Impact of viral disease hypophagia on pig jejunal function and integrity

Abstract

Pathogen challenges are often accompanied by reductions in feed intake, making it difficult to differentiate impacts of reduced feed intake from impacts of pathogen on various response parameters. Therefore, the objective of this study was to determine the impact of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) and feed intake on parameters of jejunal function and integrity in growing pigs. Twenty-four pigs (11.34 ± 1.54 kg BW) were randomly selected and allotted to 1 of 3 treatments (n = 8 pigs/treatment): 1) PRRSV naïve, ad libitum fed (Ad), 2) PRRSV-inoculated, ad libitum fed (PRRS+), and 3) PRRSV naïve, pair-fed to the PRRS+ pigs' daily feed intake (PF). At 17 days post inoculation, all pigs were euthanized and the jejunum was collected for analysis. At days post inoculation 17, PRRS+ and PF pigs had decreased (P < 0.05) transepithelial resistance compared with Ad pigs; whereas fluorescein isothiocyanate-dextran 4 kDa permeability was not different among treatments. Active glucose transport was increased (P < 0.05) in PRRS+ and PF pigs compared with Ad pigs. Brush border carbohydrase activity was reduced in PRRS+ pigs compared with PF pigs for lactase (55%; P = 0.015), sucrase (37%; P = 0.002), and maltase (30%; P = 0.015). For all three carbohydrases, Ad pigs had activities intermediate that of PRRS+ and PF pigs. The mRNA abundance of the tight junction proteins claudin 2, claudin 3, claudin 4, occludin, and zonula occludens-1 were reduced in PRRS+ pigs compared with Ad pigs; however, neither the total protein abundance nor the cellular compartmentalization of these tight junction proteins differed among treatments. Taken together, this study demonstrates that the changes that occur to intestinal epithelium structure, function, and integrity during a systemic PRRSV challenge can be partially explained by reductions in feed intake. Further, long term adaptation to PRRSV challenge and caloric restriction does reduce intestinal transepithelial resistance but does not appear to reduce the integrity of tight junction protein complexes.

Damage to intestinal barrier integrity in piglets caused by porcine reproductive and respiratory syndrome virus infection

“…Previous studies indicated that PRRSV infection impairs the lungs and intestine [ 17 ] and affects jejunal function and integrity due to hypophagia [ 18 ]. However, its impact on intestinal barrier function and the correspond mechanism of intestinal barrier injury remain unclear.…”

Dairy Cows Are Limited in Their Ability to Increase Glucose Availability for Immune Function during Disease

“…Among them, increased glucose removal from the plasma pool [ 25 , 78 ], a shift in glucose transporter expression [ 79 ], and the depletion of glycogen stores [ 43 ] may increase glucose availability to immune cells to some degree. A reduced energy demand from the digestive tract following hypophagia, as reflected by reduced cell migration and turnover [ 80 , 81 ], may also increase glucose availability for other tissues. In total, however, the contribution of glucogenic C by these adaptations is expected to be low in dairy cows during early lactation, as glycogen depots are generally exhausted after calving [ 82 , 83 ], while homeostasis of plasma glucose is tightly regulated [ 84 ].…”

Lawsonia intracellularis infected enterocytes lack sucrase-isomaltase which contributes to reduced pig digestive capacity

“…Further, the reduction in feed efficiency observed in non-vaccinated pigs was not observed in vaccinated pigs. These data suggest that vaccination prevents disease associated losses in feed efficiency and reductions in growth were largely due to reduced feed intake [ 13 , 31 ].…”

“…Hematoxylin and eosin slides were also used to evaluate intestinal morphology. Images were taken at 4 × magnification using a DP80 Olympus Camera mounted on an OLYMPUS BX 53/43 microscope (Olympus Scientific, Waltham, MA, USA), and 15 well orientated villus and crypt pairs (ileum) or 15 crypts (cecum and colon) were measured using OLYMPUS CellSens Dimension 1.16 software (Olympus Scientific) as previously described [ 13 ].…”