Effect of exogenous leukotriene B4 (LTB4) on BALB/c mice splenocyte production of Th1 and Th2 lymphokines |
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| Institution: | 1. Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA;2. Penn Cardiovascular Outcomes, Quality, and Evaluative Research Center, University of Pennsylvania, Philadelphia, PA;3. Penn Center for Health Incentives and Behavioral Economics, University of Pennsylvania, Philadelphia, PA;4. Leonard Davis Institute of Health Economics, University of Pennsylvania, Philadelphia, PA;5. Penn Center for Digital Cardiology, University of Pennsylvania, Philadelphia, PA;6. Ascension Health, St. Louis, MO;7. Department of Medical Ethics and Health Policy, University of Pennsylvania, Philadelphia, PA;8. Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT;9. The Wharton School, University of Pennsylvania, Philadelphia, PA |
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| Abstract: | The effect of exogenous leukotriene B4 (LTB4) on the production of cytokines typical of Th1 (interleukin-2 and interferon-γ) and Th2 (interleukin-4 and interleukin-10) lymphocytes was studied. Splenocytes were stimulated with concanavalin A (ConA) with or without different concentrations of LTB4 (3 × 10−10 to 3 × 10−7M) for various times in the presence of BW 755C to inhibit the endogenous synthesis of eicosanoids. LTB4 was not able to induce cytokine secretion by itself. However, LTB4 augmented ConA spleen cell production of interleukin-2 (IL-2) and interferon-γ (IFN-γ) from Th1 cells and interleukin-4 (IL-4) and interleukin-10 (IL-10) from Th2 cells more than the controls treated with ConA alone. The pre-exposition of splenocytes to LTB4 for 3 h made these cells more sensitive to ConA in terms of IL-2 and IL-10 production than those treated with LTB4 at the onset of the incubation and maintained during the whole culture period. The results suggest that LTB4 may participate as a component of the signal transduction process for ConA-induced Th1 and Th2 cytokine production in a timedependent manner. |
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