Polymorphonuclear leukocyte adhesion

Inoue T, Sakai Y, Morooka S, Hayashi T, Takayanagi K, Takabatake Y. Expression of polymorphonuclear leukocyte adhesion molecules and its clinical significance in patients treated with percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1996 28 1127-1133. 

Lumpkin, M. D. The regulation of ACTH secretion by IL-1. Science 238, 452-454 (1987). Luscinskas, F. W., Brock, A. F., Amaout, M. A., and Gimbrone, M. A., Jr. Endothelial-leukocyte adhesion molecule-1-dependent and leukocyte (CDll/CD18)-dependent mechanisms contribute to polymorphonuclear leukocyte adhesion to cytokine-activated human vascular endothelium. J. Immunol. 142, 2257-2263 (1989). 

Del Maschio A, Zanetti A, Corada M, Rival Y, Ruco L, Lampugnani MG, Dejana E Polymorphonuclear leukocyte adhesion triggers the disorganization of endothelial cell-to-cell adherens junctions. J Cell Biol 1996 135 497-510. 

Spagnulo, P., Ellner, J. and Hassid, A. (1980). Thromboxane A2 mediates augmented polymorphonuclear leukocyte adhesiveness. ]. Clin. Invest., 66, 406-414... 

Key PMN, polymorphonuclear leukocytes EC, endothelial cell lymphs, lymphocytes CD, cluster of differentiation iCAM, intercellular adhesion molecule LFA-1, lymphocyte function-associated antigen-1 PECAM-1, platelet endothelial cell adhesion cell molecule-1. 

Early infiltration of polymorphonuclear leukocytes and monocyte/macro-phages into the transplanted organ occurs soon after reperfusion of the transplant is initiated. In the context of transplantation, oxygen deprivation and general tissue stress of the graft leads to the activation of proinflammatory cytokines and the upregulation of the adhesion molecules required for leukocyte... 

J. A. McDonald, B. J. Baum, D, M. Roseubeg, J. A. Kdman,S. C. Brin, and R. G. Crystal. Destruction of a imJor extracellular adhesive glycoprotein (fibronccrin) of human fibroblasts by neutral proteases from polymorphonuclear leukocyte granules. Lab. Invest. 40350 (1979). 

Bevilacqua M. P., Pober J. S., Wheeler M. E., Cotran R. S., and Gimbrone M. A., Jr. (1985) Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines. J. Clin. Invest. 76, 2003-2011. 

Figure 31.4. Time coui se of cellular and molecular acdvadon folowing stioke. Diagrammadc representadon of die dme course of cellular acdvadori (PNL, polymorphonuclear leukocytes M(j), macrophages) and inflammatory molecular expression (GM, granulocyte and monocyte coloriy-sdmuladng factor ICAM, soluble intercellular adhesion molecule-1 VCAM, soluble vascular- cell adliesiori molecule-1 TNF-a, tumor necrosis factor a IL-1(5, interleukin 1(5 IL-6, interleukin 6 IL-8, interleukin 8 IL-10, interleukin 10) in human brain, cerebrospinal fluid (CSF) and blood after sUoke. Reproduced from Nilupul Perera M, Ma HK, Arakawa S, Howells DW, Markus R, Rowe CC, Donnan GA (2006). InPammation following stroke. J Clin Neurosci, 13 1-8 (with permission from Elsevier).

Dorovin-Zis K, Bowman PD, Prameya R (1992) Adhesion and migration of human polymorphonuclear leukocytes across cultured bovine brain micro vessel endothelial cells. J Neuropathol Exp Neurol. 51(2) 194-205. 

Yoshida, N., Yoshikawa, T., Manabe, H., Terasawa, Y., Kondo, M., Noguchi, N., and Niki, E. (1999) Vitamin E protects against polymorphonuclear leukocyte-dependent adhesion to endothelial ce h. JLeukoc Biol 65, 757-63. 

Inflammatory cells infiltrating postischemic tissue are considered to contribute to disability after cerebral ischemia [5,8,17]. Identification of factors involved in the selective recruitment and accumulation of inflammatory cells into ischemic brain tissue and the mechanisms behind the entry of leukocytes through the blood-brain barrier into sites of ischemia are not completely understood [5,8]. Locally produced proinflammatory cytokines such as TNF-a, IL-1 P, and IL-6 initiate the inflammatory process. TNF-a and IL-1 P mRNA elevate in the brain after experimental middle cerebral artery occlusion [5,51,81]. While, IL-1 p and TNF-a play a major role in promoting adhesion between endothelial cells and leukocytes, they are poor attractants for polymorphonuclear leukocytes and monocytes [7]. Astrocytes and endothelial cells can respond in vitro to such proinflammatory cytokines with enhanced expression of chemokines, which results in the influx of leukocytes to areas of inflammation [5,8,103]. 

Several conditions are associated with altered C2GnTl activity or expression. C2GnTl activity is increased specifically in the heart tissues of diabetic or hyperglycemic rats. An increase in C2GnTl expression in polymorphonuclear leukocytes was found in patients with type 1 and 2 diabetes. The high C2GnTl activity may possibly promote leukocyte-endothelial cell adhesion and capillary occlusions. The mechanisms of these alterations remain to be shown. 

Barnett CC, Moore EE, Moore FA, Biffl WL, Partrick DA Soluble intercellular adhesion molecule-1 provokes polymorphonuclear leukocyte elastase release by CD18. Surgery 1996 120 395 04. 

Malawista, S.E., de Boisfleury Chevance, A. and Boxer, L.A. (2000). Random locomotion and chemotaxis of human blood polymorphonuclear leukocytes from a patient with leukocyte adhesion deficiency-1. Normal displacement in close quarters via chimneying. Cell Motil. Cytoskeleton 46, 183-189. 

In an intestinal ischemia-reperfusion mouse model, acute inflammation is a rapid tissue response, presenting higher levels of TNF-a, adhesion molecules (E-selectin and ICAM-1), polymorphonuclear leukocytes accumulation, and NFkB activation. These processes are significantly attenuated in CORM-2-treated mice [71]. More recently, the same authors have found anti-inflammatory effect of CORM-2 in a mouse model of acute colitis, where this molecule has inhibited the production of keratinocyte chemoattractant and TNF-a in... 

The effects of 16-, 17-, 18-, 19-, and 20-HETE have been studied to varying degrees. Activated polymorphonuclear leukocytes (PMNs) are known to produce 16-HETE. In vitro, 16(7 )-HETE inhibits human PMN adhesion and aggregation. Administration of 16-HETE to rabbits with thromboembolic stroke leads to reduction in intracranial pressure [59]. Synthesis of leukot-liene B4, a pro-inflammatory molecule, is also increased by 16(7 )-HETE. Carroll et al. demonstrated that 16(7 )-HETE promotes vasodilation of renal arteries in a COX-dependent manner [60], Furthermore, 16(5)-HETE inhibits the activity of the adenosine triphosphatase (ATPase) in the renal proximal tubule [60], Similarly, 17(iS)-HETE inhibits proximal tubule ATPase activity while 17(i )-HETE is inactive in this system. 

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