Expression of CD11b as an Adhesion Molecule on Neutrophils in Children with Kawasaki Disease
-
Behzad Heidari
,
Reza Amin
,
Sara Kashef
,
Soheila Alyasin
,
Mozhgan Moghtaderi
,
Maneli Aminshahidi
,
Mehdi Kalani
Abstract
Inflammation of blood vessels is a characteristic feature of Kawasaki disease. Neutrophils play a key role in the inflammatory responses where movement of neutrophils toward the site of inflammation depends on CD11b/CD18 expression as adhesion molecules on these cells. The purpose of this study was to investigate CD11b/CD18 expression in patients with Kawasaki disease upon diagnosis and after treatment.
The study included 20 children with Kawasaki disease aged from 3 months to 8 years. Mean fluorescence intensity of CD11b levels on diagnosis and at 1-2 and 6 weeks after intravenous immunoglobulin (IVIG) therapy was measured in these patients. Level of CD11b was measured in age-matched healthy children and febrile children (each 21) as negative and positive controls, respectively.
Mean fluorescence intensity of CD11b in Kawasaki patients was lower than that of the control groups before and after 1-2 weeks of IVIG therapy. There were no significant differences in CD11b in Kawasaki patients either with aneurysm or without aneurysm.
The CD11b levels at the diagnosis time and after treatment with IVIG in our patients with Kawasaki were lower than the control groups.
1. Newburger JW, Takahashi M, Gerber MA, Gewitz MH, Tani LY, Burns JC. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Pediatrics 2004; 114(6):1708-33.
2. Koyanagi H, Yanagawa H, Nakamura Y, Yashiro M.Leukocyte counts in patients with Kawasaki disease: from the results of nationwide surveys of Kawasaki disease in Japan. ActaPaediatr 1997; 86(12):1328–32.
3. Ghio M, Contini P, Negrini S, Proietti M, Gonella R, Ubezio G. sHLA-I contaminating molecules as novel mechanism of ex vivo/in vitro transcriptional and posttranscriptional modulation of transforming growth factor-beta in CD8+ T lymphocytes and neutrophils after intravenous immunoglobulin treatment. Transfusion 2010; 50(3):547-55.
4. Ley K. Pathways and bottlenecks in the web of inflammatory adhesion molecules and chemoattractants. Immunol Res. 2001;24(1):87-95.
5. Luo BH, Carman CV, Springer TA. Structural basis of integrin regulation and signaling. Annu Rev Immunol 2007; 25:619-47.
6. Schymeinsky J, Mócsai A, Walzog B. Neutrophil activationviabeta2integrins (CD11/CD18): molecular mechanisms and clinical implications.ThrombHaemost 2007; 98(2):262-73.
7. Dajani AS, Taubert KA, Takahashi M, Bierman FZ, Freed MD, Ferrieri P, et al. Guidelines for long- termmanagement of patients with Kawasakidisease. Report from the Committee on Rheumatic Fever, Endocarditis, and KawasakiDisease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation 1994; 89(2):916-22.
8. Arjunan K, Daniels SR, Meyer RA, Schwartz DC, Barron H, Kaplan S. Coronary artery caliber in normal children and patients with Kawasaki disease but without aneurysms: an echocardiographic and angiographic study. J Am CollCardiol 1986; 8(5):1119-24.
9. Kobayashi T, Kimura H, Okada Y, Inoue Y, Kobayashi T, Shinohara M, et al. Increased CD11b expression on polymorphonuclear leucocytes and cytokine profiles in patients with Kawasaki disease. Clin Exp Immunol 2007;148(1):112-8.
10. Harlan JM, Winn RK. Leukocyte-endothelial interactions:clinical trials of anti-adhesion therapy. Crit Care Med 2002; 30(5 Suppl):S214-9.
11. Kubo M, Motomura Y. Transcriptional regulation of the anti-inflammatory cytokine IL-10 in acquired immune cells. Front Immunol 2012; 3:275.
12. Casulli S, Topçu S, Fattoum L, von Gunten S, Simon HU, Teillaud JL, et al. A differential concentration-dependent effect of IVIg on neutrophil functions: relevance for anti- microbial and anti-inflammatory mechanisms. PLoS One 2011; 6(10):e26469.
13. Kimura H, Kato M, Ikeda M, Nagai A, Okada Y, Naito S, et al. Sulfonated human immunoglobulin enhances CD16- linked CD11b expression on human neutrophils. Cell Biol Int 2003; 27(11):913-9.
14. Macmillan HF, Rowter D, Lee T, Issekutz AC. Autoimmunity.Intravenous immunoglobulin G selectively inhibits IL-1α-induced neutrophil-endothelial cell adhesion. Autoimmunity 2010; 43(8):619-27.
15. Anthony RM, Nimmerjahn F, Ashline DJ, Reinhold VN, Paulson JC, Ravetch JV. Recapitulation of IVIGanti- inflammatory activity with a recombinantIgG Fc. Science 2008; 320(5874):373-6.
16. Ghio M, Contini P, Setti M, Ubezio G, Mazzei C, Tripodi G. sHLA-I Contamination, a novel mechanism to explain ex vivo/in vitro modulation of IL-10 synthesis and release in CD8(+) T lymphocytes and in neutrophils followingintravenous immunoglobulin infusion. J Clin Immunol 2010; 30(3):384-92.
17. Overbeek SA, Braber S, Henricks PA, Kleinjan M, Kamp VM, Georgiou NA, et al. Cigarettesmokeinduces β2- integrin-dependent neutrophil migration across human endothelium. Respir Res 2011; 12:75.
18. Niwa Y, Yanagida I, Somiya K. [Enhanced neutrophilic functions in mucocutaneous lymph node syndrome (MCLS). With special reference to the possible role of increased active oxygen generation in the pathogenesis of coronary thromboarteritis]. Rinsho Ketsueki 1984; 25(5):619-26.
19. Takahashi K, Oharaseki T, Yokouchi Y. Pathogenesis of Kawasaki disease. Clin Exp Immunol 2011; 164(Suppl1):20-2.
| Files | ||
| Issue | Vol 13, No 4 (2014) | |
| Section | Articles | |
| Keywords | ||
| Adhesion molecules CD11b Flowcytometry Integrin IVIG Kawasaki disease Vascular aneurysm | ||
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