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Ann Thorac Surg 2007;84:2137-2138. doi:10.1016/j.athoracsur.2007.06.007
© 2007 The Society of Thoracic Surgeons
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Correspondence

Decreasing the Expression of LFA-1 and ICAM-1 as Well as Hindering Their Interaction as the Major Mechanism for Statin-Induced Neutrophil Dysfunction

Mohammad R. Namazi, MD

Department of Dermatology, Shiraz University of Medical Sciences, Faghihi Hospital, Shiraz, Iran

(Email: namazi_mr{at}yahoo.com).

To the Editor:

I read with great interest the article by Chello and colleagues [1].

This work shows that simvastatin markedly suppresses the functional activity of neutrophils, which is underscored by reduced expression of CD11b (p < 0.01 at 24 hours) and a significantly less percentage of cells positive for nitro-blue tetrazolium (p < 0.01 at 12 and 24 hours) compared with a placebo. I would like to complement the discussion of Chello and coworkers [1] by introducing a major route through which statins could suppress the activity of neutrophils.

The most important adhesion protein identified on neutrophils is the integrin lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18), which is the ligand for intercellular adhesion molecule-1 (ICAM-1) expressed on the endothelium. The LFA-1/ICAM-1 interaction is crucial for the ingress of neutrophils into the inflammatory sites [2]. Statins downregulate the expression of ICAM-1 and LFA-1, and through binding to LFA-1, they interfere with ICAM-1–LFA-1 interaction [3]. This important mechanism should be borne in mind as the major mechanism for statin-induced inhibition of neutrophil activity.


   References
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 References
 

  1. Chello M, Anselmi A, Spadaccio C, et al. Simvastatin increases neutrophil apoptosis and reduces inflammatory reaction after coronary surgery Ann Thoracic Surg 2007;83:1374-1380.[Abstract/Free Full Text]
  2. Haskard DO, Lee TH. The role of leukocyte-endotheial interactions in the accumulation of leukocytes in allergic inflammation Am Rev Respir Dis 1992;145:S10-S13.[Medline]
  3. Namazi MR. Statins: novel additions to the dermatologic arsenal? Exp Dermatol 2004;13:337-339.[Medline]




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