Dietary intake of probiotic yogurt, which has beneficial effects on intestinal microecology, is associated with a lower incidence of hypertension. Recent studies have shown that the gut microbiota plays a vital role in the development of hypertension. However, the impact of the gut microbiota in the antihypertensive effect of probiotic yogurt remains unclear. Here, we evaluated the impact of the gut microbiota in the antihypertensive effect of probiotic yogurt in spontaneously hypertensive rats (SHR). SHR were treated with probiotic yogurt (0.2 mL per 100 g body weight) (SHR-Y group) for seven weeks and compared with whole milk-treated (0.2 mL per 100 g body weight) SHR (SHR group) and with normotensive Wistar-Kyoto rats (WKY group). The blood pressure and heart function of the rats in the WKY, SHR, and SHR-Y groups were measured. Fecal microbiota was assessed by 16S ribosomal RNA (16S rRNA) gene sequencing. To investigate whether probiotic yogurt prevents hypertension in spontaneously hypertensive rats through the gut microbiota, we co-housed SHR rats (SHR^COH) with SHR-Y rats (SHR^COH-Y), thus allowing the transfer of microbiota via coprophagy. Compared with whole milk, supplementation of probiotic yogurt significantly reduced the blood pressure, heart rate (HR), and cardiac function. We found that the probiotic yogurt modified the gut microbiota populations and increased the alpha diversity. Gut microbiota remodeling by co-housing partly rescued the increase of blood pressure and impaired the cardiac function of SHR rats. Moreover, probiotic yogurt modulated the gut microbiota in mice by increasing the abundance of short-chain fatty acid (SCFA)-producing bacteria and SCFA levels (acetic acid, propionic acid, butyric acid, and valeic acid) in the feces. Together, the presented data revealed that probiotic yogurt exhibited antihypertensive effects in SHR rats via remodeling of the gut microbiota.

Pulmonary embolism (PE) is a common and potentially fatal condition in the emergency department, and early identification of modifiable risk factors for prevention and management is highly desirable. Although gut dysbiosis is associated with a high incidence of venous thromboembolism, the role and mechanisms of the gut microbiome in the pathogenesis of venous thromboembolism, especially PE, remain unexplored. Here, we attempted to elucidate the benefits of the gut microbiome in the pathogenesis of PE using multiple antibiotics and fecal microbiota transplantation (FMT) for early intervention in a classical mouse model of PE. The results showed that early administration of various antibiotics (except ampicillin) could inhibit pulmonary thrombosis to a certain extent and reduced mortality in young and old mice with PE. Among them, vancomycin has the best inhibitory effect on PE. With the help of gut microbiota sequencing analysis, we found that antibiotic treatment can reshape the gut microbiota; especially vancomycin can significantly improve the gut microbiota structure in PE mice. Furthermore, FMT could transfer vancomycin-modified gut microbes into mice and inhibit the pathogenesis of PE, possibly due to increased intestinal colonization by Parasutterella. These data elucidate the underlying molecular mechanism by which early administration of vancomycin can remodel the gut microbiota to suppress PE, providing new clues for clinical optimization and development of PE prevention strategies.