Diarrheal diseases and PEM are major causes of child morbidity and mortality worldwide. Diarrhea may be prolonged by PEM, therefore, we hypothesized that PEM delays intestinal recovery following viral enteritis. Two-dolci pigs (n=24) were infected with rotavirus, and PEM was superimposed on half by diluting formula 50%. Twelve pigs were not infected. Two d post-infection, severe diarrhea and 11 % weight loss were accompanied by increased intestinal PGE2 (9-fold) and MHC gene expression (marker of inflammation), 60% reduced villus height and 78% reduced lactase activity in infected compared to noninfected pigs (P<0.05). Nine d post-infection, diarrhea persisted, weight gain was 59% lower, and villus height and lactase activity remained 50% reduced in infected compared to noninfected pigs (P<0.05). Plasma IGF-I was reduced 68% and intestinal PGEj was 2-fold higher in infected-PEM compared to infected full-fed pigs (P<0.05). Sixteen d post-infection, full-fed pigs had recovered from rolaviral infection, reflected by lack of diarrhea, and similar weight gain, intestinal PGE2 and MHC gene expression, villus height and lactase activity compared to noninfected pigs. However, diarrhea and lower weight gain persisted, and plasma IGF-I, villus height and alkaline phosphatase activity remained reduced in infectedPEM compared to infected full-fed pigs (P<0.05). Overall, PEM prolonged diarrhea and delayed small-intestinal recovery which suggests that improving nutritional status is essential to support rapid recovery from viral enteritis. Identification of indices of intestinal inflammation affected by PEM facilitates efforts to design therapeutic strategies based on nutrient immunomodulation.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology