chemotaxis

(redirected from Chemotactic factors)
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Related to Chemotactic factors: histamine, chemotaxin

che·mo·tax·is

 (kē′mō-tăk′sĭs, kĕm′ō-)
n.
The characteristic movement or orientation of an organism or cell along a chemical concentration gradient either toward or away from the chemical stimulus.

che′mo·tac′tic (-tăk′tĭk) adj.
che′mo·tac′ti·cal·ly adv.

chemotaxis

(ˌkɛməʊˈtæksɪs)
n
(Microbiology) the movement of a microorganism or cell in response to a chemical stimulus
ˌchemoˈtactic adj
ˌchemoˈtactically adv

che•mo•tax•is

(ˌki moʊˈtæk sɪs, ˌkɛm oʊ-)

n.
oriented movement toward or away from a chemical stimulus.
[1890–95]
che`mo•tac′tic (-tɪk) adj.
che`mo•tac′ti•cal•ly, adv.

chemotaxis

the property of some plants and animals of moving toward or away from certain chemicals.
See also: Motion
ThesaurusAntonymsRelated WordsSynonymsLegend:
Noun1.chemotaxis - movement by a cell or organism in reaction to a chemical stimulus
taxis - a locomotor response toward or away from an external stimulus by a motile (and usually simple) organism
negative chemotaxis - movement away from a chemical stimulus
positive chemotaxis - movement toward a chemical stimulus
Translations
chemotassi

che·mo·tax·is

, positive chemotaxis, negative chemotaxis
n. quimiotaxis, movimiento de un organismo o célula como reacción a un estímulo químico.
References in periodicals archive ?
Differential effect of saturated and unsaturated free fatty acids on the generation of monocyte adhesion and chemotactic factors by adipocytes: dissociation of adipocyte hypertrophy from inflammation.
Injury to blood vessels in the area leads to hematoma, and this clot activates the release of chemotactic factors.
As a result of binding of autoantibodies, histamine, triptase-like proteases, chemotactic factors, leukotriens and cytokines (TNF-[alpha], IL-1, IL-4, IL-5) are released from basophils and mast cells.
14) An in vitro study of purified KL-6 concluded that the biomarker is one of the chemotactic factors for most fibroblasts and that increased KL-6 in the epithelial lining fluid in small airways could actually be one cause of the intra-alveolar fibrosis in ILDs.
As such, it is possible that the relative ability of CRP, neutrophil counts and eosinopenia in differentiating infections is different, depending on the severity of systemic inflammation and amount of chemotactic factors released into the systemic circulation.
Some of the evidence that implicates pyrin as a regulator of inflammation includes its interaction with leukocyte cytoskeleton, the death domain contained within the protein and its ability to deregulate chemotactic factors.
C5a, through binding to its receptor C5aR, induces expression of additional adhesion molecules and chemotactic factors, thus perpetually amplifying the destructive inflammatory cascade.