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Contrary to the induction phase, corticosteroids do not modify the time-dependent decay of PCT and CRP when the underlying infectious disease (CAP) is adequately treated(Figure 2). Thus, the increase in IL-6 may be a consequence of an increased inflammatory response to infection. We conclude that the increase in IL-6 is not the result of a response to an established infectious disease. It is the result of a state-dependent inflammatory response to infection.
Immunological Regulation of Immunoglobulinemia. We recently reported a study of immune activation to chronic stress and chronic infection in the skin in rats. In the skin, corticosteroids attenuated the hyperpermeability and hyperinflammation of mice (25). These findings indicated that corticosteroid inhibition of the inflammation-induced immune activation in rat skin could influence its long-term consequences (26). However, our study was limited by an immunocompromised mouse model and the lack of clinical trials involving human patients. The possibility might exist that immunocompromised humans have altered cytokine levels and might not manifest the inflammatory response in the skin. Similarly, it is possible that immunocompromising individuals who respond well to immune activation have low levels of cytokine levels, but remain susceptible to immunogenic insults (27). It is worth noting that our study tested IL-6 only, which might suggest that it is not a direct mediator of the immune response as previously described in studies of innate immune responses. In addition, as IL-6 secretion is highly regulated by the cytokine receptor tyrosine kinase, our results might not generalize to the presence of tyrosine kinase deficiency. Finally, a previous study reported that the magnitude of the inflammatory response to chronic infection was not altered by the cytokine corticosterone, whereas an altered inflammatory response to chronic mild stress was altered by both corticosterone and glucocorticoids (28). Together, the observed variation in the inflammatory response to chronic infection and the inability of these immune alterations to alter the immune response to acute infection suggest that the immune response to infection might be not regulated by the cytokine receptor tyrosine kinase, but would be regulated by other factors, such as other cytokines or chemokines, like leukotrienes and others. This would require further studies.
To conclude, our data suggest that cytokines (IL-6 and IL-10) may not play a causal role in mediating changes in the immune response to infection, and that these changes are not directly regulated by the cytokine receptor tyrosine kinase. This data is consistent with the work of Hirsch
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