BackgroundPig diarrhea causes high mortality and large economic losses in the swine industry. Transmissible gastroenteritis virus (TGEV) causes pig diarrhea, with 100% mortality in piglets less than 2 weeks old. No investigation has yet been made of the small intestine of piglets that survived infection by TGEV.MethodsIn this study, we evaluated the impact of TGEV infection on the small intestine of recovered pigs.ResultsHistological analyses showed that TGEV infection led to villi atrophy, and reduced villous height and crypt depth. The number of SIgA positive cells, CD3+T cells, and dendritic cells (DCs) in jejunum decreased after TGEV infection in vivo. In contrast, microfold cell (M cell) numbers and cell proliferation increased in infected pigs. TGEV infection also significantly enhanced the mRNA expression levels of cytokine IL-1β, IL-6, TNF-α, IL-10, and TGF-β. Additionally, lower gene copy numbers of Lactobacillus, and higher numbers of Enterobacteriaceae, were detected in mucosal scraping samples from TGEV-infected pigs.ConclusionsTGEV infection damages the small intestine, impairs immune functions, and increases pathogenic bacterial loading, all of which may facilitate secondary infections by other pathogens. These findings help quantify the impact of TGEV infection and clarify the pathogenic mechanisms underlying its effects in pigs.

The nasal mucosa is the body's first barrier against pathogens entering through the respiratory tract. The respiratory immune system of pigs has more similarities with humans than the mouse respiratory system does, and so was selected as the animal model in the present study. To evaluate the effects of Bacillus subtilis as a potential probiotic to stimulate local immune responses, piglets were intranasally administered with Dylight 488-labeled B. subtilis (WB800-green fluorescent protein). The results revealed that B. subtilis was able to reach the lamina propria of the nasal mucosa, nasopharyngeal tonsils and soft palate tonsils. Piglets were subsequently administered intranasally with B. subtilis (WB800) at 3, 12 and 28 days. The results revealed that, following administration with B. subtilis, the number of dendritic cells, immunoglobulin A+ B cells and T cells in the nasal mucosa and tonsils significantly increased (P<0.05). No obvious differences were observed in the morphological structure following B. subtilis administration. There were no statistical differences were observed in the expression of interleukin (IL)-1β, tumor necrosis factor-α and IL-8 mRNA between the B. subtilis treated group and the control group in the nasal mucosa, nasopharyngeal tonsil or soft palate tonsil. Toll-like receptor (TLR)-2 and TLR-9 mRNA expression in the tonsils was significantly increased following B. subtilis administration compared with the control group (P<0.05). The results demonstrate that B. subtilis administration increases the number of immune cells in the nasal mucosa and tonsils of piglets and stimulates nasal mucosal and tonsillar immunity. The present study lays the foundation for further study into the intranasal administration of B. subtilis in humans to enhance the immunity of human nasal mucosa to respiratory diseases.

Objective The aim of this study was to identify and validate ferroptosis-related markers in ulcerative colitis (UC) to explore new directions for UC diagnosis and treatment. Methods We screened UC chips and ferroptosis-related genes from the Gene Expression Omnibus (GEO), FerrDb, and GeneCards databases. The differentially expressed genes (DEGs) and ferroptosis-related DEGs between the UC group and normal controls were analyzed using bioinformatics methods. Enrichment analysis, protein–protein interaction analysis, and hub genes were screened. Peripheral blood chip and animal experiments were used to validate the ferroptosis-related hub genes. Finally, hub gene–transcription factor, hub gene–microRNA (miRNA), and hub gene–drug interaction networks were constructed. Results Overall, 26 ferroptosis-related DEGs were identified that were significantly enriched in energy pathways and metabolism. We identified ten ferroptosis-related hub genes from the protein–protein interaction network: IL6, PTGS2, HIF1A, CD44, MUC1, CAV1, NOS2, CXCL2, SCD, and ACSL4. In the peripheral blood chip GSE94648, CD44 and MUC1 were upregulated, which was consistent with the expression trend in GSE75214. Animal experiments showed that CD44 expression was significantly increased in the colon. Conclusions Our findings indicate that CD44 and MUC1 may be ferroptosis-related markers in UC.

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