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Porcine epidemic diarrhea (PED) is a highly contagious intestinal infection primarily affecting pigs. It is caused by the porcine epidemic diarrhea virus (PEDV). PEDV targets the villus tissue cells in the small intestine and mesenteric lymph nodes, resulting in shortened intestinal villi and, in extreme cases, causing necrosis of the intestinal lining. Moreover, PEDV infection can disrupt the balance of the intestinal microflora, leading to an overgrowth of harmful bacteria like Escherichia coli. Exosomes, tiny membrane vesicles ranging from 30 to 150 nm in size, contain a complex mixture of RNA and proteins. MicroRNA (miRNA) regulates various cell signaling, development, and disease progression processes. This study extracted exosomes from both groups and performed high-throughput miRNA sequencing and bioinformatics techniques to investigate differences in miRNA expression within exosomes isolated from PEDV-infected porcine small intestine tissue compared to healthy controls. Notably, two miRNA types displayed upregulation in infected exosomes, while 12 exhibited downregulation. These findings unveil abnormal miRNA regulation patterns in PEDV-infected intestinal exosomes, shedding light on the intricate interplay between PEDV and its host. This will enable further exploration of the relationship between these miRNA changes and signaling pathways, enlightening PEDV pathogenesis and potential therapeutic targets.

Abstract Toxoplasma gondii is thought to infect all nucleated cells in warm-blooded animals, including poultry, mammals, and humans. However, it is unclear whether T. gondii can infect chicken erythrocytes due to the nucleated nature of these cells. Due to the special role of chicken erythrocytes in innate immunity, we investigated the cell‒cell interaction between T. gondii and erythrocytes to elucidate the role of chicken erythrocytes in T. gondii infection. Cellular apoptosis was analyzed by transwell assay and flow cytometry. An immunofluorescence method was used to examine the reorganization of vimentin during T. gondii infection in both Vero cells and chicken erythrocytes. The reorganization of actin was evaluated to further examine the invasion capacity of tachyzoites on chicken erythrocytes during infection. We discovered that T. gondii can adhere to but not invade chicken erythrocytes and eventually cause apoptosis in chicken erythrocytes. When tachyzoites were cocultured with chicken erythrocytes in vitro, the transcriptional levels of T. gondii MIC3, ROP16, and ROP18 were significantly decreased. In addition, the rearrangement of host cell vimentin, a type III cytoskeleton protein regulated by T. gondii infection, was not observed. Similarly, the parasite-induced ring-shaped actin structure was not formed in the host-parasite junction. T. gondii (RH strain) tachyzoites preferentially invaded Vero cells and replicated in chicken blood monocytes, but they were not found in chicken erythrocytes. These findings showed that although T. gondii could attach to the surface of chicken erythrocytes, but couldn’t invade successfully. Interestingly, we found that the T. gondii secretome, lysates, and intact tachyzoites could cause apoptosis of chicken erythrocytes, which suggested a complex mechanism involved in the apoptosis of chicken erythrocytes induced by T. gondii. This study elucidated that T. gondii could not infect nucleated chicken erythrocytes and enriched our understanding of the transmission mechanism of T. gondii among avian species.

Background: Eimeria species are obligate intracellular apicomplexan parasites, causing great economic losses in the poultry industry. Currently wild-and attenuated- type anticoccidial vaccines are used to control coccidiosis. However, their use in fast growing broilers is limited by vaccination side effects caused by medium and/or low immunogenic Eimeria spp. There is, therefore, a need for a vaccine with high immunogenicity for broilers. Methods: The avian yolk sac IgY Fc is the avian counterpart of the mammalian IgG Fc, which enhances immunogenicity of Fc-fusion proteins. Here, we developed a stable transgenic Eimeria mitis expressing IgY Fc (Emi.chFc) and investigated whether the avian IgY Fc fragment enhances the immunogenicity of E. mitis. Two-week-old broilers were immunized with either Emi.chFc or wild type Eimeria and challenged with wild type E. mitis to analyze the protective properties of transgenic Emi.chFc. Results: Chickens immunized with Emi.chFc had significantly lower oocyst output, in comparison with PBS, mock control (transgenic E. mitis expressing HA1 from H9N2 avian influenza virus) and wildtype E. mitis immunized groups after challenge, indicating that IgY Fc enhanced the immunogenicity of E. mitis. Conclusions: Our findings suggest that IgY Fc-expressing Eimeria may be a better coccidiosis vaccine, and transgenic Eimeria expressing Fc-fused exogenous antigens may be used as a novel vaccine-delivery vehicle against a wide variety of pathogens. [ABSTRACT FROM AUTHOR]