Warm-up exercise suppresses platelet-eosinophil/neutrophil aggregation and platelet-promoted release of eosinophil/neutrophil oxidant products enhanced by severe exercise in men

Summary

Heterotypic platelet-eosinophil/neutrophil aggregation and subsequent release of eosinophil/neutrophil oxidant products contribute to pathogenesis of conditions such as asthma and inflammatory bowel diseases. This study investigates whether warmup exercise (WUE) affects platelet-eosinophil/neutrophil interaction mediated by high-intensity exercise (HIE). Twenty-three healthy sedentary men performed on three occasions light-intensity exercise (LIE, 40%VO_2max for 40 min) and HIE (80%VO_2max for 40 min) with and without WUE (40%VO_2max for 20 min). Before and immediately after exercise, platelet-eosinophil and platelet-neutrophil aggregation (PEA and PNA), reactive oxygen species production of eosinophils and neutrophils (EROS and NROS) enhanced by platelets, and adhesion molecule expression on platelets, eosinophils, and neutrophils were measured. The results of this study demonstrated that HIE enhanced PEA, PNA, and platelet-induced EROS and NROS, was accompanied by increased expressions of Mac-1 on eosinophils and neutrophils and P-selectin on platelets at 5 dyne/cm² of shear stress, 100 µg/ml lipopolysaccharide, and 1 µM N-formylmethionyl-leucyl-phenylalanine treatments, whereas the enhancement of HIE on platelet-eosinophil/neutrophil interaction was suppressed by WUE. Conversely, LIE significantly reduced PEA and PNA, suppressed platelet-induced EROS and NROS, and down-regulated eosinophil/neutrophil Mac-1 and platelet P-selectin expressions under various stimuli and shear flow conditions. Moreover, these effects were more pronounced in platelet interaction with eosinophils than with neutrophils. It is concluded that HIE enhances hetero-aggregation, adhesion molecules expressions, and subsequent oxidative bursts mediated by platelets and eosinophils/neutrophils, this effect diminishes after WUE. However, LIE minimizes the risk of thromboinflammation.

