Excessive prostaglandin E2 production by suppressor monocytes in head and neck cancer patients

Charles M. Balch, P. A. Dougherty, A. B. Tilden

Research output: Contribution to journalArticle

Abstract

The proliferative response of peripheral blood mononuclear cells (PBMC) to the mitogens PHA and Con A was significantly depressed in 86% of 45 head and neck cancer patients compared with 44 normal controls. This depression of immune competence was greatest in older patients and in those with more advanced disease stages. The abnormal mitogen responses could be restored toward normal (especially with Con A stimulation) by incubating the cells with either of two prostaglandin synthetase inhibitors (indomethacin or RO-205720). This augmentation of immune response was independent on other factors, including the primary tumor site, disease stage, treatment (surgery, radiation therapy, or chemotherapy) or the patient's age or race. The most likely explanation for this depressed level of immunocompetence was an excessive production of PGE2 by suppressor cells. This was confirmed by the finding that PBMC from patients produced more PGE2 than PBMC from normal individuals (8.4 ng/ml vs. 5.2 ng/ml, p = 0.002). This difference was greatest among patients less than 60 years of age whose cultured PBMC produced 91% more PGE2 than controls (p2 was produced by a population of monocytes defined by a monoclonal antibody and purified with a fluorescence-activated cell sorter. Patients with epidermoid cancer of the head and neck thus have an abnormality of immunoregulatory monocytes that can contribute significantly to their depression of cellular immunity by elaborating prostaglandin E2. This abnormality could be partially corrected in vitro by incubating their PBMC with a prostaglandin synthetase inhibitor.

Original languageEnglish (US)
Pages (from-to)645-650
Number of pages6
JournalAnnals of Surgery
Volume196
Issue number6
StatePublished - 1982
Externally publishedYes

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Head and Neck Neoplasms
Dinoprostone
Monocytes
Blood Cells
Prostaglandin Antagonists
Prostaglandin-Endoperoxide Synthases
Mitogens
Immunocompetence
Cellular Immunity
Indomethacin
Mental Competency
Radiotherapy
Fluorescence
Monoclonal Antibodies
Drug Therapy
Population
Neoplasms

ASJC Scopus subject areas

  • Surgery

Cite this

Excessive prostaglandin E2 production by suppressor monocytes in head and neck cancer patients. / Balch, Charles M.; Dougherty, P. A.; Tilden, A. B.

In: Annals of Surgery, Vol. 196, No. 6, 1982, p. 645-650.

Research output: Contribution to journalArticle

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AU - Dougherty, P. A.

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AB - The proliferative response of peripheral blood mononuclear cells (PBMC) to the mitogens PHA and Con A was significantly depressed in 86% of 45 head and neck cancer patients compared with 44 normal controls. This depression of immune competence was greatest in older patients and in those with more advanced disease stages. The abnormal mitogen responses could be restored toward normal (especially with Con A stimulation) by incubating the cells with either of two prostaglandin synthetase inhibitors (indomethacin or RO-205720). This augmentation of immune response was independent on other factors, including the primary tumor site, disease stage, treatment (surgery, radiation therapy, or chemotherapy) or the patient's age or race. The most likely explanation for this depressed level of immunocompetence was an excessive production of PGE2 by suppressor cells. This was confirmed by the finding that PBMC from patients produced more PGE2 than PBMC from normal individuals (8.4 ng/ml vs. 5.2 ng/ml, p = 0.002). This difference was greatest among patients less than 60 years of age whose cultured PBMC produced 91% more PGE2 than controls (p2 was produced by a population of monocytes defined by a monoclonal antibody and purified with a fluorescence-activated cell sorter. Patients with epidermoid cancer of the head and neck thus have an abnormality of immunoregulatory monocytes that can contribute significantly to their depression of cellular immunity by elaborating prostaglandin E2. This abnormality could be partially corrected in vitro by incubating their PBMC with a prostaglandin synthetase inhibitor.

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