Tuberculosis and Respiratory Diseases

The Korean Academy of Tuberculosis and Respiratory Diseases (대한결핵및호흡기학회)
권호 표지
DOI QR코드

DOI QR Code

Moxifloxacin Alleviates Oleic Acid-provoked Neutrophilic Respiratory Burst in the Rat Lung through the Inhibition of Cytosolic Phospholipase $A_2$

Moxifloxacin의 Cytosolic Phospholipase $A_2$ 억제효과가 흰 쥐 호중구의 Respiratory Burst에 미치는 영향

  • Lee, Young-Man (Department of Physiology, Daegu Catholic University School of Medicine)
  • 이영만 (대구가톨릭대학교 의과대학 생리학교실)
  • Received : 2010.08.05
  • Accepted : 2010.09.16
  • Published : 2010.10.30
Download PDF
⟨ Previous Next ⟩

Abstract

Background: According to the notion of the immunoregulatory functions of moxifloxacin (MFX), the effect of MFX on the neutrophilic respiratory burst in conjunction with the expression of cytosolic phospholipase $A_2$ ($cPLA_2$) was investigated. Methods: The effects and possible mechanisms of MFX on neutrophilic respiratory burst in oleic acid (OA)-induced acutely injured rats lung and OA-stimulated, isolated murine neutrophils were probed, associated with the expression of cytosolic phospholipase $A_2$ in vivo and in vitro. Results: In the OA-induced acutely-injured lungs, neutrophils were accumulated, which was attenuated by MFX. The parameters denoting a neutrophilic respiratory burst, such as nitro blue tetrazolium reaction, cytochrome-c reduction, neutrophil aggregation, $H_2O_2$ production in neutrophils revealed increased neutrophilic respiratory burst by OA, and MFX decreased all of these parameters. In addition, the enhanced expression of $cPLA_2$ in the lung and isolated murine neutrophils by OA were decreased by MFX. Conclusion: MFX suppresses the OA-induced neutrophilic respiratory burst by the suppression of $cPLA_2$ in neutrophils.

