Effects of thermal environment on response to acute peripheral lipopolysaccharide challenge exposure in neonatal pigs

John J. Klir From the Animal Physiology Unit, Agricultural Research Service, United States Department of Agriculture (Klir, Matteri) and the Department of Animal Science (Shahbazian, Fritsche), University of Missouri, Columbia, MO 65211. Dr. Becker is self employed.

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L. Masoud Shahbazian From the Animal Physiology Unit, Agricultural Research Service, United States Department of Agriculture (Klir, Matteri) and the Department of Animal Science (Shahbazian, Fritsche), University of Missouri, Columbia, MO 65211. Dr. Becker is self employed.

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Robert L. Matteri From the Animal Physiology Unit, Agricultural Research Service, United States Department of Agriculture (Klir, Matteri) and the Department of Animal Science (Shahbazian, Fritsche), University of Missouri, Columbia, MO 65211. Dr. Becker is self employed.

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Kevin L. Fritsche From the Animal Physiology Unit, Agricultural Research Service, United States Department of Agriculture (Klir, Matteri) and the Department of Animal Science (Shahbazian, Fritsche), University of Missouri, Columbia, MO 65211. Dr. Becker is self employed.

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B. Ann Becker From the Animal Physiology Unit, Agricultural Research Service, United States Department of Agriculture (Klir, Matteri) and the Department of Animal Science (Shahbazian, Fritsche), University of Missouri, Columbia, MO 65211. Dr. Becker is self employed.

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Abstract

Objective

To evaluate effects of thermal environment on response to acute peripheral lipopolysaccharide (LPS) challenge exposure in neonatal pigs.

Animals

26 neonatal pigs.

Procedure

Pigs were assigned to the following treatment groups: 1 warm environment/LPS; 2 warm environment/saline solution; 3 cool environment/LPS; and 4 cool environment/saline solution. For each pig given LPS. 1 littermate of the same sex was given saline solution. Sows with baby pigs were housed in a warm (32 C) or cool (21 C) thermal environment. At 28 days of age, pigs were given 150 µg/kg of body weight of Escherichia coli LPS or saline solution intraperitoneally as a control. Rectal temperature and signs of sickness were monitored for 3 hours after LPS administration, when pigs were euthanatized and blood samples were collected to determine serum concentrations of tumor necrosis factor (TNF) α and cortisol. To determine in vitro production of TNFα, alveolar macrophages were collected by tracheal lavage and incubated for 24 hours at 37 or 41 C, with or without LPS (10 µg/ml).

Results

Thermal environment had a significant (P = 0.0004) effect on rectal temperature; LPS administration induced a febrile response (P = 0.0007) only in pigs in the warm environment. All LPS-injected pigs developed signs of endotoxemia; serum TNFα and cortisol concentrations were significantly increased (TNFα, P = 0.003; cortisol, P = 0.0001); there was no significant in vivo thermal effect on serum TNFα and cortisol concentrations. LPS-stimulated alveolar macrophages produced significantly less (P = 0.0086) TNFα when incubated at 41 C.

Conclusions

Thermal environment can have a significant impact on the response of neonatal pigs exposed to bacterial endotoxins. (Am J Vet Res 1997; 58:364-369)

Abstract

Objective

To evaluate effects of thermal environment on response to acute peripheral lipopolysaccharide (LPS) challenge exposure in neonatal pigs.

Animals

26 neonatal pigs.

Procedure

Pigs were assigned to the following treatment groups: 1 warm environment/LPS; 2 warm environment/saline solution; 3 cool environment/LPS; and 4 cool environment/saline solution. For each pig given LPS. 1 littermate of the same sex was given saline solution. Sows with baby pigs were housed in a warm (32 C) or cool (21 C) thermal environment. At 28 days of age, pigs were given 150 µg/kg of body weight of Escherichia coli LPS or saline solution intraperitoneally as a control. Rectal temperature and signs of sickness were monitored for 3 hours after LPS administration, when pigs were euthanatized and blood samples were collected to determine serum concentrations of tumor necrosis factor (TNF) α and cortisol. To determine in vitro production of TNFα, alveolar macrophages were collected by tracheal lavage and incubated for 24 hours at 37 or 41 C, with or without LPS (10 µg/ml).

Results

Thermal environment had a significant (P = 0.0004) effect on rectal temperature; LPS administration induced a febrile response (P = 0.0007) only in pigs in the warm environment. All LPS-injected pigs developed signs of endotoxemia; serum TNFα and cortisol concentrations were significantly increased (TNFα, P = 0.003; cortisol, P = 0.0001); there was no significant in vivo thermal effect on serum TNFα and cortisol concentrations. LPS-stimulated alveolar macrophages produced significantly less (P = 0.0086) TNFα when incubated at 41 C.

Conclusions

Thermal environment can have a significant impact on the response of neonatal pigs exposed to bacterial endotoxins. (Am J Vet Res 1997; 58:364-369)

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