Chemotaxis activation mechanism

As already mentioned, molecular cross talk seems to be the prerequisite mechanism for most of root microbial infections. Indeed the initial step of any root colonization involves the movement of microbes to the plant root surface bacterial movement can be passive, via soil water flux, or active, via specific induction of flagellar activity by plant released compounds (chemotaxis) (Chaps. 4 and 7). Other important steps are adsorption and anchoring to the root surface. 

Mechanisms of Complement Activation. Complement is a major mediator of the inflammatory response. Complement recruits and enlists the participation of humoral and cellular effector systems, induces histamine release from mast cells and directs migration of leukocytes (chemotaxis), in addition to producing phagocytosis and the release of lysosomal constituents from phagocytes. 

Involvement of complement activation in the etiology of the acute byssinotic reaction could explain the pathogenic mechanism of histamine release, non-histamine-mediated bronchoconstriction, chemotaxis, endotoxin and bacterial proteolytic enzyme action. Bronchoconstriction experienced in the acute byssinotic reaction might be attributed to the combined action of C3a and C5a mediated histamine release and non-histamine mediated kinin activity. The presence of PMN in the nasal airways of byssinotics might be explained by the chemotactic action of C5a and the C567 complex. 

Migration of cells in response to stimuli is responsible for several physiological functions mostly in the case of inflammatory responses and immune functions. The transwell chemotaxis assay is useful to study mechanisms of migration during chemotaxis. The main purpose of this assay is to determine if a molecule of interest exhibits chemotactic activity. Molecules that... 

The opioids modulate the immune system by effects on lymphocyte proliferation, antibody production, and chemotaxis. In addition, leucocytes migrate to the site of tissue injury and release opioid peptides, which in turn help counter inflammatory pain. However, natural killer cell cytolytic activity and lymphocyte proliferative responses to mitogens are usually inhibited by opioids. Although the mechanisms involved are complex, activation of central opioid receptors could... 

The anti-inflammatory activity of the NSAIDs is mediated chiefly through inhibition of biosynthesis of prostaglandins (Figure 36-2). Various NSAIDs have additional possible mechanisms of action, including inhibition of chemotaxis, down-regulation of interleukin-1 production, decreased production of free radicals and superoxide, and interference with calcium-mediated intracellular events. Aspirin irreversibly acetylates and blocks platelet cyclooxygenase, while most non-COX-selective NSAIDs are reversible inhibitors. 

FIGURE 12-26 The two-component signaling mechanism in bacterial chemotaxis. When an attractant ligand (A) binds to the receptor domain of the membrane-bound receptor, a protein His kinase in the cytosolic domain (component 1) is activated and autophosphorylates on a His residue. This phosphoryl group is then transferred to an Asp residue on component 2 (in some cases a separate protein in others, another domain of the receptor protein). After phosphorylation on Asp, component 2 moves to the base of the flagellum, where it determines the direction of rotation of the flagellar motor. 

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