IL-1 Receptor Contributes to the Maintenance of the Intestinal Barrier via IL-22 during Obesity and Metabolic Syndrome in Experimental Model.

Intestinal permeability and bacterial translocation are increased in obesity and metabolic syndrome (MS). ILC3 cells contribute to the integrity of intestinal epithelium by producing IL-22 via IL-1β and IL-23. This study investigates the role of IL-1R1 in inducing ILC3 cells and conferring protection during obesity and MS.

Murine response to the opportunistic bacterium Pseudomonas aeruginosa infection in gut dysbiosis caused by 5-fluorouracil chemotherapy-induced mucositis.

Aims: This manuscript aims to explain the relationship between mucositis caused by 5-FU over gut bacterial species and susceptibility to opportunistic infection caused by P. aeruginosa.

Main Methods: BALB/c mice were intraperitoneally treated with PBS or 5-FU.

and Gut Immune System: A Good Friendship That Attenuates Inflammatory Bowel Disease, Obesity, and Diabetes.

is a Gram-negative anaerobic mucus-layer-degrading bacterium that colonizes the intestinal mucosa of humans and rodents. Metagenomic data have shown an inverse correlation between the abundance of and diseases such as inflammatory bowel disease (IBD), obesity, and diabetes. Thus, in recent decades, the potential of this bacterium as an immunomodulatory probiotic for autoimmune and chronic inflammatory diseases has been explored in experimental models.

The role of IL-10 in immune responses against Pseudomonas aeruginosa during acute lung infection.

Pseudomonas aeruginosa is considered an opportunistic pathogen of great clinical importance. The clearance of this bacterium occurs through recognition of the pathogen by innate immune system receptors, leading to a lung inflammatory response. However, this response must be controlled via immunoregulatory pathways.

Vancomycin-induced gut dysbiosis during Pseudomonas aeruginosa pulmonary infection in a mice model.

Pseudomonas aeruginosa is one of the most common opportunistic pathogens causing respiratory infections in hospitals. Vancomycin, the antimicrobial agent usually used to treat bacterial nosocomial infections, is associated with gut dysbiosis. As a lung-gut immunologic axis has been described, this study aimed to evaluate both the immunologic and histopathologic effects on the lungs and the large intestine resulting from vancomycin-induced gut dysbiosis in the P.