Carbonate buffer mixture and fecal microbiota transplantation hold promising therapeutic effects on oligofructose-induced diarrhea in horses.

Diarrhea is a common gastrointestinal disorder in horses, with diet-induced diarrhea being an emerging challenge. This study aimed to investigate the gut microbiota differences in healthy and diet-induced diarrheic horses and evaluate the effectiveness of fecal microbiota transplantation (FMT) and carbonate buffer mixture (CBM) as potential therapeutic approaches. Twenty healthy horses were included in the study, with four groups: Control, Diarrhea, CBM, and FMT. Diarrhea was induced using oligofructose, and fecal samples were collected for microbiota analysis. FMT and CBM treatments were administered orally using donor fecal matter, and formula mixture, respectively. Clinical parameters, serum levels, intestinal tissue histopathology, and fecal microbiota profiles were evaluated. The results showed that diarrhea induction disbalanced the gut microbiota with decreased diversity and richness, affected clinical parameters including elevated body temperature and diarrhea score, and decreased fecal pH, increased inflammatory responses such as increased serum LPS, IL-17A, lactic acid and total protein, and caused damage in the colon tissue. CBM and FMT treatments altered the gut microbiota composition, restoring it towards a healthier profile compared to diarrheic, restored the gut microbiota composition to healthier states, improved clinical symptoms including decreased body temperature and diarrhea score, and increased fecal pH, decreased inflammatory responses such as increased serum LPS, IL-17A, lactic acid and total protein, and repaired tissue damage. CBM and FMT Spearman correlation analysis identified specific bacterial taxa associated with host parameters and inflammation. FMT and CBM treatments showed promising therapeutic effects in managing oligofructose-induced diarrhea in horses. The findings provide valuable insights into the management and treatment of diarrhea in horses and suggest the potential of combined CBM and FMT approaches for optimal therapeutic outcomes.

The rumen microbiota contributed to the development of mastitis induced by subclinical ketosis.

BACKGROUND: Mastitis is a serious disease which affects animal husbandry, particularly in cow breeding. The etiology of mastitis is complex and its pathological mechanism is not yet fully understood. Our previous research in clinical investigation has revealed that subclinical ketosis can increase the number of somatic cell counts (SCC) in milk, although the underlying mechanism remains unclear. Recent studies have further confirmed the significant role of mastitis. RESULTS: In this study, we aimed to examine the SCC, rumen microbiota, and metabolites in the milkmen of cows with subclinical ketosis. Additionally, we conducted a rumen microbiota transplant into mice to investigate the potential association between rumen microbiota disturbance and mastitis induced by subclinical ketosis in dairy cows. The study has found that cows with subclinical ketosis have a higher SCC in their milk compared to healthy cows. Additionally, there were significant differences in the rumen microbiota and the level of volatile fatty acid (VFA) between cows with subclinical ketosis and healthy cows. Moreover, transplanting the rumen microbiota from subclinical ketosis and mastitis cows into mice can induce mammary inflammation and liver function damage than transplanting the rumen flora from healthy dairy cows. CONCLUSIONS: In addition to the infection of mammary gland by pathogenic microorganisms, there is also an endogenous therapeutic pathway mediated by rumen microbiota. Targeted rumen microbiota modulation may be an effective way to prevent and control mastitis in dairy cows.

The Prevention Effect of Bacillus subtilis on Escherichia coli-Induced Mastitis in Mice by Suppressing the NF-κB and MAPK Signaling Pathways.

Mastitis, common inflammation of the mammary gland, caused by various factors, is a challenge for the dairy industry. Escherichia coli (E. coli), a Gram-negative opportunistic pathogen, is one of the major pathogens causing clinical mastitis which is characterized by reduced milk production and recognizable clinical symptoms. Bacillus subtilis (B. subtilis) has been reported to have the ability to limit the colonization of pathogens and has immune-stimulatory effects on epithelial cells. The purpose of this study was to explore the preventive role of B. subtilis H28 on E. coli-induced mastitis in mice. The mastitis model was established by nipple duct injection of E. coli into mice, while B. subtilis H28 was utilized 2 h before E. coli injection. Furthermore, pathological changes in the mammary gland were evaluated by hematoxylin-eosin (H&E) staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of proinflammatory cytokines (TNF-α, IL-1ß, and IL-6). We also observed changes in Toll-like receptor 4 (TLR4), nuclear transcription factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) expression by using western blotting. The results revealed that B. subtilis H28 pretreatment reduced neutrophil infiltration in the mammary gland tissues, significantly decreased the secretion of TNF-α, IL-1ß, and IL-6, and downregulated the activation of TLR4 and the phosphorylation of p65 NF-κB, IκB, p38, and ERK. In conclusion, our results indicated that B. subtilis H28 can ameliorate E. coli-induced mastitis and suggest a new method for the prevention of mastitis.

Gut microbiota involved in leptospiral infections.

Leptospirosis is a re-emerging zoonotic disease worldwide. Intestinal bleeding is a common but neglected symptom in severe leptospirosis. The regulatory mechanism of the gut microbiota on leptospirosis is still unclear. In this study, we found that Leptospira interrogans infection changed the composition of the gut microbiota in mice. Weight loss and an increased leptospiral load in organs were observed in the gut microbiota-depleted mice compared with those in the control mice. Moreover, fecal microbiota transplantation (FMT) to the microbiota-depleted mice reversed these effects. The phagocytosis response and inflammatory response in bone marrow-derived macrophages and thioglycolate-induced peritoneal macrophages were diminished in the microbiota-depleted mice after infection. However, the phagocytosis response and inflammatory response in resident peritoneal macrophage were not affected in the microbiota-depleted mice after infection. The diminished macrophage disappearance reaction (bacterial entry into the peritoneum acutely induced macrophage adherence to form local clots and out of the fluid phase) led to an increased leptospiral load in the peritoneal cavity in the microbiota-depleted mice. In addition, the impaired capacity of macrophages to clear leptospires increased leptospiral dissemination in Leptospira-infected microbiota-depleted mice. Our study identified the microbiota as an endogenous defense against L. interrogans infection. Modulating the structure and function of the gut microbiota may provide new individualized preventative strategies for the control of leptospirosis and related spirochetal infections.

Emergency vaccine immunization protects hamsters against acute leptospirosis.

Leptospirosis, caused by pathogenic Leptospira, is a global critical zoonotic disease in terms of mortality and morbidity. Vaccines are often used to prevent leptospirosis. However, few studies have reported the therapeutic effect of a vaccine against Leptospira infection. This study demonstrates the efficacy of the emergency vaccine immunization against acute leptospirosis in hamsters. Treatment with a whole-cell vaccine (Leptospira interrogans serovar Lai) at 24 h post-infection improved the survival rate of hamsters with lower leptospiral burden and minor pathological damage to organs. The vaccine also protected against multiple Leptospira serotypes acute infection. However, the protective effect of the vaccines was lost when beginning treatment at 36 h or 48 h post-infection. These results indicated that vaccines could treat acute leptospirosis in hamsters, but only if immunization is within 24 h after infection.