Biomedical subjects

C E Walsh

Publications and source records attributed to C E Walsh.

39 records · Page 3Linked to original sources

PubMed1982

Comparison of the calcium ionophore and phorbol myristate acetate on the initiation of the respiratory burst in human neutrophils.

We investigated the ability of the calcium ionophore A23187 and phorbol myristate acetate to elicit a respiratory burst in human neutrophils. In general, the ionophore was considerably more potent than phorbol myristate acetate in generating a chemiluminescent response and slightly less active in generating superoxide anion. In contrast, the ionophore caused a much smaller stimulation of glucose oxidation via the hexose monophosphate shunt. This relative inability of the ionophore to stimulate the shunt could not be ascribed to an effect on glucose transport or to a direct inhibition of any of the enzymes involved in glucose metabolism. These data suggest that different stimuli may have markedly different effects on various activities associated with the respiratory burst and emphasize the necessity for measurement of more than one parameter to assess the oxidative metabolism of the neutrophil.

Anti-Bacterial Agents↗

PubMed1981

Release and metabolism of arachidonic acid in human neutrophils.

Dual radiolabel incorporation of [3H]arachidonic acid and [14C]palmitate or [14C]stearate by human neutrophils was employed to study both the release and metabolism of arachidonic acid. Results indicate the involvement of a phospholipase A2 mechanism causing [3H]arachidonate release from membrane phospholipid. Phosphatidylinositol and phosphatidylcholine were the sources of [3H]arachidonate; about twice as much radiolabeled phosphatidylinositol was degraded as phosphatidylcholine. Challenge of neutrophils with opsonized zymosan and calcium ionophores caused the release of [3H]arachidonate; however, ionophores but not opsonized zymosan led to the production of [3H]hydroxyicosatetraenoic acid and [3H]dihydroxyicosatetraenoic acid. These products were preferentially released by neutrophils into the extracellular milieu in contrast with free [3H]arachidonate which remained cell associated. One-third of the [3H]hydroxyicosatetraenoic acid but not [3H]dihydroxyicosatetraenoic acid was reincorporated into cellular lipid, primarily phospholipid. No significant production of [3H]prostaglandin or [3H]thromboxane was detected. In contrast to zymosan and ionophore, phorbol myristate acetate, another potent stimulant of neutrophil oxidative metabolism and degranulation, did not release [3H]arachidonate.

Arachidonic Acid↗

PubMed1981

Effect of phagocytosis and ionophores on release and metabolism of arachidonic acid from human neutrophils.

Challenge of human neutrophils prelabeled with [3H] arachidonate and [14C] palmitate or [14C]-stearate with opsonized zymosan or the Ca2+ ionophores A23187 or Ionomycin caused the release of [3H], but not [14C], fatty acid. With the ionophores, but not zymosan, considerable conversion of the [3H] arachidonate to hydroxyeicosatetraenoates occurred. Although various isomers were recovered, the 5-hydroxyeicosatetraenoate appeared to be the major product. In these experiments, no [14C] products were detected such as lysophospholipid, diglyceride or monoglyceride. Although no definite statement can be made about the mechanism of release of arachidonate, our data are most easily interpreted as the result of the action of a phospholipase A2.

Anti-Bacterial Agents↗