Keywords

Warm-up - eosinophil - platelet - inflammation - thrombosis

• References

• 1 Wardlaw AJ, Moqbel R, Kay AB. Eosinophils: biology and role in disease. Adv Immunol 1995; 60: 151-266.
• 2 Gleich GJ. Mechanisms of eosinophil-associated inflammation. J Allergy Clin Immunol 2000; 105: 651-63.
• 3 Lucas R, Lou J, Morel DR. et al. TNF receptors in the microvascular pathology of acute respiratory distress syndrome and cerebral malaria. J Leukoc Biol 1997; 61: 551-8.
• 4 Obayashi Y, Yamadori I, Fujita Jet. al. The role of neutrophils in the pathogenesis of idiopathic pulmonary fibrosis. Chest 1997; 112: 1338-43.
• 5 Sustiel AM, Joseph B, Rocklin RE. et al. Asthmatic patients have neutrophils that exhibit diminished responsiveness to adenosine. Am Rev Respir Dis 1989; 140: 1556-61.
• 6 Takashi S, Okubo Y, Horie S. Contribution of CD54 to human eosinophil and neutrophil superoxide production. J Appl Physiol 2001; 91: 613-22.
• 7 Ulfman LH, Joosten DPH, van Aalst CW. et al. Platelets promote esinophil adhesion of patients with asthma to endothelium under flow conditions. Am J Respir Cell Mol Biol 2003; 28: 512-9.
• 8 Pitchford SC, Momi S, Giannini S. et al. Platelet P-selectin is required for pulmonary eosinophil and lymphocyte recruitment in a murine model of allergic inflammation. Blood 2005; 105: 2074-81.
• 9 Diacovo TG, Roth SJ, Buccola JM. et al. Neutrophil rolling, arrest, and transmigration across activated, surface-adherent platelets via sequential action of P-selectin and the ß2-integrin CD11b/CD18. Blood 1996; 88: 146-57.
• 10 Suzuki K, Sugimura K, Hasegawa K. et al. Activated platelets in ulcerative colitis enhance the production of reactive oxygen species by polymorphonuclear leukocytes. Scand J Gastroenterol 2001; 36: 1301-6.
• 11 Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994; 83: 2759-79.
• 12 Mukai HY, Ninomiya H, Mitsuhashi S. et al. Thromboembolism in a patient with transient eosinophilia. Ann Hematol 1996; 72: 93-5.
• 13 Rauch AE, Amyot KM, Dunn HG, ert al. Hypereosinophilic syndrome and myocardial infarction in a 15-year-old. Pediatr Pathol Lab Med 1997; 17: 469-86.
• 14 Coyle AJ, Page CP, Atkinson L. et al. The requirement for platelets in allergen-induced late asthmatic airway obstruction. Eosinophil infiltration and heightened airway responsiveness in allergic rabbits. Am Rev Respir Dis 1990; 142: 587-93.
• 15 Kivity S, Argaman A, Onn A. et al. Eosinophil influx into the airways in patients with exercise-induced asthma. Respir Med 2000; 94: 1200-5.
• 16 Yoshikawa T, Shoji S, Fujii T. et al. Severity of exercise-induced bronchoconstriction is related to airway eosinophilic inflammation in patients with asthma. Eur RespirJ 1998; 12: 879-84.
• 17 Gotshall RW. Exercise-induced bronchoconstriction. Drugs 2002; 62: 1725-39.
• 18 de Bisschop C, Guenard H, Desnot P. et al. Reduction of exercise-induced asthma in children by short, repeated warm ups. Br J Sports Med 1999; 33: 100-4.
• 19 Helenius IJ, Tikkanen HO, Haahtela T. Association between training and risk of asthma in elite athletes. Thorax 1997; 51: 157-60.
• 20 Spector SL. Update on exercise-induced asthma. Ann Allergy 1993; 71: 571-7.
• 21 Savov JD, Gavett SH, Brass DM. et al. Neutrophils playa critical role in development of LPS-induced airway disease. Am J Physiol Lung Cell Mol Physiol 2002; 283: L952-62.
• 22 George CL, Jin H, Wohlford-Lenane CL. et al. Endotoxin responsiveness and subchronic grain dust-induced airway disease. Am J Physiol Lung Cell Mol Physiol 2001; 280: L203-13.
• 23 McCarty OJT, Tien N, Bochner BS. et al. Exogenous eosinophil activation converts PSGL-1-dependent binding to CD18-dependent stable adhesion to platelets in shear flow. Am J Physiol 2003; 284: C1223-34.
• 24 Nagata KT, Todoroki TN, Katagiri Y. et al. Activated platelets induce superoxide anion release by monocytes and neutrophils through P-selectin (CD62). J Immunol 1993; 151: 3267-73.
• 25 Wang JS, Cheng L-J. The effect of strenuous acute exercise on α2-adrenergic agonist-potentiated platelet activation. Arteriosclero Thromb Vasc Biol 1999; 19: 1559-65.
• 26 Wang JS. Intense exercise increases shear-induced platelet aggregation through enhancement of von Willebrand factor binding, glycoprotein IIb/IIIa activation and P-selectin expression. Eur J Appl Physiol 2004; 91: 741-7.
• 27 Wang JS, Chow SE, Chen J-K. Strenuous, acute exercise affects reciprocal modulation of platelet and polymorphonuclear leukocyte activities under shear flow in men. J Thromb Haemost 2003; 01: 2031-7.
• 28 Blom M, Tool AT, Mul FP. et al. Eosinophils isolated with two different methods show different characteristics of activation. J Immunol Meth 1995; 178: 183-93.
• 29 Wang JS, Li Y-S, Chen J-C. Effects of exercise training and deconditioning on platelet aggregation induced by alternating shear stress in men. Arteriosclero Thromb Vasc Biol 2005; 25: 454-60.
• 30 Wang JS. Strenuous, acute exercise suppresses polymorphonuclear leukocyte respiratory burst under adherence to surface-adherent platelets in men. Thromb Haemost 2004; 92: 1076-85.
• 31 Rothe G, Valet G. Measurement of phagosomal hydrogen peroxide production with dihydorhodamine 123. In: Handbook of Flow Cytometry Methods. 2nd Ed. John Wiley & Sons, Inc; New York: 1993: 155-6.
• 32 Li N, Wallen NH, Hjemdahl P. Evidence for prothrombotic effects of exercise and limited protection by aspirin. Circulation 1999; 100: 1374-9.
• 33 Cooke JP, Tsao PS. Is NO an endogenous antiatherogenic molecule?. Arterioscl Thromb 1994; 14: 653-5.
• 34 Stenberg PE, McEver RP, Shuman MA. et al. A platelet a-granule membrane protein (GMP-140) is expressed on the plasma membrane after activation. J Cell Biol 1985; 101: 880-6.
• 35 Wong CS, Gamble JR, Skinner MP. et al. Adhesion protein GMP140 inhibits superoxide anion release by human neutrophils. Proc Natl Acad Sci USA 1991; 88: 2397-401.
• 36 Michel O. Role of lipopolysaccharide (LPS) in asthma and other pulmonary conditions. J Endotoxin Res 2003; 09: 293-300.
• 37 Tanaka H, Bradley JD, Baudendistel LJ. et al. Mechanisms of increased pulmonary microvascular permeability induced by FMLP in isolated rabbit lungs. J Appl Physiol 1992; 73: 2074-82.
• 38 Wang JS, Liao CH. Moderate-intensity exercise suppresses platelet activation and polymorphonuclear leukocytes interaction with surface-adherent platelets under shear flow in men. Thromb Haemost 2004; 91: 587-94.
• 39 Paraskevaidis IA, Iliodromitis EK, Mavrogeni S. et al. Repeated exercise stress testing identifies early and late preconditioning. Intern J Cardiol 2005; 98: 221-6.
• 40 Glanemann M, Vollmar B, Nussler AK. et al. Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state. J Hepatol 2003; 38: 59-66.
• 41 Wang JS, Huang Y-H. Effects of exercise intensity on lymphocyte apoptosis induced by oxidative stress in men. Eur J Appl Physiol 2005; 95: 290-7.
• 42 Pasupathy S, Naseem KM, Homer-Vanniasinkam S. Effects of warm-up on exercise capacity, platelet activation and platelet-leucocyte aggregation in patients with claudication. Br J Surg 2005; 92: 50-5.
• 43 Kato M, Yamaguchi T, Tachibana A. et al. Differential role of an atypical protein kinase C, PKCγ, in regulation of human eosinophil and neutrophil functions. Int Arch Allergy Immunol 2005; 137 (Suppl. 01) 27-34.
• 44 Perrini S, Henriksson J, Zierath JR. et al. Exerciseinduced protein kinase C isoform-specific activation in human skeletal muscle. Diabetes 2004; 53: 21-4.
• 45 Blom M, Tool ATJ, Wever PC. et al. Human eosinophils express, relative to other circulating leukocytes, large amounts of secretory 14-kD phospholipase A2. Blood 1998; 91: 3037-43.