Leukotrienes stimulate neutrophil adhesion to mesangial cells: modulation with lipoxins

1990 ◽  
Vol 259 (5) ◽  
pp. F809-F815 ◽  
Author(s):  
H. R. Brady ◽  
U. Persson ◽  
B. J. Ballermann ◽  
B. M. Brenner ◽  
C. N. Serhan
Keyword(s):  
High Performance ◽  
Mesangial Cells ◽  
Divalent Cations ◽  
Leukotriene B4 ◽  
Polymorphonuclear Neutrophil ◽  
Induced Response ◽  
Lipoxin A4 ◽  
Leukotriene D4 ◽  
Adhesion Process

We have examined polymorphonuclear neutrophil (PMN) adhesion to mesangial cells (MC) in vitro and have assessed the actions of lipoxygenase (LO) products in this process. On exposure to either leukotriene B4 (LTB4), or leukotriene D4 (LTD4), 111In-labeled PMNs adhere to monolayers of cultured MC. These actions were rapid in onset (less than 5 min) and dependent upon leukotriene concentration (10(-9) to 10(-6) M) and the presence of divalent cations. Adhesion was sustained (0-30 min), and neither LTB4 nor LTD4 was metabolized to inactive products during PMN-MC interaction, as determined by their recovery after reverse-phase high-performance liquid chromatography. LTB4 was a PMN-directed stimulus, whereas LTD4 appeared to act on MC. A monoclonal antibody (TS 1/18) against the CD18 component of the PMN CD18/CD11 adhesion complex inhibited the LTB4-induced response, indicating involvement of this PMN glycoprotein in the adhesion process. In contrast, this antibody did not affect LTD4-induced adhesion, suggesting that this response was mediated by other adhesion epitopes. When added alone, neither lipoxin A4 (LXA4) nor lipoxin B4 (LXB4) provoked PMN adhesion to MC. In contrast, LXA4 and LXB4 at equimolar concentrations attenuated the LTD4- but not LTB4-induced response. Together, these results provide further evidence that LO-derived eicosanoids may constitute important early signals that regulate PMN-MC interaction in glomerular inflammation.

scholarly journals Lipoxin A4 induces hyperadhesiveness in human endothelial cells for neutrophils

Blood ◽  
1993 ◽  
Vol 82 (3) ◽  
pp. 948-953 ◽  
Author(s):  
R Lerner ◽  
M Heimburger ◽  
J Palmblad
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Cytosolic Calcium ◽  
Leukotriene B4 ◽  
Polymorphonuclear Neutrophil ◽  
Maximal Response ◽  
Neutrophil Granulocytes ◽  
Lipoxin A4

Abstract Lipoxin A4 (LXA4), but not lipoxin B4, induced in vitro a dose- dependent, slowly emerging hyperadhesiveness in human umbilical vein endothelial cells (HUVEC), leading to a 1.9-fold increase in the binding of neutrophils (polymorphonuclear neutrophil granulocytes [PMN]). The maximal response to LXA4 occurred at 1 nmol/L and after 30 minutes of treatment of HUVEC. These response kinetics were intermediate in comparison with those of fast-acting inducers of HUVEC adhesivity (eg, thrombin, leukotriene B4 [LTB4] or platelet activating factor [PAF]), needing 5 to 15 minutes, or to the slow inducer interleukin-1 (IL-1 beta), which requires hours. The maximal LXA4 effect was slightly lower than that of LTB4 (100 nmol/L) and thrombin (1 U/mL), and less than that of PAF (100 nmol/L) or IL-1 beta (2.5 U/mL) (2.2-, 2.0-, 2.4-, or 13.6-fold increases, respectively). The LXA4 effect was inhibited by the PAF receptor antagonist WEB-2086; however, it could not be blocked by pertussis toxin. LXA4 conferred a slow, sustained increase in HUVEC cytosolic calcium ion concentrations, whereas thrombin did so rapidly and transiently. LXA4 also caused PMN to become hyperadhesive. Thus, this novel effect of LXA4 on HUVEC appears to be associated with endogenous PAF expression and slow increases of cytosolic calcium concentrations but not pertussis- sensitive G proteins.

scholarly journals Lipoxin A4 induces hyperadhesiveness in human endothelial cells for neutrophils

Blood ◽  
1993 ◽  
Vol 82 (3) ◽  
pp. 948-953
Author(s):  
R Lerner ◽  
M Heimburger ◽  
J Palmblad
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Cytosolic Calcium ◽  
Leukotriene B4 ◽  
Polymorphonuclear Neutrophil ◽  
Maximal Response ◽  
Neutrophil Granulocytes ◽  
Lipoxin A4

