Mini ReviewCytokine regulation of cellular adhesion molecule expression in inflammation
Section snippets
Cellular adhesion molecules
The process of inflammation is central to protection of the host against infectious, and thus potentially harmful, micro-organisms, e.g., bacteria. In general, leukocytes circulating in the blood are drawn to sites of tissue injury or infection by chemoattractant gradients. However, other mechanisms are required to retard and eventually halt the movement of leukocytes in order that they can exit the blood vessel and migrate into the affected areas. The major mechanism involved in arrest of
Cytokine stimulation of CAM expression
In the early 1980 s, proinflammatory cytokines such as TNF-α, IL-1α, and IL-1β and gram-negative bacterial endotoxins (lipopolysaccharide, LPS) were demonstrated to directly stimulate increased leukocyte adhesion in cultured endothelial cells [19], [20]. Their stimulatory effect was much greater in amplitude than that of other previously studied leukocyte activators, such as leukotrienes, activated complement components, and chemotactic peptides, and has been shown to result in firm attachment
Effect of cytokine action on selectin expression
The selectins play a critical role in the migration of leukocytes to sites of inflammation by mediating the initial attachment and rolling of leukocytes on the vascular endothelium prior to integrin-dependent arrest and extravasation [1], [2], [3], [4], [5], [6], [8], [9]. Both E- and P-selectins on the endothelium probably participate in the initiation of leukocyte rolling [21]. E-selectin is not expressed on unstimulated (resting) endothelial cells in vitro, but is induced in response to
Effect of cytokine action on integrin receptors
Integrins are constitutively expressed on leukocytes, but are only able to form adhesive contacts with other cells following activation to produce structural and affinity changes in the external integrin moieties, in particular the I-domains which include binding sites for Ig-like addressin receptors [10], [11], [14], [37]. Activation appears to be a complex process involving divalent cations and stimuli transmitted through both integrins and non-integrin surface molecules resulting in
Mechanisms of adhesion molecule inductions
That many cellular adhesion molecules are induced by proinflammatory cytokines suggests that a common mechanism leading to CAM gene transcription is triggered. IL-1s and TNFs mediate their actions via distinct cell surface receptors, but downstream signalling pathways overlap considerably and involve common transcription factors. It is now clear that NF-κB is a crucial factor in both IL-1 and TNF mediated inducibility of adhesion molecules, including E-selectin, ICAM-1, VCAM-1 and MAdCAM-1 [60]
Potential therapeutic interventions for adhesion molecule-mediated inflammation
An inflammatory response begins when cells in damaged/infected tissues call for ‘help’ by secreting chemical mediators and cytokine that activate the endothelium of local blood vessels. In the majority of situations this lead to infiltration of affected tissues by activated leukocytes, a localised inflammatory reaction, tissue repair and resolution of infections. However, occasionally, and particularly in cases of massive tissue damage or overwhelming infections, the inflammatory reaction gets
Acknowledgments
I am indebted to Mrs Jenni Haynes for her expert typing of this manuscript.
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