Yangchun Cao’s research while affiliated with Northwest A&F University and other places

Clostridium difficile infection (CDI) is a significant infectious disease with limited treatment options. Pterostilbene, an active compound found in blueberries, is known for its antioxidant and anti-inflammatory properties. This study...

Background Subacute rumen acidosis (SARA) is a common metabolic disorder in ruminants that disrupts the rumen microbiome and animal health, but diagnosis is challenging due to subtle symptoms and invasive testing requirements. This study explores the potential of the buccal (oral) microbiome as a diagnostic indicator for SARA, hypothesizing an interaction with the rumen microbiome. Results The study involved 47 dairy goats, including 11 on a control diet and 36 on high-concentrate diets with increasing rumen-degradable starch. Animals were grouped based on dietary exposure and ruminal pH: Control, Low-RDS Tolerance/SARA (LRDST/LRDSS), and High-RDS Tolerance/SARA (HRDST/HRDSS). Transcriptomics of rumen epithelium showed heightened inflammatory pathway gene expression in SARA-susceptible goats compared to controls and tolerant groups. Alpha diversity of ruminal bacteria showed lower Shannon diversity in HRDSS goats compared to HRDST whereas buccal bacteria displayed significantly lower Chao1 diversity in LRDSS goats compared to HRDST. Beta diversity analyses revealed distinct patterns between SARA-affected goats and healthy controls in both ruminal and buccal microbiomes. Prevotellaceae_UCG-003 emerged as a candidate biomarker, with reduced abundance in SARA-susceptible goats in both rumen and buccal samples. Machine learning classifiers achieved high accuracy in distinguishing SARA-susceptible goats using this genus (rumen AUC = 0.807; buccal AUC = 0.779). Source tracking analysis illustrated diminished cross-population of bacteria from the buccal to rumen (2.86% to 0.25%) and vice versa (8.59% to 1.17%), signifying compromised microbial interchange in SARA-affected goats. A microbiota transplant experiment verified SARA microbiota's ability to induce pH decline, escalate inflammation-related gene expression ( MAPK10 , IL17B , FOSB , SPP1 ), disrupt microbial transfer, and reduce Prevotellaceae_UCG-003 in recipients. Conclusion Our findings highlight SARA’s dual impact on ruminal and buccal microbiota, exacerbating epithelial inflammation gene expression. Shifts in the buccal microbiome, specifically reductions in Prevotellaceae_UCG-003 , mirror ruminal changes and can be influenced by inter-compartmental bacterial transmission, thereby offering a non-invasive diagnostic approach for SARA.

This review summarizes the mechanisms of hepatic glycolipid metabolism disorders caused by the negative energy balance encountered in periparturient dairy cows and the relevant research on nutritional additives as a therapeutic option. Factors such as dietary management, hormonal regulation, and overall metabolic stress in the body of the transition cow all contribute greatly to fatty liver formation. Nutritional strategies, such as using gluconeogenic precursors, growth factor, natural plant extracts, and methyl donors can positively modulate the negative effects of fatty liver in periparturient dairy cows. Choline, a methyl donor as a feed additive in transition cows minimizes lipid accumulation in the liver by increasing the efficiency of lipoprotein transport. In conclusion, the disruption of hepatic gluconeogenesis, changes in hormone levels, oxidative stress, and endoplasmic reticulum stress during the transition period in dairy cows collectively disturb hepatic anabolic homeostasis. This disruption promotes the formation of fatty liver and reduces lactation performance in dairy cows. Understanding the specific physiological phenomena of hepatic lipid metabolism disorders in transition cows and intervening with nutritional additives will reduce the negative effects of transition stress and improve animal health.

Clostridium difficile infection (CDI) is a growing global health threat, presenting significant challenges to public health. Advances in metabolomics and proteomics have enhanced our understanding of human physiology, particularly the influence of gut microbiota and dietary components on diseases like CDI. This review explores recent insights into CDI pathogenesis, including the infection cycle, toxin mechanisms, spore structure, germination, and therapeutic strategies targeting spore formation and germination. We also examine the role of gut microbiota and metabolites in CDI progression, along with the impact of diet on disease pathology through microbiota modulation and immune regulation. We aim to guide the development of precise, individualized dietary strategies to regulate gut microbiota and immune responses, offering innovative therapeutic options for CDI prevention.

Background Despite the growing number of studies investigating the connection between host genetics and the rumen microbiota, there remains a dearth of systematic research exploring the composition, function, and metabolic traits of highly heritable rumen microbiota influenced by host genetics. Furthermore, the impact of these highly heritable subsets on lactation performance in cows remains unknown. To address this gap, we collected and analyzed whole-genome resequencing data, rumen metagenomes, rumen metabolomes and short-chain fatty acids (SCFAs) content, and lactation performance phenotypes from a cohort of 304 dairy cows. Results The results indicated that the proportions of highly heritable subsets (h² ≥ 0.2) of the rumen microbial composition (55%), function (39% KEGG and 28% CAZy), and metabolites (18%) decreased sequentially. Moreover, the highly heritable microbes can increase energy-corrected milk (ECM) production by reducing the rumen acetate/propionate ratio, according to the structural equation model (SEM) analysis (CFI = 0.898). Furthermore, the highly heritable enzymes involved in the SCFA synthesis metabolic pathway can promote the synthesis of propionate and inhibit the acetate synthesis. Next, the same significant SNP variants were used to integrate information from genome-wide association studies (GWASs), microbiome-GWASs, metabolome-GWASs, and microbiome-wide association studies (mWASs). The identified single nucleotide polymorphisms (SNPs) of rs43470227 and rs43472732 on SLC30A9 (Zn²⁺ transport) (P < 0.05/nSNPs) can affect the abundance of rumen microbes such as Prevotella_sp., Prevotella_sp._E15-22, Prevotella_sp._E13-27, which have the oligosaccharide-degradation enzymes genes, including the GH10, GH13, GH43, GH95, and GH115 families. The identified SNPs of chr25:11,177 on 5s_rRNA (small ribosomal RNA) (P < 0.05/nSNPs) were linked to ECM, the abundance alteration of Pseudobutyrivibrio_sp. (a genus that was also showed to be linked to the ECM production via the mWASs analysis), GH24 (lysozyme), and 9,10,13-TriHOME (linoleic acid metabolism). Moreover, ECM, and the abundances of Pseudobutyrivibrio sp., GH24, and 9,10,13-TRIHOME were significantly greater in the GG genotype than in the AG genotype at chr25:11,177 (P < 0.05). By further the SEM analysis, GH24 was positively correlated with Pseudobutyrivibrio sp., which was positively correlated with 9,10,13-triHOME and subsequently positively correlated with ECM (CFI = 0.942). Conclusion Our comprehensive study revealed the distinct heritability patterns of rumen microbial composition, function, and metabolism. Additionally, we shed light on the influence of host SNP variants on the rumen microbes with carbohydrate metabolism and their subsequent effects on lactation performance. Collectively, these findings offer compelling evidence for the host-microbe interactions, wherein cows actively modulate their rumen microbiota through SNP variants to regulate their own lactation performance. C1VA69ck9huqCRa2wNrTKWVideo Abstract