Keywords

References

  1. Ware LB. Advances in the pathogenesis and treatment of the acute respiratory distress syndrome. Clin Pul Med 2003;10:208-18. https://doi.org/10.1097/01.cpm.0000080904.11193.27
  2. Kitsiouli E, Nakos G, Lekka ME. Phospholipase A2 subclasses in acute respiratory distress syndrome. Biochim Biophys Acta 2009;1792:941-53.
  3. Nakos G, Kitsiouli E, Hatzidaki E, Koulouras V, Touqui L, Lekka ME. Phospholipases A2 and platelet-activating- factor acetylhydrolase in patients with acute respiratory distress syndrome. Crit Care Med 2005;33:772-9. https://doi.org/10.1097/01.CCM.0000158519.80090.74
  4. Stommer P, Steinmann U. Phospholipase A2 induced diffuse alveolar damage: effect of indomethacin and dexamethasone upon morphology and plasma-histamine level. Klin Wochenschr 1989;67:171-6. https://doi.org/10.1007/BF01711347
  5. Schaloske RH, Dennis EA. The phospholipase A2 superfamily and its group numbering system. Biochim Biophys Acta 2006;1761:1246-59. https://doi.org/10.1016/j.bbalip.2006.07.011
  6. Wheeler DS. Phospholipase A2 and acute lung injury: it's just not that simple. Crit Care Med 2005;33:904-5. https://doi.org/10.1097/01.CCM.0000159694.64555.F8
  7. Pruzanski W, Vadas P. Phospholipase A2: a mediator between proximal and distal effectors of inflammation. Immunol Today 1991;12:143-6.
  8. Arbibe L, Vial D, Touqui L. Phospholipase A2 and acute respiratory distress syndrome. Prog Surg 1997;24: 79-87. https://doi.org/10.1159/000075455
  9. Kramer RM, Sharp JD. Structure, function and regulation of $Ca^{2+}$-sensitive cytosolic phospholipase A2 ($cPLA_2$). FEBS Lett 1997;410:49-53. https://doi.org/10.1016/S0014-5793(97)00322-0
  10. Dana R, Malech HL, Levy R. The requirement for phospholipase A2 for activation of the assembled NADPH oxidase in human neutrophils. Biochem J 1994;297: 217-23.
  11. Lucas KK, Dennis EA. The ABC's of Group IV cytosolic phospholipase A2. Biochim Biophys Acta 2004;1636: 213-8 https://doi.org/10.1016/j.bbalip.2003.12.009
  12. Huang HC, Shieh CC, Yu WL, Cheng KC, Chen CC, Chang ST, et al. Comparing the protective effects of ciprofloxacin, moxifloxacin and levofloxacin in mice with lipopolysaccharide-induced acute lung injuries. Respirology 2008;13:47-52. https://doi.org/10.1111/j.1440-1843.2007.01192.x
  13. Wang JP, Raung SL, Huang LJ, Kuo SC. Involvement of cyclic AMP generation in the inhibition of respiratory burst by 2-phenyl-4-quinolone (YT-1) in rat neutrophils. Biochem Pharmacol 1998;56:1505-14. https://doi.org/10.1016/S0006-2952(98)00265-2
  14. Weiner RE, Sasso DE, Gionfriddo MA, Syrbu SI, Smilowitz HM, Vento J, et al. Early detection of bleomycin- induced lung injury in rat using indium-111-labeled antibody directed against intercellular adhesion molecule-1. J Nucl Med 1998;39:723-8.
  15. Goldblum SE, Wu KM, Jay M. Lung myeloperoxidase as a measure of pulmonary leukostasis in rabbits. J Appl Physiol 1985;59:1978-85.
  16. Hobson J, Wright J, Churg A. Histochemical evidence for generation of active oxygen species on the apical surface of cigarette-smoke-exposed tracheal explants. Am J Pathol 1991;139:573-80.
  17. Haslett C, Guthrie LA, Kopaniak MM, Johnston RB Jr, Henson PM. Modulation of multiple neutrophil functions by preparative methods or trace concentrations of bacterial lipopolysaccharide. Am J Pathol 1985;119: 101-10.
  18. Botha AJ, Moore FA, Moore EE, Fontes B, Banerjee A, Peterson VM. Postinjury neutrophil priming and activation states: therapeutic challenges. Shock 1995;3:157-66.
  19. Dalhoff A, Shalit I. Immunomodulatory effects of quinolones. Lancet Inf Dis 2003;3:359-71. https://doi.org/10.1016/S1473-3099(03)00658-3
  20. Koksel O, Cinel I, Tamer L, Cinel L, Ozdulger A, Kanik A, et al. N-acetylcysteine inhibits peroxynitrite-mediated damage in oleic acid-induced lung injury. Pulm Pharmacol Ther 2004;17:263-70. https://doi.org/10.1016/j.pupt.2004.05.002
  21. Karagiorga G, Nakos G, Galiatsou E, Lekka ME. Biochemical parameters of bronchoalveolar lavage fluid in fat embolism. Intensive Care Med 2006;32:116-23. https://doi.org/10.1007/s00134-005-2868-x
  22. Julien M, Hoeffel JM, Flick MR. Oleic acid lung injury in sheep. J Appl Physiol 1986;60:433-40. https://doi.org/10.1152/jappl.1986.60.2.433
  23. Lee YM, Kim BY, Park YY. Role of the PLA2-activated neutrophilic oxidative stress in oleic acid-induced acute lung injury. Tuberc Respir Dis 2010;68:55-61. https://doi.org/10.4046/trd.2010.68.2.55
  24. Shmelzer Z, Haddad N, Admon E, Pessach I, Leto TL, Eitan-Hazan Z, et al. Unique targeting of cytosolic phospholipase A2 to plasma membranes mediated by the NADPH oxidase in phagocytes. J Cell Biol 2003; 162:683-92. https://doi.org/10.1083/jcb.200211056
  25. Leslie CC. Properties and regulation of cytosolic phospholipase A2. J Biol Chem 1997;272:16709-12. https://doi.org/10.1074/jbc.272.27.16709
  26. Ghosh M, Tucker DE, Burchett SA, Leslie CC. Properties of the Group IV phospholipase A2 family. Prog Lipid Res 2006;45:487-510. https://doi.org/10.1016/j.plipres.2006.05.003
  27. Nagase T, Uozumi N, Ishii S, Kume K, Izumi T, Ouchi Y, et al. Acute lung injury by sepsis and acid aspiration: a key role for cytosolic phospholipase A2. Nat Immunol 2000;1:42-6. https://doi.org/10.1038/76897
  28. Magrioti V, Kokotos G. Phospholipase A2 inhibitors as potential therapeutic agents for the treatment of inflammatory diseases. Expert Opin Ther Pat 2010;20: 1-18. https://doi.org/10.1517/13543770903463905