1.
Effect of cortisol and/or DHEA on THP1-derived macrophages infected with Mycobacterium tuberculosis.
Bongiovanni, B, Mata-Espinosa, D, D'Attilio, L, Leon-Contreras, JC, Marquez-Velasco, R, Bottasso, O, Hernandez-Pando, R, Bay, ML
Tuberculosis (Edinburgh, Scotland). 2015;(5):562-9
Abstract
Tuberculosis (TB) is a major health problem requiring an appropriate cell immune response to be controlled. Macrophages play a central role in the response against Mycobacterium tuberculosis (Mtb). Given our prior studies in which adrenal steroids were found to modify the cellular immune responses from TB patients, it was sensible to analyze the immunomodulatory capability of cortisol and DHEA on macrophages infected with Mtb. The human macrophage-like THP-1 cells were infected with the H37Rv strain of Mtb and treated with Cortisol and DHEA at different doses. We monitored phagocytosis, intracellular-bacterial growth, autophagosoma formation, as well as cytokine gene expression and production. Cultures exposed to cortisol showed a decreased production of IL-1β, TNF-α, with DHEA being unable to modify the pattern of cytokine production or to reverse the cortisol inhibitory effects. Interestingly the intra-macrophagic bacterial burden was found reduced by DHEA treatment. While this effect was not related to a different cytokine pattern, in terms their production or mRNA expression, DHEA treatment did promote autophagy in Mtb-infected macrophages, irrespective of Cortisol presence. In essence, the better control of Mtb load by DHEA-treated macrophages seems to be dependent on an autophagic mechanism. The present results are relevant for two reasons as autophagy is not only important for clearance of mycobacteria but also for the prevention of tissue damage.
2.
Vitamin C supplementation and salivary immune function following exercise-heat stress.
Carrillo, AE, Murphy, RJ, Cheung, SS
International journal of sports physiology and performance. 2008;(4):516-30
Abstract
PURPOSE Prolonged physical exertion and environmental heat stress may elicit postexercise depression of immune cell function, increasing upper respiratory tract infection (URTI) susceptibility. We investigated the effects of acute and short-term vitamin C (VC) compared with placebo (PL) supplementation on URTI susceptibility, salivary immunoglobulin A (s-IgA), and cortisol responses in healthy individuals following prolonged exercise-heat stress. METHODS Twelve participants were randomized into the VC or PL group in a double-blind design. For 12 days, participants consumed 3x500 mg tablets of VC or PL per day, with testing completed at baseline, then following acute (1 d) and short-term (8 d) supplementation. Participants performed 120.1+/-49.6 min of cycling at 54+/-6% VO2max in a hot (34.8+/-1.0 degrees C and 13+/-3% relative humidity) environment, with saliva samples collected at pre-, post-, and 72 h postexercise. Health logs specifying URTI symptoms were completed for 7 days postexercise. RESULTS A 2x3x3 mixed ANOVA with a post hoc Bonferroni correction factor revealed a significant linear trend in postexercise cortisol attenuation in the VC group, 21.7+/-15.1 nmol/L (mean+/-SD) at baseline, to 13.5+/-10.0 at acute, to 7.6+/-4.2 after short term (P=.032). No differences were detected in ratio of s-IgA to protein or URTI symptoms between groups. CONCLUSIONS These data suggest that vitamin C supplementation can decrease postexercise cortisol in individuals performing exercise similar to that of a half-marathon or marathon in hot conditions. However, no changes in s-IgA and URTI were evident, possibly due to previous moderate training and reduced physical and psychological stress compared with athletes participating in ultramarathons.