Lipoxin A4 (LXA4), but not lipoxin B4, induced in vitro a dose- dependent, slowly emerging hyperadhesiveness in human umbilical vein endothelial cells (HUVEC), leading to a 1.9-fold increase in the binding of neutrophils (polymorphonuclear neutrophil granulocytes [PMN]). The maximal response to LXA4 occurred at 1 nmol/L and after 30 minutes of treatment of HUVEC. These response kinetics were intermediate in comparison with those of fast-acting inducers of HUVEC adhesivity (eg, thrombin, leukotriene B4 [LTB4] or platelet activating factor [PAF]), needing 5 to 15 minutes, or to the slow inducer interleukin-1 (IL-1 beta), which requires hours. The maximal LXA4 effect was slightly lower than that of LTB4 (100 nmol/L) and thrombin (1 U/mL), and less than that of PAF (100 nmol/L) or IL-1 beta (2.5 U/mL) (2.2-, 2.0-, 2.4-, or 13.6-fold increases, respectively). The LXA4 effect was inhibited by the PAF receptor antagonist WEB-2086; however, it could not be blocked by pertussis toxin. LXA4 conferred a slow, sustained increase in HUVEC cytosolic calcium ion concentrations, whereas thrombin did so rapidly and transiently. LXA4 also caused PMN to become hyperadhesive. Thus, this novel effect of LXA4 on HUVEC appears to be associated with endogenous PAF expression and slow increases of cytosolic calcium concentrations but not pertussis- sensitive G proteins.

scholarly journals Sugar, vitamin C, and polyphenols in commercial apple beverages and their effects on antioxidant and anti-inflammatory activities in vitro

2021 ◽  
Vol 13 ◽  
Author(s):  
Claudine Loong ◽  
Latasha Leo ◽  
Wai Mun Loke
Keyword(s):  
Vitamin C ◽  
High Performance ◽  
Lipid Hydroperoxide ◽  
Radical Scavenging ◽  
Leukotriene B4 ◽  
Detection Methods ◽  
Myeloperoxidase Activity ◽  
Hydroperoxide Formation ◽  
Anti Inflammatory

The concentrations of sugar, vitamin C, and polyphenols, as well as antioxidant and anti-inflammatory capacity of commercial apple beverage products in Singapore, were not known. The concentrations of vitamin C, total polyphenol content, and specific polyphenols, quercetin, and catechin of commercial apple beverages were determined using their respective high-performance liquid chromatography – ultraviolet detection methods. 1,1-diphenyl-2-picrylhydrazyl assay and in vitro studies were conducted to examine the antioxidant and anti-inflammatory capacity. The apple beverages (n=17) exhibited significant antioxidant (DPPH radical scavenging assay, inhibition of cellular F2-isoprostanes and lipid hydroperoxide formation) and anti-inflammatory (inhibition of cellular leukotriene B4 formation and myeloperoxidase activity) capacity, which were found to be associated with vitamin C (10.35±1.18g/ 100g), total polyphenols (9.9±1.2mg GAE/ 100g), catechin (1.60±0.10mg/ 100g), and quercetin (0.46±0.09mg/ 100g) concentrations in the beverages. A separate simulation experiment demonstrated that antioxidant and anti-inflammatory capacity were augmented by increasing vitamin C, total and specific polyphenol concentrations.

scholarly journals Physical exercise increases urinary excretion of lipoxin A4 and related compounds

2003 ◽  
Vol 94 (6) ◽  
pp. 2237-2240 ◽  
Author(s):  
Sebastiano Gangemi ◽  
Graziella Luciotti ◽  
Etrusca D'Urbano ◽  
Agostino Mallamace ◽  
Domenico Santoro ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
High Performance ◽  
Reversed Phase ◽  
Strenuous Exercise ◽  
Lipoxin A4 ◽  
Safeguard Mechanism ◽  
First Time ◽  
Related Compounds

Lipoxins (LX) are lipoxygenase-derived eicosanoids with potent anti-inflammatory activities and vascular bed-dependent vasodilatory actions. LX can be formed in vitro and in vivo in a number of conditions, and we have reported that immunoreactive LXA4 (iLXA4) is physiologically excreted with human urine. Using a recently developed LX extraction method coupled to an ELISA, we examined whether iLXA4 excretion was modified by strenuous exercise, which is known to trigger potential LX-forming events. Maximal exertion significantly increased iLXA4 urinary excretion in nine healthy volunteers (0.061 ± 0.023 vs. 0.113 ± 0.057 ng/mg creatinine; P = 0.028). iLXA4 levels returned to baseline after 6 h and increased, although at a smaller extent, after 24 h. A significant correlation ( r = 0.988) was denoted between iLXA4 ELISA measurements and reversed-phase high-performance liquid chromatography quantitation of a previously described urinary tetraene, confirming its LXA4-related nature. These findings show for the first time that an increase in excretion of LXA4-related compounds can be observed in response to strenuous exercise. This may be the reflection of an enhanced LX biosynthesis, which may represent a safeguard mechanism that keeps the inflammatory reaction triggered by physical stress under control.

