Cryptosporidiosis is a zoonotic protozoan parasite-born disease, equally significant in both animals and humans, especially affecting immunocompromised individuals (e.g., AIDS patients) and neonates. The prime concerns of this review article are to demonstrate the disruption of the intestinal barrier and variations in the gut microbiome during cryptosporidiosis, and to explore host gut–parasite interactions that can lead to the development of novel therapeutics. The review concluded that the enteric barrier is particularly maintained by tight junction proteins (e.g., occludin, claudin, and ZO-1, etc.) and mucosal immunity, both of which are severely compromised during Cryptosporidium spp. infections, resulting in increased intestinal barrier permeability, inflammatory responses, diarrhea, and ultimately death in severe cases. Cryptosporidium-induced dysbiosis is characterized by reduced microbial diversity and richness, a shift from commensal to pathogenic bacteria, as evidenced by increased pro-inflammatory taxa like Proteobacteria, and reduced proportions of beneficial SCFAs producing bacteria, e.g., Firmicutes. Recent investigations have highlighted the interrelations between gut microbiota and epithelial barrier integrity, especially during cryptosporidiosis, demonstrating the modulations regarding tight junctions (TJs), immune reactions, and SCFA production, all of which are main players in alleviating this protozoal parasitic infection. This review comprehensively describes the fine details underlying these impairments, including autophagy-mediated TJs’ degradation, inflammasome activation, and gut microbiome-driven alterations in metabolic pathways, providing the latest relevant, and well-organized piece of knowledge regarding intestinal barrier alterations and microbial shifts during cryptosporidiosis. This work emphasizes the future need for longitudinal studies and advanced sequencing techniques to understand host gut microbiota–parasite interactions, aiming to formulate innovative strategies to mitigate cryptosporidiosis.

Yaks are important food animals in China; however, bacterial diarrheal diseases frequently occur on the plateau, with limited effective therapies. The objective of this research was to evaluate the effectiveness of Lactobacillus salivarius (LS) and berberine in alleviating diarrhea in yak calves. For this purpose, eighteen healthy yak calves were divided into control (JC), infected (JM), and treatment (JT) groups. Yaks in the JT group were treated with 2 × 10¹⁰ CFU/calf L. salivarius and 20 mg/kg berberine, and yaks in the JM and JT groups were induced with multi-drug-resistant Escherichia coli. The results showed that the weight growth rate in the JM group was significantly lower than that in the JC and JT groups. The diarrhea score in the JM group was significantly higher than that in both the JC and JT groups. Additionally, the contents of T-AOC, SOD, GSH-Px, and IL-10 were significantly lower in the JM group than those in the JC and JT groups, while MDA, TNF-α, IL-1β, and IL-6 were significantly higher in the JM group. Microbiota sequencing identified two phyla and twenty-seven genera as significant among the yak groups. Notably, probiotic genera such as Faecalibaculum and Parvibacter were observed, alongside harmful genera, including Marvinbryantia and Lachnospiraceae UCG-001. Our findings indicate that treatment with L. salivarius and berberine significantly reduced diarrhea incidence, improved growth performance, and positively modulated intestinal microbiota, which could provide novel insights for developing new therapies for ruminant diarrhea.

This study aims to explore the therapeutic potential of Angelicae Pubescentis Radix (APR), a traditional Chinese medicine that is widely known for its anti-inflammatory, anti-oxidative, and anti-microbial properties, using a mouse model. In this study, 30 mice were selected and divided into three groups: control group (CD), infection group (ED), and treatment group (TD). Mice in the TD were gavaged with APR oil (0.15 mL/kg/day) for 20 days, while mice in the CD and ED received an equal volume of normal saline. On the 21st day, mice in the ED and TD were infected with multi-drug-resistant E. coli (1 × 10⁷ CFU/mL) derived from diarrheal yak. Twenty-four hours later, all mice were euthanized, and blood, organs, and intestinal samples were collected for analysis. The results of intestinal sections and intestinal bacterial load revealed that APR treatment significantly reduced (p < 0.05) both bacterial load and intestinal injury. Serum analysis indicated that APR treatment also alleviated the inflammation and oxidative stress induced by E. coli infection. Intestinal microbiota sequencing further showed that APR treatment increased the abundance of intestinal probiotics such as Ligilactobacillus, Paludicola, and Blautia_A_1417806 while also enhancing the enrichment of functional pathways associated with antioxidant defense. In conclusion, APR treatment effectively alleviates diseases caused by E. coli infection, promotes the growth of beneficial intestinal bacteria, and improves the antioxidant capacity in animals. Additionally, these findings confirm APR’s role in addressing immediate effects rather than chronic adaptations. Future studies should investigate the prolonged effects of APR treatment beyond the acute phase.