Abstract

Chemotaxis is the oriented or directed locomotion induced by a gradient of chemical substance. A variety of chemical substances or chemotactic factors for leukocytes are demonstrable, of which the most generally important are C5a and probably the lymphokines. However, the synthetic formyl methionyl chemotactic peptides have proved valuable in establishing that the initial event in neutrophil chemotaxis is the reversible binding of the synthetic peptide to a specific receptor on the neutrophil surface. Binding to the same receptor also initiates other functions of the neutrophil. The initial signal is transduced into the effector mechanism of locomotion through parallel sequential changes in ion fluxes, increased arachidonic acid metabolism, methylation processes, possibly changes in membrane potential, and so on. The neutrophils are stimulated to move through activation of their microfilament-actomyosin system, and the movement is possibly affected through changes in microtubule assembly. Humoral defects in the generation of chemotactic factors and cell-directed defects in chemotactic responsiveness are frequently associated with recurrent infections. The Chediak-Higashi, Kartagener's, and leukocyte actin dysfunction syndromes are examples of genetically determined defects in neutrophil locomotion. Among the acquired cellular defects is the hyperglobulinemia E syndrome. Also of interest to allergists are present explorations of the role of mast cell-derived neutrophil chemotactic factors as an element in the pathogenesis of the inflammation of the airways associated with asthma.

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