scholarly journals Reduced 15-lipoxygenase 2 and lipoxin A4/leukotriene B4 ratio in children with cystic fibrosis

2014 ◽  
Vol 44 (2) ◽  
pp. 394-404 ◽  
Author(s):  
F. C. Ringholz ◽  
P. J. Buchanan ◽  
D. T. Clarke ◽  
R. G. Millar ◽  
M. McDermott ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Leukotriene B4 ◽  
Lipoxin A4

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.

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 Activation of Lipoxin a4 Receptors by Aspirin-Triggered Lipoxins and Select Peptides Evokes Ligand-Specific Responses in Inflammation

2000 ◽  
Vol 191 (7) ◽  
pp. 1197-1208 ◽  
Author(s):  
Nan Chiang ◽  
Iolanda M. Fierro ◽  
Karsten Gronert ◽  
Charles N. Serhan
Keyword(s):  
Tissue Injury ◽  
Leukotriene B4 ◽  
Peptide Ligands ◽  
Peptide Fragments ◽  
Transmembrane Segment ◽  
Small Peptides ◽  
Lipoxin A4 ◽  
Chimeric Receptors ◽  
Chemotactic Peptides ◽  
Endogenous Lipids

Lipoxin (LX) A4 and aspirin-triggered LX (ATL) are endogenous lipids that regulate leukocyte trafficking via specific LXA4 receptors (ALXRs) and mediate antiinflammation and resolution. ATL analogues dramatically inhibited human neutrophil (polymorphonuclear leukocyte [PMN]) responses evoked by a potent necrotactic peptide derived from mitochondria as well as a rogue synthetic chemotactic peptide. These bioactive lipid analogues and small peptides each selectively competed for specific 3H-LXA4 binding with recombinant human ALXR, and its N-glycosylation proved essential for peptide but not LXA4 recognition. Chimeric receptors constructed from receptors with opposing functions, namely ALXR and leukotriene B4 receptors (BLTs), revealed that the seventh transmembrane segment and adjacent regions of ALXR are essential for LXA4 recognition, and additional regions of ALXR are required for high affinity binding of the peptide ligands. Together, these findings are the first to indicate that a single seven-transmembrane receptor can switch recognition as well as function with certain chemotactic peptides to inhibitory with ATL and LX (lipid ligands). Moreover, they suggest that ALXR activation by LX or ATL can protect the host from potentially deleterious PMN responses associated with innate immunity as well as direct effector responses in tissue injury by recognition of peptide fragments.

The absorption and effect of dietary supplementation with omega-3 fatty acids on serum leukotriene B4, in patients with cystic fibrosis

1994 ◽  
Vol 18 (4) ◽  
pp. 211-217 ◽  
Author(s):  
Lawrence E. Kurlandsky ◽  
Maurice R. Bennink ◽  
Phyllis M. Webb ◽  
Pamela J. Ulrich ◽  
Lawrence J. Baer
Keyword(s):  
Cystic Fibrosis ◽  
Fatty Acids ◽  
Dietary Supplementation ◽  
Leukotriene B4 ◽  
Omega 3 Fatty Acids ◽  
Omega 3

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.

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