In the case of the ER stress response to tunicamycin there were small increases in some proinflammatory cytokines, but these were orders of magnitude lower than concentrations observed in response to infection-related stimuli, and in particular there was no substantial induction of TNF-a, IL-1β, and IL-6, the cytokines best described to induce the HPA axis. Here, IL1B is linked to infection.