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Article

Malnutrition Modifies Pig Small Intestinal Inflammatory Responses to Rotavirus

Ruurd T. Zijlstra^*,1, Barbara A. McCracken^*, Jack Odle^*,,2, Sharon M. Donovan^,**, Howard B. Gelberg, Bryon W. Petschow, Federico A. Zuckermann and H. Rex Gaskins^*,,3

Division of Nutritional Sciences, Departments of ^* Animal Sciences, ^** Food Science and Human Nutrition, and Veterinary Pathobiology, University of Illinois at Urbana-Champaign and Mead Johnson Research Center, Evansville, IN

³To whom correspondence should be addressed.

Infectious diarrheal diseases and malnutrition are major causes of child morbidity and mortality. In this study, malnutrition was superimposed on rotavirus infection in neonatal piglets to simulate the combined intestinal stress of viral enteritis in malnourished infants. Two-day-old piglets were assigned to three treatment groups as follows: 1) noninfected, fully nourished; 2) infected, fully nourished; and 3) infected, malnourished. Intestinal indices of inflammation were monitored over the subsequent 2-wk period. Intestinal damage and diarrhea were observed within 2 d of rotavirus infection and began to subside in nourished piglets by d 9 but persisted through d 16 postinfection in malnourished piglets. Rotavirus upregulated small intestinal expression of major histocompatibility complex (MHC) class I and class II genes; malnutrition intensified MHC class I gene expression and suppressed MHC class II expression. Jejunal CD4⁺ and CD8⁺ T-lymphocyte numbers were elevated for infected, nourished piglets on d 2, 9 and 16 postinfection. Malnutrition did not significantly affect the local expansion of T cell subsets in response to rotavirus. Intestinal prostaglandin E₂ (PGE₂) concentrations were elevated early after rotavirus infection independent of nutritional state. By d 9, PGE₂ concentrations returned to baseline in infected, nourished piglets but remained elevated in malnourished piglets, corresponding to diarrhea observations. Together, the results identify intestinal indices of inflammation that are modulated by malnutrition and prompt reconsideration of current models of rotavirus pathophysiology.

KEY WORDS: • rotavirus • inflammation • malnutrition • pigs • small intestine

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