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, overwrapping 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 3 groups: Group 1, rats were administered LPS intraperitoneally (200 μg/kg); Group 2, rats received saline at volume equal to that administered in the LPS group; Group 3, rats received no treatment. Pups were placed in custom-made chambers maintained at ambient temperature of 33 °C. Body surface temperature was continuously monitored for 4 h. Thereafter, the rats were euthanized and serum was 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.