Effects of Erythromycin, Josamycin and Spiramycin on Rat Polymorphonuclear Leukocyte Chemotaxis

Chemotherapy ◽  
1986 ◽  
Vol 32 (4) ◽  
pp. 379-382 ◽  
Author(s):  
A. Eyraud ◽  
J. Descotes ◽  
J.Y. Lombard ◽  
A. Laschi-Loquerie ◽  
P. Tachon ◽  
...  
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Leukocyte Chemotaxis

Effect of Some Anti-Inflammatory Drugs on Human Neutrophil Chemotaxis

1994 ◽  
Vol 22 (2) ◽  
pp. 100-106 ◽  
Author(s):  
G Hasçelik ◽  
B ŞLener ◽  
Z Hasçelik
Keyword(s):  
Acetylsalicylic Acid ◽  
Polymorphonuclear Leukocyte ◽  
Polymorphonuclear Leukocytes ◽  
Diclofenac Sodium ◽  
Tiaprofenic Acid ◽  
Boyden Chamber ◽  
Random Migration ◽  
Leukocyte Chemotaxis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

The effects of piroxicam, tenoxicam, diclofenac sodium, acetylsalicylic acid and tiaprofenic acid on the chemotaxis and random migration of human polymorphonuclear leukocytes were investigated, using zymosan-activated serum as chemo-attractant, with a modified Boyden chamber technique. All five compounds significantly reduced chemotaxis. The random migration of polymorphonuclear leukocytes was inhibited by piroxicam, diclofenac sodium and tiaprofenic acid but not by tenoxicam or acetylsalicylic acid. The inhibitory effect of these non-steroidal anti-inflammatory drugs on polymorphonuclear leukocyte chemotaxis and on random migration was generally dose-dependent. The results suggest that the drugs studied may have a direct effect on polymorphonuclear leukocyte chemotaxis and that this activity may contribute to their anti-inflammatory properties.

Cellular augmentation of polymorphonuclear leukocyte chemotaxis

1979 ◽  
Vol 236 (1) ◽  
pp. C22-C29 ◽  
Author(s):  
A. Takeuchi ◽  
R. H. Persellin
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Polymorphonuclear Leukocytes ◽  
Cellular Response ◽  
Active Component ◽  
Cell Contact ◽  
Cytoplasmic Fraction ◽  
Activated Neutrophils ◽  
Leukocyte Chemotaxis ◽  
Number Of Cells ◽  
Insufficient Number

The density of neutrophils influences the number of cells that will respond to a chemoattractant, endotoxin-activated serium. When fewer than 3 x 10(5) polymorphonuclear leukocytes (PMN) were placed in the top compartment of a modified Boyden chemotaxis chamber, the cellular response was weak. Complete membrane penetration by activated neutrophils rarely was observed. When this number of PMN was exceeded, however, both the number of cells and the percentage of neutrophils responding to the leukoattractant increased. The density of cells required for effective chemotactic response to occur was such that intimate cell-to-cell contact was suggested. This indicated that PMN exerted a kinetic influence upon one another. Extracts of disrupted PMN induced an otherwise insufficient number of neutrophils to respond to the chemotactic stimulus. The active component was isolated in the cytoplasmic fraction (postcentrifugation, 100,000 x g, 60 min) of PMN, but was not present in other subcellular fractions. This cytoplasmic augmentor of chemotaxis (CACh) increased random mobility of neutrophils, but was not, itself, a chemotactic factor. These findings suggest that PMN cooperate in their response to a leukotactic stimulus.

scholarly journals Endothelial-secreted arachidonic acid metabolites modulate polymorphonuclear leukocyte chemotaxis and diapedesis in vitro

Blood ◽  
1988 ◽  
Vol 71 (3) ◽  
pp. 771-779 ◽  
Author(s):  
J Doukas ◽  
HB Hechtman ◽  
D Shepro
Keyword(s):  
Arachidonic Acid ◽  
Polymorphonuclear Leukocyte ◽  
Thromboxane A2 ◽  
In Vitro Assays ◽  
General Effect ◽  
Random Motility ◽  
Acid Metabolites ◽  
Leukocyte Chemotaxis ◽  
High Doses

Abstract The influence of endothelial cells (ECs) on polymorphonuclear leukocyte (PMN) motility was examined using in vitro assays of PMN diapedesis and chemotaxis. ECs are seen to release arachidonic acid (20:4) metabolites that directly increase or decrease PMN movement, with their general effect being enhanced motility. This effect can be increased or decreased by treating ECs with stimulators or inhibitors of 20:4 metabolism, respectively. The metabolites include thromboxane B2, which increases PMN random motility, chemotaxis, and diapedesis in a dose- responsive manner and which acts as a chemoattractant; 6-keto-PGF1 alpha, which increases chemotaxis and diapedesis at high doses but decreases these responses at low doses; and a lipoxygenase-derived metabolite, suggested to be 5-hydroxyeicosatetraenoic acid, which increases chemotaxis and diapedesis. Thromboxane A2 and prostacyclin mimetics also affect chemotaxis in qualitatively similar manners as TxB2 and 6-keto-PGF1 alpha, respectively, but display greater potency. EC release of these metabolites is also seen to be substratum modulated, with an increased production by cells cultured on extracellular matrices. These results suggest that ECs are capable of modulating PMN motility and suggest a role for ECs in the control of PMN diapedesis.

Polymorphonuclear leukocyte chemotaxis in sporotrichosis

1982 ◽  
Vol 79 (1) ◽  
pp. 39-41 ◽  
Author(s):  
H. Hachisuka ◽  
S. Tajiri ◽  
K. Hongo ◽  
Y. Sasai
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Leukocyte Chemotaxis

Very rapid assay of polymorphonuclear leukocyte chemotaxis in vitro

1989 ◽  
Vol 22 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Watanabe Kazuyoshi ◽  
Kinoshita Shigemi ◽  
Nakagawa Hideo
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Rapid Assay ◽  
Leukocyte Chemotaxis

Etretinate therapy reduces polymorphonuclear leukocyte chemotaxis—enhancing properties of psoriatic serum

1985 ◽  
Vol 13 (3) ◽  
pp. 437-443 ◽  
Author(s):  
Charles N. Ellis ◽  
Sewon Kang ◽  
Roy C. Grekin ◽  
John J. Voorhees ◽  
Joseph Silva
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Leukocyte Chemotaxis
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