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Neutrophil chemotaxis

Although controversial, findings as to how chronically administered morphine modulates neutrophil chemotaxis and function, a growing consensus believes that morphine is suppressive in the recruitment and functional aspects of these cells during an innate immune response. When peripheral human blood neutrophils were pretreated with exogenous opioids, lL-8-induced chemotaxis was inhibited (Grimm et al. 1998). Conversely, Simpkins et al. reported an increase in neutrophil chemotaxis... [Pg.342]

Wandall, J.H. (1992). Effects of omeprazole on neutrophil chemotaxis, superoxidc production, degranulation and translocation of cytochrome b 245. Gut 33, 617-621. [Pg.173]

Anonymous 1988. New York, Connecticut act to restrict TBT-based paints. Ecology USA, June 6, 1988 107. Arakawa, Y. and O. Wada, 1984. Inhibition of neutrophil chemotaxis by organotin compounds. Biochem. Biophys. Res. Comm. 123 543-548. [Pg.626]

Apart from being a potent activator of neutrophil chemotaxis, IL-8 can also induce degranulation and reactive oxygen metabolite production in human neutrophils. These activities are usually very low or undetectable but are augmented when neutrophil suspensions are pretreated with cytochala-sin B. Addition of IL-8 also induces elevations in intracellular free Ca2+. [Pg.95]

Harvath, L. (1990). Regulation of neutrophil chemotaxis Correlations with actin polymerization. Cancer Invest. 8, 651-4. [Pg.147]

Histamine inhibits neutrophil chemotaxis due to HR2 triggering, which is mimicked by impromidine (HR2 agonist), but not by betahistine (HRl agonist). In addition, histamine inhibits neutrophil activation, superoxide formation and degranulation via HR2 [40]. Downregulation of... [Pg.72]

Chen Y, Corriden R, Inoue Y, Yip L, Hashiguchi N. Zinkernagel A, Nizet V. Insel PA. Junger WG ATP release guides neutrophil chemotaxis via P2Y2 and A3 receptors. Science 2006 314 1792-1795. [Pg.199]

Pfizer s tenidap (CP-66,248) (157), another enolic compound, was also more potent (500-fold) toward CO over 5-LO inhibition in human ISN (0.032 /iM and 18 /iM, respectively) [379-381]. Efficacy in rheumatoid arthritis clinical trials has been reported [380,382] in patients, serum levels of acute phase proteins and synovial fluid levels of IL-1 were reduced by tenidap, in contrast to the lack of this effect with NSAIDs. Besides CO/5-LO inhibition, a variety of in vitro activities have been reported, including a number of effects on monocyte functions and differentiation [379], inhibition of neutrophil degranulation [382], inhibition of the activation of neutrophil collagenase [383], inhibition of leukocyte-endothelial cell adhesion [384], and inhibition of LTB4-induced neutrophil chemotaxis [385]. Al-... [Pg.37]

Harvath, L., Balke, J. A., Christiansen, N. P., Russell, A. A., and Skubitz, K. M. (1991) Selected antibodies to leukocyte common antigen (CD45) inhibit human neutrophil chemotaxis. J. Immunol. 146, 949-957. [Pg.290]

It is important to examine the fluorescent conjugate for biological activity and confirm that the coupling procedure does not destroy the chemoattractant stimulatory activity. We evaluate neutrophil chemotaxis in a 48-well micro-chemotaxis chamber (7) as previously described in detail (8) and briefly outlined below. [Pg.302]

Harvath, L., Falk, W., and Leonard, E. J. (1980) Rapid quantitation of neutrophil chemotaxis use of a polyvinylpyrrolidone-free polycarbonate membrane in a multiwell assembly. J. Immunol. Methods 37, 39-45. [Pg.308]

IL-18 augments T- and NK-cell maturation, cytotoxicity and cytokine production. It stimulates TH differentiation, promotes secretion of TNF-a, IFN-y and GM-CSF and enhances NK cell cytotoxicity by increasing FasL expression. IL-8-mediated neutrophil chemotaxis is promoted by IL-18 via its effects on TNF-a and IFN-y, which are stimulatory in action. It plays an important role in maintaining synovial inflammation and inducing joint destruction in rheumatoid arthritis. In synovium of patients with rheumatoid arthritis, enhanced levels of TNF-a and IL-1 are associated with augmented expression of IL-18. [Pg.43]

Kobayashi H, Kitamura K, Nagai K, Nakao Y, Fusetani N, van Soest RWM, Matsunaga S (2007) Carteramine A, an Inhibitor of Neutrophil Chemotaxis, from the Marine Sponge... [Pg.440]

Culpitt SV, de Matos C, Russell RE, et al. Effect of theophylline on induced sputum inflammatory indices and neutrophil chemotaxis in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2002 165 1371-1376. [Pg.385]

Johnston, C.S., Martin, L.J., and Cai, X. Antihistamine effect of supplemental ascorbic acid and neutrophil chemotaxis. J Am Coll Nutr, 11,172-176,1992. [Pg.187]

Parekh T, Saxena B, Reibman J, Cronstein BN, Gold LI. Neutrophil chemotaxis in response to TGF-P isoforms (TGF-Pl, TGF-P2, TGF-P3) is mediated by fibronectin. Journal of Immunology 1994, 152, 2456-2466. [Pg.79]

Bik decreases ischemia/reperfusion injury by inhibiting proteases that cause kinin release [4, 99]. Reversion to a normal blood pressure occurs in two ways through inhibition of kallikrein with protease inhibitors and by destruction of kinins by kinase. Bik decreases kinin formation through their effect on kallikrein. The duration of kinin formation and destruction ranges from 2 to 30 min [100, 101]. After 30 min, little kinin activity is detectable. As inflammation abates, so does neutrophil chemotaxis and endothelial adherence to the basement membrane. PAR also regulates vascular tone and participates in response to vascular injury. Bik inhibits PAR activation [79, 80],... [Pg.239]


See other pages where Neutrophil chemotaxis is mentioned: [Pg.136]    [Pg.137]    [Pg.171]    [Pg.250]    [Pg.63]    [Pg.573]    [Pg.540]    [Pg.79]    [Pg.94]    [Pg.104]    [Pg.280]    [Pg.72]    [Pg.193]    [Pg.300]    [Pg.373]    [Pg.88]    [Pg.400]    [Pg.1201]    [Pg.300]    [Pg.627]    [Pg.253]    [Pg.254]    [Pg.1352]    [Pg.65]    [Pg.8]    [Pg.34]    [Pg.239]    [Pg.240]   
See also in sourсe #XX -- [ Pg.24 , Pg.233 ]

See also in sourсe #XX -- [ Pg.204 , Pg.221 , Pg.222 ]




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