Thermal and Cytokine Responses to Endotoxin Challenge During Early Life

Sudden infant death syndrome (SIDS) remains the leading cause of infant mortality beyond the neonatal period. An increase in body temperature as a result of high environmental temperature, over-wrapping of infants and/or infection are associated with SIDS. Endotoxins such as lipopolysaccharide (LPS) and heat stress may perturb cardiorespiratory function and thermoregulation. Although LPS-mediated body temperature and cytokine responses are well-documented in older animals, the capacity of LPS to induce fever and cytokine response in young rats remains unclear. Therefore, we sought to investigate the acute effects of LPS on body temperature and cytokine concentrations in rat pups. Postnatal day 7 rat pups were divided into three groups. Group 1 was administered LPS intraperitoneally (200µg/kg). Group 2 received saline at volume equal to LPS group. Group 3 received no treatment. Pups were placed in custom-made chambers maintained at ambient temperature of 33°C. Body surface temperature was continuously monitored for four hours. Thereafter, the rats were euthanized and serum collected for cytokine analysis. We demonstrate that LPS treatment increased MIP-1α, IL-10, MCP-1, IP-10, fractalkine and TNF-α with no concurrent rise in body surface temperature. Although neonatal rats produced an array of cytokines in response to LPS, there was no evidence of fever.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author