scholarly journals Lipoxin A4 Antagonizes the Mitogenic Effects of Leukotriene D4 in Human Renal Mesangial Cells

2000 ◽  
Vol 275 (36) ◽  
pp. 27566-27575 ◽  
Author(s):  
Blaithin McMahon ◽  
Catherine Stenson ◽  
Fiona McPhillips ◽  
Aine Fanning ◽  
Hugh R. Brady ◽  
...  
Keyword(s):  
Mesangial Cells ◽  
Lipoxin A4 ◽  
Leukotriene D4

scholarly journals Arachidonic acid in postshock mesenteric lymph induces pulmonary synthesis of leukotriene B4

2008 ◽  
Vol 104 (4) ◽  
pp. 1161-1166 ◽  
Author(s):  
Janeen R. Jordan ◽  
Ernest E. Moore ◽  
Eric L. Sarin ◽  
Sagar S. Damle ◽  
Sara B. Kashuk ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Lung Injury ◽  
Ischemia Reperfusion ◽  
Leukotriene B4 ◽  
Polymorphonuclear Neutrophil ◽  
Sprague Dawley ◽  
Bioactive Lipids ◽  
Mesenteric Lymph ◽  
Sprague Dawley Rats

Mesenteric lymph is the mechanistic link between splanchnic hypoperfusion and acute lung injury (ALI), but the culprit mediator(s) remains elusive. Previous work has shown that administration of a phospholipase A2(PLA2) inhibitor attenuated postshock ALI and also identified a non-ionic lipid within the postshock mesenteric lymph (PSML) responsible for polymorphonuclear neutrophil (PMN) priming. Consequently, we hypothesized that gut-derived leukotriene B4(LTB4) is a key mediator in the pathogenesis of ALI. Trauma/hemorrhagic shock (T/HS) was induced in male Sprague-Dawley rats and the mesenteric duct cannulated for lymph collection/diversion. PSML, arachidonic acid (AA), and a LTB4receptor antagonist were added to PMNs in vitro. LC/MS/MS was employed to identify bioactive lipids in PSML and the lungs. T/HS increased AA in PSML and increased LTB4and PMNs in the lung. Lymph diversion decreased lung LTB4by 75% and PMNs by 40%. PSML stimulated PMN priming (11.56 ± 1.25 vs. 3.95 ± 0.29 nmol O2−/min; 3.75 × 105cells/ml; P < 0.01) that was attenuated by LTB4receptor blockade (2.64 ± 0.58; P < 0.01). AA stimulated PMNs to produce LTB4, and AA-induced PMN priming was attenuated by LTB4receptor antagonism. Collectively, these data indicate that splanchnic ischemia/reperfusion activates gut PLA2-mediated release of AA into the lymph where it is delivered to the lungs, provoking LTB4production and subsequent PMN-mediated lung injury.

Bronchoalveolar cell activation after inhalation of a bronchoconstricting agent

1988 ◽  
Vol 64 (4) ◽  
pp. 1615-1623 ◽  
Author(s):  
J. A. Cooper ◽  
W. W. Merrill ◽  
J. A. Rankin ◽  
Y. Sibille ◽  
M. G. Buck
Keyword(s):  
Bronchoalveolar Lavage ◽  
Cell Activation ◽  
Leukotriene B4 ◽  
Thromboxane B2 ◽  
Polymorphonuclear Neutrophil ◽  
Pulmonary Cells ◽  
Fluid Levels ◽  
Culture Supernatants

Airway inflammation is thought to be an important determinant of bronchoconstriction and bronchial hyperreactivity. We have recently demonstrated that bronchoconstriction induced by an aqueous extract of cotton bracts (CBE) is associated with bronchoalveolar complement activation, release of polymorphonuclear neutrophil (PMN) chemoattractants by pulmonary cells, and increased numbers of bronchoalveolar lavage PMN's. In the present study we performed bronchoalveolar lavage (BAL) on subjects after CBE or control (saline) challenge and examined whether BAL cells were activated in vitro to produce other inflammatory agonists. After CBE administration, cultured BAL cells released increased amounts of the reactive O2 species, superoxide (O2-.), and the cyclooxygenase products prostaglandin E2 and thromboxane B2. Although none of these in vitro parameters of BAL cell activation appeared to correlate with the degree of bronchoconstriction induced by CBE, BAL fluid levels of thromboxane B2 were also increased after CBE administration and in vivo amounts of this eicasanoid did correlate with the degree of bronchoconstriction induced by CBE (r = 0.50, P less than 0.04). Finally, although cell culture supernatants were highly chemotactic for PMN's, concentrations of leukotriene B4 were not increased, suggesting other chemotaxins were released by BAL cells in this setting. We conclude that CBE administration activates bronchoalveolar cells to release reactive O2 species and cyclooxygenase products that may be important in the bronchoconstricting response to CBE.

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