ARS | Publication request: TOLL-LIKE RECEPTORS 2 (TLR2) AND 4 (TLR4) OF PORCINE BLOOD LEUKOCYTES DURING HEAT-STRESS

Submitted to: Veterinary Immunology International Symposium
Publication Type: Abstract Only
Publication Acceptance Date: March 3, 2004
Publication Date: July 25, 2004
Citation: Eicher, S.D., Sartin, J.L., Schwartz, D.D., Lay, Jr., D.C., Cheng, H. 2004. Toll-like receptors 2 (TLR2) and 4 (TLR4) of porcine blood leukocytes during heat-stress [absreact]. Veterinary Immunology International Symposium. p. 240.

Technical Abstract: Toll-like receptors (TLR) are becoming well-characterized for mice, but not much is known about their role during acute heat stress in swine. Heat stress is a common problem for swine and humans. In humans, heat shock proteins are recognized by TLR4 and TLR2. Our objective was to determine if acute heat stress would alter TLR2 or TLR4 in swine. Twelve barrows, weighing approximately 45 kg were assigned randomly to control or heat-stress treatments. The control room was maintained at 21.1°C throughout the study. The heat stress pigs were housed in a pre-heated room at 32.2°C for 24 hours. Jugular blood was collected from 3 pigs from each group at 12 and 24 hours after exposure to heat stress. Following blood collection, the pigs were euthanized and then lung tissues were collected. RNA was extracted from whole blood using QIAamp (Qiagen) whole blood extraction kits and from lung tissues using RNeasy mini-kits (Qiagen) and subjected to real-time RT-PCR using Taqman probes. Toll-like receptor 2 tended (P < 0.10) to be elevated in the heat stress group by 24 hours, but not by 12 hours in the blood leukocytes. Toll-like receptor 4 was increased by 24 hours (P < 0.05), but not by 12 hours in blood leukocytes. These data show that porcine TLR4 is most responsive to heat stress as TLR4 is to heat shock proteins in humans and mice, but a lag of more than 12 h is necessary to see the effect. Additionally, by 24 h post-heat exposure, upregulation of TLR2 expression is not as strong as TLR4 upregulation, but as in mice, it appears that both TLRs are involved.