRP3 is not necessary for treating MRSA urinary tract infections, with or without our catheterization. At 24 hours after ascending UTI treatment, mice lacking in NLRP3 activity displayed comparable MRSA burden and comparable inflammation in the bladder and kidney tissues.
More research is expected on the topic. However, with the knowledge we have so far, medical personnel could perform targeted interventions for UTIs caused by MRSA.
Many schools of thought have proposed that NLRP3 plays a role in UTI, MRSA in particular. The results above propose that they’re dispensable. Overall, our findings support NLRP3 having little to no influence, if any, on the development of urinary immune responses against acute MRSA UTI.