The porcine interferon (PoIFN) complex represents an ideal model for studying IFN evolution which has resulted from viral pressure during domestication. Bama and Banna miniature pigs are the two Chinese miniature pig breeds that have been developed as laboratory animal models for studying virus infection, pathogenesis, and vaccine evaluation. However, the PoIFN complex of such miniature pig breeds remains to be studied. In the present study, we cloned PoIFN-β genes from Bama and Banna miniature pigs, detected their PoIFN-β tissue expression profiles, prepared recombinant PoIFN-β (rPoIFN-β) using the E. coli expression system, and measured their antiviral activities against three different pig viruses. At the amino acid sequence level, PoIFN-βs of the two miniature pig breeds were identical, which shared 100% identity with that of Congjiang Xiang pigs, 99.4–100% identity with that of domestic pigs, and 99.5% identity with that of three species of African wild boars. The tissue expression profiles of PoIFN-β mRNA differed not only between the two miniature pig breeds but between miniature pigs and domestic pigs as well. The four promoter domains of PoIFN-β of the two miniature pig breeds were identical with that of humans, domestic pigs, and three species of African wild boars. The recombinant PoIFN-β prepared from the two miniature pig breeds showed dose-dependent pre-infection and post-infection antiviral activities against vesicular stomatitis virus, porcine respiratory and reproductive syndrome virus, and pig pseudorabies virus. This study provided evidence for the high sequence conservation of PoIFN-β genes within the Suidae family with different tissue expression profiles and antiviral activities.

Food allergy (FA) pathogenesis is closely associated with perturbations of the enteric ecosystem; however, comparative studies examining how distinct allergen triggers differentially affect the enteric mycobiome (total fungal community residing in the gastrointestinal tract) and the enteric bacteriome (total bacterial community residing in the gastrointestinal tract) remain limited. Mapping these allergen-specific patterns of dysbiosis is critical for understanding the pathogenesis and designing targeted therapies. We investigated betanin, a naturally occurring bioactive compound with potent antioxidant and anti-inflammatory properties as a prophylactic agent capable of resolving allergen-specific dysbiosis and restoring immune homeostasis and intestinal barrier integrity. We established parallel peanut and ovalbumin (OVA) FA mouse models, administered betanin prophylactically across the sensitization and challenge phases, and evaluated its effects on the allergic outcomes. Efficacy was assessed by measuring anaphylactic symptom scores, allergic biomarkers (total IgE), allergen-specific IgE, histamine, and mast cell protease-1 (mMCPT-1), Th1/Th2 cytokine profiles, and their associated transcription factors (GATA3 and T-bet), intestinal barrier integrity markers, and tight junction protein expression. Allergen-specific microbial shifts were characterized by using ITS2 and 16S rRNA amplicon sequencing. Betanin significantly attenuated the anaphylactic symptoms in both models. It suppressed the Th2-driven allergic cascade, evidenced by GATA3 downregulation and concurrent reductions in IL-4, IL-5, IL-13, allergen-specific IgE, histamine, and mMCPT-1. Betanin intervention notably restored intestinal villus architecture, indicating improved intestinal structural integrity, which was further supported by the upregulated tight junction proteins (i.e., claudin-1, occludin, and tight junction protein 1). Furthermore, betanin restored allergic-associated dysbiosis with both mycobiome and bacteriome enriching Lachnospiraceae (a well-known family associated with short-chain fatty acid production) and suppressing pathobionts Desulfovibrio. These results suggest that prophylactic betanin administration attenuated IgE-mediated anaphylaxis in two murine allergen models through coordinated immunomodulation, intestinal barrier structure integrity, and enteric microbiome remodeling.

Interferons play a major role in innate immunity and disease resistance. Porcine interferon alpha has 17 subtypes, and their gene sequences, tissue expression profiles, and antiviral activities have been primarily studied in domestic pigs but not in minipigs. Bama minipigs are genetically stable disease-resistant and making them as laboratory animal models for bioscience studies. To define the potential mechanism for disease resistance, in this study, we cloned 17 subtypes of Porcine interferon alpha genes in Bama minipigs using high fidelity polymerase chain reaction and subsequent sequencing. Sequence alignment showed that the 17 porcine interferon alpha subtypes were 98%-100 % homologous in those of domestic pigs. However, significantly different tissue expression profiles of PoIFN-α subtypes were found in the two pig species using real-time quantitative RT-PCR. Among the 10 different Bama minipig tissues tested, significant expression of multi-subtype porcine interferon alpha was detected in the lymph nodes and spleen, whereas no or low expression of fewer subtypes was detected in the heart, lung, brain, and small intestine. Sequence analysis revealed that the porcine interferon alpha promoters were almost similar between the two pig species. A cytopathic effect inhibition assay showed that the recombinant 17 porcine interferon alpha subtypes purified from mammalian cells had significantly different antiviral profile against vesicular stomatitis virus, porcine pseudorabies virus and porcine reproductive and respiratory syndrome virus compared with those in domestic pigs. Our findings provide evidence that porcine interferon alpha subtypes are highly conserved between Bama minipigs and domestic pigs but show varied tissue expression pattern and antiviral capabilities, which may contribute to their differences in disease resistance.