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Abstract

Click to add/remove this article to your list of 'My Favorites' Reduced Baseline and Post-Exercise Leukocyte mRNA Expression of Inflammatory Cytokines in Type 1 DM Children during Ex-Vivo Incubation

Year: 2006

Abstract Number: 1009-P

Authors: PIETRO R. GALASSETTI, JAIME ROSA, REBECCA L. FLORES, ANDRIA PONTELLO, JENNIFER LARSON, MASATO MITSUHASHI.

Institutions: Orange, CA; Irvine, CA.

Results: Introduction Alterations in immune function are known to occur in Type 1 Diabetes (T1DM), causing increased susceptibility to infection. We hypothesized that this may be due in part to reduced leukocyte inflammatory/chemotactic cytokine signaling in response to stimuli requiring inflammatory activation, such as physical exercise.

Methods To test this hypothesis we studied 11 T1DM and 11 control children, age 11-15 years, at rest and after 30min of intense cycling exercise performed in euglycemic conditions. Blood samples were obtained immediately before (pre) and at the end (end) of exercise; leukocytes were incubated ex-vivo for 2 hours, after which analysis of mRNA expression was performed on triplicate 60 uL whole blood aliquots applied to 96-well filterplates; followed by mRNA purification and cDNA synthesis. Real time PCR with SYBR Green fluorescence detection was employed to amplify target mRNAs.

Results Leukocyte mRNA expression of the pro-inflammatory cytokines IL-1β and IL-6, and of the neutrophil chemotactic factor IL-8 were significantly reduced in T1DM children, both at baseline and end exercise. No differences were observed in mRNA expression of IFNγ or the apoptosis regulator FasL.[figure1]Conclusion While ex-vivo leukocyte incubation from healthy children, at rest and after exercise, induced robust increases in pro-inflammatory/chemotactic signaling, these effects seem markedly reduced in age matched T1DM children. Our data suggest a potential role of altered stress-induced leukocyte signaling for the increased susceptibility to infection that occurs in diabetic patients.

Category: Exercise - Human

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