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Protein Malnutrition Modifies Innate Immunity and Gene Expression by Intestinal Epithelial Cells and Human Rotavirus Infection in Neonatal Gnotobiotic Pigs
In pigs infected with HRV at PTD10, there was a uniform decrease in the function and/or frequencies of natural killer cells, plasmacytoid dendritic cells, and CD103+ and apoptotic mononuclear cells and altered gene expression profiles of intestinal epithelial cells. In pilot experiments, to evaluate the effects of protein malnutrition on immune function and enteric infection, we infected pigs with HRV at 3 and 10 days after HIFM transplantation to evaluate protein malnutrition/HRV infection effects in the context of developing and established intestinal microbiomes, respectively. The neonatal pigs infected with HRV at 3 days after HIFM transplantation had poor health, high mortality rates, and enhanced HRV shedding/diarrhea, unlike pigs infected at 10 days after HIFM transplantation or germfree pigs. The GF pigs on the protein-deficient diet became stunted compared to their sufficient-diet counterparts; however, stunting and edema were less evident in GF pigs than in HIFM-transplanted protein-deficient pigs. Protein deficiency differentially affects SOX9, CgA, MUC2, villin, and PCNA gene mRNA levels of IECs.SOX9, MUC2, villin, PCNA, and CgA gene mRNA levels were lower in jejunal IECs of protein-deficient pigs than in those of sufficient HIFM/HRV-infected pigs, as demonstrated by quantitative reverse transcription-PCR.
However, only MUC2 and villin mRNA levels were lower in protein-deficient pigs than in protein-sufficient non-HRV-inoculated pigs, while CgA, PCNA, and SOX9 mRNA levels were higher. Protein deficiency decreased the frequencies of natural killer cells among intestinal and splenic mononuclear cells and significantly decreased the NK function of splenic MNCs. Similarly, frequencies of intestinal plasmacytoid dendritic cells and CD103+ MNCs were significantly lower in protein-deficient pigs than in protein-sufficient pigs. To evaluate if the malnutrition-associated altered microbiota is sufficient to induce stunting and other clinical parameters associated with malnutrition in a naive host, we transplanted neonatal Gn piglets on the sufficient and deficient diets with HIFM from large intestinal contents of protein-deficient and -sufficient pigs. Stunting of the pigs on the deficient diet that were transplanted with sHIFM or dHIFM was indistinguishable from that of pigs transplanted with dHIFM.
Likewise sHIFM failed to rescue pigs on a deficient diet from stunting. Here, we report on the establishment of a neonatal Gn pig model of protein malnutrition-the first HIFM-transplanted large-animal model that most fully recapitulates all of the major aspects of kwashiorkor and EED.In this study, we reproduced the main clinical parameters associated with protein malnutrition stunting, hypoproteinemia, hypoalbuminemia, hypoglycemia, and edema in neonatal Gn pigs. Because protein-deficient HIFM-transplanted pigs with or without HRV were more stunted than protein-deficient GF pigs infected with HRV, we conclude that the altered microbiota and not HRV infection alone plays a major role in the development of stunting in protein deficiency. Finally, our observations suggest that the intestinal microbiota enhances epithelial proliferation and IEC barrier function, which is evident from the higher PCNA and villin mRNA levels in HIFM-transplanted pigs than in GF pigs. In conclusion, our results indicate that early-life protein malnutrition in an HIFM-transplanted neonatal Gn pig model accurately reproduces the major aspects of protein malnutrition, including clinical signs, suppressed immunity, increased severity of enteric infection, intestinal dysbiosis, and disrupted epithelial barrier and homeostasis.
What is a Mangalitsa Pig?
The Mangalica grows slower than the leaner and meatier breeds that began to replace it, and fewer farmers wanted to take the time. All good reasons to stop raising Mangalica pigs, and as traditional farming fell by the wayside, the Mangalica became less and less common a sight at Hungarian farms. In the early 1990s there were just 198 Mangalica pigs left and a Hungarian animal geneticist became alarmed. Cooperatives of farmers were formed to protect the breed, and over 20 years, as the numbers stabilized, traditional Mangalica sausage with sweet paprika became available in the Hungarian markets again. There are even a few specialized farmers raising Mangalica pigs in the United States today.
Slow Food, an international organization that preserves traditional foods, endangered animal breeds, and stands against the industrialization of food has listed the Mangalica pig in its Ark of Taste, recognizing it as a breed worth saving. Eating MangalicaThe Mangalica is one of the fattiest pigs in the world; on average 65-70% of the carcass is fat, and lean meat is only 30 – 35% of the carcass, compared to over 50% in modern breeds. The meat of the Mangalica pig is reddish, highly marbled with creamy white fat, and is high in omega-3 fatty acids and natural antioxidants. Mangalica lard is lighter, and melts at a lower temperature, than lard from other pigs, because it contains more unsaturated fat. Because of the high fat content, cured Mangalica pork products can spend a longer time drying, which deepens the flavor without losing moisture.
While the Mangalica pig will never be raised in great numbers, and as an artisanal product costs more than other heritage breed pork, it is gaining adherents who relish the intense flavor and abundant fat. If people keep eating them, it’s safe to say that the Mangalica is back and fatter than ever.