Food is often contaminated with Escherichia coli (E. coli) bacteria strains, which have been associated with different diseases, including urinary tract infections. The consumption of meat by humans is a potential route of transmission of antimicrobial resistance, and food-producing animals have been associated as a major reservoir of resistant bacterial strains. The aim of this study was to determine the presence of the E. coli strains producing the CNF-1 toxin in pig kidneys. Pig kidneys were collected from a Mexican slaughterhouse and classified according to their coloration into reddish kidneys (RK) and yellowish kidneys (YK). A tissue sample from each kidney was processed for histological analysis, the presence of E. coli was determined by conventional PCR assay, and the CNF-1 toxin was detected by both conventional PCR and Western blotting. Herein, an inflammatory cell infiltrate was found in all collected kidneys, regardless of macroscopic differences. Surprisingly, E. coli and the CNF-1 toxin were detected in all kidney samples. We clearly demonstrate contamination by CNF-1 toxin-producing E. coli in pork kidneys from a slaughterhouse, even in those without apparent damage. This suggests that pork may serve as a reservoir for pathogens, representing an important risk to human health.

La obesidad es una enfermedad crónica que se caracteriza por un IMC superior a 30 causado por el exceso de grasa corporal, afecta a millones de personas en el mundo y representa un problema de salud pública en ascenso considerando sus múltiples complicaciones. El espermatozoide es una célula altamente especializada conformada por cabeza, pieza intermedia y cola, que cumple con la función principal de fecundar el ovocito. Durante el trayecto en el tracto reproductor femenino, el espermatozoide lleva a cabo un proceso de capacitación donde posteriormente realizará la reacción acrosomal, proceso que permite penetrar la zona pelúcida del ovocito. En este estudio se evaluó el efecto del aumento de tejido adiposo sobre la fisiología espermática en un modelo murino, se observó un incremento en la reacción acrosomal espontánea, lo que sugiere un compromiso de la obesidad en la fertilidad masculina. Aunque la identificación de proteínas acetiladas no arrojó resultados concluyentes, los hallazgos refuerzan la hipótesis de que la obesidad afecta procesos celulares esenciales en los espermatozoides.

Background: Diets high in fat and carbohydrates, like fructose, trigger colon inflammation, increase intestinal permeability, and drive dysbiosis. However, the effects of obesogenic diets on gut microbiota, including Clostridium and Bacteroides, remain unknown. Understanding how these diets damage the colon is critical. Methods: Using a controlled preclinical obesity model, we compared the effects over time of High-Fat Diet (HFD), High-Fructose Diet (HFrD), and their combination (HFHFrD). Diet-induced dysbiosis was assessed at 4 and 8 weeks via qPCR using primers specific to bacterial phyla and species. In addition, intestinal inflammation, atrophy, and mucin production were evaluated by digital pathology after 8 weeks of diet exposure. Results: both HFrD and HFHFrD mice exhibited marked intestinal inflammation, atrophy, and damage, alongside altered production of neutral and mixed mucins. HFD-fed mice displayed a 15-fold surge in Clostridium/Bacteroides ratio at 4 weeks. At 8 weeks, HFrD-fed mice showed a striking 10-fold rise in microbial relative abundance compared to the other diets. Both HFrD and HFHFrD triggered an early increase in Bacteroides species, but significance emerged only at 8 weeks. Conclusions: Although all obesogenic diets induced inflammation, atrophy, epithelial damage, and altered mucin patterns, HFrD and HFHFrD caused pronounced disruptions to barrier function and dysbiosis. Critically, HFD consistently raised the Firmicutes/Bacteroidetes ratio at 4 and 8 weeks, while the Clostridium/Bacteroides ratio spiked only at 4 weeks. Obesogenic diets fundamentally shifted microbial load and diversity. Therefore, bacterial ratios, such as Clostridium/Bacteroides, may signal dysbiosis and tissue damage from obesogenic diets, but further research is required for confirmation.