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S Krilis

Publications and source records attributed to S Krilis.

5 recordsLinked to original sources
PubMed1990

Lipoxin A4 inhibits phosphoinositide hydrolysis in human neutrophils.

Lipoxins (LX) are trihydroxytetraene metabolites derived from arachidonic acid via an interaction between the 5- and 15-lipoxygenases. Preincubation of [3H] myo-inositol labeled PMN with 10-7M and 10-5M LXA4 for 1 minute at 37 degrees C resulted in a concentration dependent inhibition of the generation of [3H] IP3 and [3H] IP in cells subsequently stimulated by increasing doses of LTB4 or FMLP for 1 minute at 37 degrees C. Preincubation of PMN with LXA4 did not inhibit specific binding of [3H] LTB4 to PMN. These results indicate that LXA4 inhibits chemotactic factor-induced phosphoinositide hydrolysis at a post-receptor level.

Dose-Response Relationship, Drug↗
PubMed1990

Human tumour necrosis factor-alpha (TNF-alpha) directly stimulates arachidonic acid release in human neutrophils.

The ability of tumour necrosis factor-alpha (TNF-alpha) to directly stimulate phospholipid turnover from human neutrophils was studied. Stimulation with recombinant human (rH) TNF-alpha induced the release of significant amounts of radioactivity from [3H]arachidonic acid-labelled neutrophils. This stimulation was equipotent to that induced by the bacterial tripeptide formyl-methionyl-leucylphenylalanine (FMLP). The time of maximum stimulated release varied between donors, with the most common maximal stimulation being 45 min. Dose-response experiments indicated that 100-1000 U/ml rH TNF-alpha were required for the maximum stimulatory effect. High-performance liquid chromatography analysis of the supernatants revealed that the radioactivity was associated with arachidonic acid, but not with its metabolites, indicating that TNF-alpha stimulates the release of arachidonic acid from cellular phospholipids but does not stimulate its metabolism. A comparison of TNF-alpha with other cytokines indicated that stimulation of arachidonic acid release paralleled the 'priming' of neutrophils for enhanced superoxide production, raising the possibility that phospholipid turnover and priming of neutrophils are causally related.

Arachidonic Acids↗
PubMedDate not supplied

15-hydroxyeicosatetraenoic acid synthesis from exogenous arachidonate by bronchial mucosa.

Arachidonate metabolism in bronchial mucosa was investigated. Bronchial biopsies from four asthmatics and three non-asthmatic controls were challenged with 300, 465, 650 and 960 mOsm/kg saline in the presence of [3H]arachidonate. Supernatants were analysed by reverse-phase high-performance liquid chromatography. The major arachidonate metabolite was identified as 15-monohydroxyeicosatetraenoic acid (15-HETE), with significantly higher production in biopsies from asthmatics than controls. Statistical analysis of the full model explained 81% of the variation (F = 14.8; df = 6, 21; P less than 0.001). Hyperosmolarity and the presence of sarcoid had no significant effect on 15-HETE synthesis, reducing R2 by only 6%.

Adult↗