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Title: CIRCULATING CORTISOL, TUMOR NECROSIS FACTOR ALPHA, INTERLEUKIN-1 BETA, AND INTERFERON GAMMA IN PIGS INFECTED WITH ACTINOBACILLUS PLEUROPNEUMONIAE

Author
item BALAJI, R - KANSAS STATE UNIVERSITY
item WRIGHT, K - CYAGRA, LLC
item TURNER, J - KANSAS STATE UNIVERSITY
item HILL, C - KANSAS STATE UNIVERSITY
item DRITZ, S - KANSAS STATE UNIVERSITY
item FENWICK, B - KANSAS STATE UNIVERSITY
item Carroll, Jeffery - Jeff Carroll
item ZANNELLI, M - PIERCE-ENDOGEN, INC.
item BEAUSANG, L - PIERCE-ENDOGEN, INC.
item MINTON, J - KANSAS STATE UNIVERSITY

Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/15/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary: The swine industry suffers substantial economic losses each year due to neonatal morbidity and mortality. For the past 5 years, our laboratory has been investigating acute disease models to evaluate various environmental and nutritional strategies to reduce the severity of disease challenges on the health and well-being of neonatal pigs. An endotoxic model to mimic acute disease responses was used in the majority of this work. However, utilizing an endotoxin to induce sickness in the young pig may not appropriately mimic a live bacterial challenge. The objective of this study was to determine the behavioral, endocrine and immune responses of the young pig to a live bacterial challenge which would mimic pneumonia in the young pig. We found that, while the pneumonia model does indeed elicit some of the expected behavioral and endocrine responses typically associated with disease and typically observed in the endotoxic model, there is no significant change in circulating cytokines. An increase in circulating cytokines is a typical response associated with an endotoxic challenge. Thus, this study demonstrates that, while endotoxic models provide important information regarding the basic regulation of immune function, they may not be the most appropriate model to simulate some disease challenges experienced by the neonatal pig. The results also demonstrate the importance of evaluating various models in order to accurately reflect disease challenges in the young pig. Results from this study will be of interest primarily to scientists working in the area of swine health and immunology.

Technical Abstract: This study evaluated the time course of systemic cytokine concentrations in an acute model of pneumonia in pigs challenged intranasally with Actinobacillus pleuropneumoniae (APP). Feed intake and serum cortisol were measured as overt clinical and systemic markers of disease onset, respectively; serum TNFalpha and IL-1beta as representative systemic inflammatory markers; and IFNgamma as a systemic marker of Th1 lymphocyte activation. Crossbred barrows (n=15), approximately 5 wk of age, were housed in a controlled facility at 25 deg C and under continuous light. Pigs had free access to water and an unmedicated diet. One wk prior to disease challenge, pigs were fitted nonsurgically with venous catheters. At challenge, pigs were given 500 million CFU APP intranasally (n = 8) or sterile growth media intranasally (CON; n = 7). Feed intake was estimated by the change in feeder weight at 12 h intervals from -12 to 84 h relative to the time of disease challenge. Blood sampling began 12 h prior to challenge and continued until 72 h after challenge. Pigs were sampled at -12, -6, and 0 h, then at 90 min intervals until 12 h post-challenge, continuing at 3 h intervals until 24 h post-challenge, then again at 6 h intervals until 72 h after challenge. Feed intake was reduced in APP pigs from 0 to 12 h (P<.001), 24 to 36 h (P<.001), 48 to 72 h (P<.05), and 72 to 84 h (P<.05). APP-challenged pigs had elevated serum cortisol from 180 min to 18 h post-challenge (P<.001) and also at 36 (P<.05), 42 (P<.001), and 60 (P<.05) h following infection. Circulating cytokines were not affected by disease challenge. Thus, in this study, weaned pigs demonstrated expected behavioral and endocrine signs of disease in the absence of significant changes in circulating inflammatory cytokines.