Chemotaxis

The mechanistic basis of this remarkable sensitivity has remained puzzhng. It was proposed to be rooted in the lateral assemblies of bacterial chemoreceptors and signaling components within the plasma membrane [204]. To test this hypothesis, Kiessling and coworkers generated polymeric attractants to probe the consequences of perturbing chemoreceptor clustering. 

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These steioids aie capable of preventing or suppressing the development of the sweUing, redness, local heat, and tenderness which characterize inflammation. They inhibit not only the acute symptoms of the inflammatory process, such as edema, fibrin deposition, and capillary dilatation, but also the chronic manifestations. There is evidence that glucocorticoids induce the synthesis of a protein that inhibits phosphoHpase A 2 (60), diminishing the release of arachidonic acid from phosphoHpids (Fig. 2), thereby reducing chemotaxis and inflammation. 

Vinca alkaloids (vincristine, vinblastine, vindesine) are derived from the periwinkle plant (Vinca rosea), they bind to tubulin and inhibit its polymerization into microtubules and spindle formation, thus producing metaphase arrest. They are cell cycle specific and interfere also with other cellular activities that involve microtubules, such as leukocyte phagocytosis, chemotaxis, and axonal transport in neurons. Vincristine is mainly neurotoxic and mildly hematotoxic, vinblastine is myelosuppressive with veiy low neurotoxicity whereas vindesine has both, moderate myelotoxicity and neurotoxicity. 

During bone formation, a series of sequential changes occur in cells in the osteoblast lineage, including osteoblast chemotaxis, proliferation and differentiation, which in turn is followed by formation of mineralised bone and cessation of osteoblast activity. The osteoblast changes are preceded by osteoclast apoptosis, which may be dependent on active TGF- 3 released from the resorbed bone. This is followed by chemotactic attraction of osteoblasts or their precursors to the sites of the resorption defect. Chemotactic attraction of osteoblast precursors is likely mediated by local factors produced during the resorption process. 

CC, and one CX3C and XC chemokine receptors have been cloned so far [2]. Receptor binding initiates a cascade of intracellular events mediated by the receptor-associated heterotrimeric G-proteins. These G-protein subunits trigger various effector enzymes that lead to the activation not only of chemotaxis but also to a wide range of fimctions in different leukocytes such as an increase in the respiratory burst, degranulation, phagocytosis, and lipid mediator synthesis. 

Chemotaxis is the detection of and coordinated movement toward a chemical compound by a cell or organism, e.g., neutrophils move towards an area of infection because of chemicals released by infected tissues. 

Tubulin is a major component of the cellular cytoskele-ton. Tubulin polymers (microtubules) are important for cell division (mitotic spindle) and the chemotaxis and phagocytosis of neutrophils. Prevention of tubulin polymerisation by colchicine accounts for the therapeutic effects of this drug in acute gouty arthritis and its anti-mitotic effects. 

Vinca alkaloids are derived from the Madagascar periwinkle plant, Catharanthus roseus. The main alkaloids are vincristine, vinblastine and vindesine. Vinca alkaloids are cell-cycle-specific agents and block cells in mitosis. This cellular activity is due to their ability to bind specifically to tubulin and to block the ability of the protein to polymerize into microtubules. This prevents spindle formation in mitosing cells and causes arrest at metaphase. Vinca alkaloids also inhibit other cellular activities that involve microtubules, such as leukocyte phagocytosis and chemotaxis as well as axonal transport in neurons. Side effects of the vinca alkaloids such as their neurotoxicity may be due to disruption of these functions. 

Devreotes, P.N. (1988). Chemotaxis in eukaryotic cells A focus on leukocytes and Dictyostelium. Ann. Rev. Cell Biol. 4, 649-686. 

Cells respond to some extracellular factors such as leukotriene B (Ford-Hutchin-son et al., 1980) by increasing the locomotion rate in an undirected manner as opposed to chemotaxis. This mechanism, known as chemokinesis, is likely on purely statistical grounds to result in cells accumulating at the site of origin of this stimulus (Wilkinson, 1987). The differentiation of factors that are chemotactic from chemokinetic responses can be difficult, but this has been greatly facilitated using the Boyden chamber (Lackie, 1986). 

Andre, E., Brink, M., Gerisch, G., Isenberg, G., Noegel, A., Schleicher, M., Segall, J.E., Wallraff, E. (1989). A Dictyostelium mutant deficient in severin, an F-actin fragmenting protein, shows normal motility and chemotaxis. J. Cell Biol. 108, 985-995. 

These stimuli elicit a complex series of responses that result in cell functions such as chemotaxis and release of inflammatory compounds, oxidants, and proteases. Probably related to chemotaxis is a rapid, transient actin polymerization response. Inflammation results in part from the release of proteases and myeloperoxidase normally stored in granules inside the cell (5) and from oxidants produced by an NADPH-oxidase system (6) located primarily... 

This mediator, apart from aggregating platelets and stimulating many cells types, is a very potent mediator in allergic reactions causing bronchoconstriction with a 1,000 times more potency than histamine. It is able to increase vascular permeability and cause chemotaxis and degranulation of eosinophils and neutrophils [14-16]. 

In contrast to E. coli, B. subtilis cells do not enter a 4-h lag phase. Instead, they continue growth with a generation time of more than 24 h and induce the synthesis of 36 CSPs which function at various levels of cellular physiology, such as protein synthesis, carbohydrate uptake and chemotaxis [120]. 

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