PMID- 2548801
OWN - NLM
STAT- MEDLINE
DCOM- 19890927
LR  - 20190820
IS  - 0143-5221 (Print)
IS  - 0143-5221 (Linking)
VI  - 77
IP  - 2
DP  - 1989 Aug
TI  - Lipoxin A4 and lipoxin B4 inhibit chemotactic responses of human neutrophils 
      stimulated by leukotriene B4 and N-formyl-L-methionyl-L-leucyl-L-phenylalanine.
PG  - 195-203
AB  - 1. Lipoxin A4 (LXA4) and lipoxin B4 (LXB4) have been evaluated for their 
      capacities to modulate neutrophil (PMN) migration and endothelial cell adherence 
      using compounds prepared by total chemical synthesis. 2. Increased PMN migration 
      was seen with concentrations of LXA4 from 10(-9) mol/l to 10(-7) mol/l. LXA4 was 
      100-fold less potent than leukotriene B4 (LTB4) and it elicited only one-half of 
      the maximal response of LTB4. 3. The (5S,6S,15S)-isomer of LXA4 induced only a 
      weak migratory response and LXB4 was inactive, suggesting that the activity of 
      LXA4 was stereospecific. 4. Modified chequerboard analysis indicated that LXA4 
      was a chemokinetic agent. 5. Preincubation of PMN with increasing concentrations 
      of LXA4 induced a very similar dose- and time-dependent inhibition of the 
      subsequent response to 10(-7) mol/l LTB4 or 10(-7) mol/l 
      N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP). The inhibition was observed 
      at 10(-10) mol/l LXA4; the concentration which produced 50% inhibition was 10(-8) 
      mol/l and 100% inhibition of PMN locomotion occurred at 10(-6) mol/l LXA4. 6. The 
      (5S,6S,15S)-isomers of LXA4 and LXB4 were 5- and 100-fold less potent than LXA4, 
      respectively, in suppressing LTB4- or FMLP-induced PMN migration. 7. 
      Preincubation of PMN with LXA4 led to a suppression of calcium mobilization, as 
      assessed by Quin2-AM fluorescence, when the cells were subsequently stimulated 
      under optimal conditions by LTB4 or FMLP. 8. These results suggest that the 
      inhibitory activity of lipoxins may be related to the capacity of these molecules 
      to regulate calcium ion mobilization.
FAU - Lee, T H
AU  - Lee TH
AD  - Department of Allergy and Allied Respiratory Disorders, United Medical School, 
      Guy's Hospital, London.
FAU - Horton, C E
AU  - Horton CE
FAU - Kyan-Aung, U
AU  - Kyan-Aung U
FAU - Haskard, D
AU  - Haskard D
FAU - Crea, A E
AU  - Crea AE
FAU - Spur, B W
AU  - Spur BW
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Hydroxyeicosatetraenoic Acids)
RN  - 0 (Lipoxins)
RN  - 0 (lipoxin A4)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 92950-25-9 (lipoxin B4)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Calcium/blood
MH  - Cell Adhesion/drug effects
MH  - Chemotaxis, Leukocyte/*drug effects
MH  - Humans
MH  - Hydroxyeicosatetraenoic Acids/*pharmacology
MH  - Isomerism
MH  - Leukotriene B4
MH  - *Lipoxins
MH  - N-Formylmethionine Leucyl-Phenylalanine
MH  - Neutrophils/drug effects/metabolism
EDAT- 1989/08/01 00:00
MHDA- 1989/08/01 00:01
CRDT- 1989/08/01 00:00
PHST- 1989/08/01 00:00 [pubmed]
PHST- 1989/08/01 00:01 [medline]
PHST- 1989/08/01 00:00 [entrez]
AID - 10.1042/cs0770195 [doi]
PST - ppublish
SO  - Clin Sci (Lond). 1989 Aug;77(2):195-203. doi: 10.1042/cs0770195.