Effects of salicylate and phenobarbital on lymphocyte proliferation and function

John D. Gabourel; Gordon H. Davies; Marvin B. Rittenberg

doi:10.1016/0090-1229(77)90029-0

Effects of salicylate and phenobarbital on lymphocyte proliferation and function

John D. Gabourel
, Gordon H. Davies
, Marvin B. Rittenberg

Molecular Microbiology and Immunology

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

Salicylate inhibited the response of human peripheral lymphocytes to phytohemagglutinim (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), and X-irradiated allogeneic lymphocytes. In addition, salicylate suppressed the generation of cytotoxic lymphocytes (CL) in vitro. The effect was dose dependent with over 90% inhibition at 48 mg%. Once CL were generated, however, the drug had little effect on their ability to lyse target cells. Sodium salicylate also suppressed the proliferative response of parental mouse thymocytes adoptively transferred into lethally irradiated F₁ hybrid recipients as assessed by splenic uptake of [¹²⁵I] iododeoxyuridine. High-dose, chronic treatment of both thymocyte donors and recipients was necessary to effect a 20-60% suppression. Similar chronic treatment of mice depressed the number of splenic plaque-forming cells by 48-72% when assayed 4 days after primary challenge with sheep erythrocytes. On the contrary, we could find no effect of phenobarbital on the response to PHA, mixed lymphocyte culture, or on the generation of CL.

Original language	English (US)
Pages (from-to)	53-61
Number of pages	9
Journal	Clinical Immunology and Immunopathology
Volume	7
Issue number	1
DOIs	https://doi.org/10.1016/0090-1229(77)90029-0
State	Published - Jan 1977

Funding

This work was supported by grants to Dr. Gabourel from the U.S. Public Health Service, CA/GM 14360, and from the Carl I. and Alma Johnson Foundation Trust. Parts of these studies were done while Dr. Gabourel was on sabbatical leave at the Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia. The authors are grateful to Charlotte Carothers, Patrick Muller. and Adriana Vasil for expert technical assistance. They also wish to thank Dr. J. F. A. P. Miller for providing facilities and help during the early phases of this work.

Funders	Funder number
Carl I. and Alma Johnson Foundation Trust
U.S. Public Health Service	CA/GM 14360

ASJC Scopus subject areas

Immunology and Allergy
Pathology and Forensic Medicine
Immunology

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10.1016/0090-1229(77)90029-0

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title = "Effects of salicylate and phenobarbital on lymphocyte proliferation and function",

abstract = "Salicylate inhibited the response of human peripheral lymphocytes to phytohemagglutinim (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), and X-irradiated allogeneic lymphocytes. In addition, salicylate suppressed the generation of cytotoxic lymphocytes (CL) in vitro. The effect was dose dependent with over 90\% inhibition at 48 mg\%. Once CL were generated, however, the drug had little effect on their ability to lyse target cells. Sodium salicylate also suppressed the proliferative response of parental mouse thymocytes adoptively transferred into lethally irradiated F1 hybrid recipients as assessed by splenic uptake of [125I] iododeoxyuridine. High-dose, chronic treatment of both thymocyte donors and recipients was necessary to effect a 20-60\% suppression. Similar chronic treatment of mice depressed the number of splenic plaque-forming cells by 48-72\% when assayed 4 days after primary challenge with sheep erythrocytes. On the contrary, we could find no effect of phenobarbital on the response to PHA, mixed lymphocyte culture, or on the generation of CL.",

author = "Gabourel, \{John D.\} and Davies, \{Gordon H.\} and Rittenberg, \{Marvin B.\}",

note = "Funding Information: This work was supported by grants to Dr. Gabourel from the U.S. Public Health Service, CA/GM 14360, and from the Carl I. and Alma Johnson Foundation Trust. Parts of these studies were done while Dr. Gabourel was on sabbatical leave at the Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia. The authors are grateful to Charlotte Carothers, Patrick Muller. and Adriana Vasil for expert technical assistance. They also wish to thank Dr. J. F. A. P. Miller for providing facilities and help during the early phases of this work.",

year = "1977",

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doi = "10.1016/0090-1229(77)90029-0",

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AU - Gabourel, John D.

AU - Davies, Gordon H.

AU - Rittenberg, Marvin B.

N1 - Funding Information: This work was supported by grants to Dr. Gabourel from the U.S. Public Health Service, CA/GM 14360, and from the Carl I. and Alma Johnson Foundation Trust. Parts of these studies were done while Dr. Gabourel was on sabbatical leave at the Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia. The authors are grateful to Charlotte Carothers, Patrick Muller. and Adriana Vasil for expert technical assistance. They also wish to thank Dr. J. F. A. P. Miller for providing facilities and help during the early phases of this work.

PY - 1977/1

Y1 - 1977/1

N2 - Salicylate inhibited the response of human peripheral lymphocytes to phytohemagglutinim (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), and X-irradiated allogeneic lymphocytes. In addition, salicylate suppressed the generation of cytotoxic lymphocytes (CL) in vitro. The effect was dose dependent with over 90% inhibition at 48 mg%. Once CL were generated, however, the drug had little effect on their ability to lyse target cells. Sodium salicylate also suppressed the proliferative response of parental mouse thymocytes adoptively transferred into lethally irradiated F1 hybrid recipients as assessed by splenic uptake of [125I] iododeoxyuridine. High-dose, chronic treatment of both thymocyte donors and recipients was necessary to effect a 20-60% suppression. Similar chronic treatment of mice depressed the number of splenic plaque-forming cells by 48-72% when assayed 4 days after primary challenge with sheep erythrocytes. On the contrary, we could find no effect of phenobarbital on the response to PHA, mixed lymphocyte culture, or on the generation of CL.

AB - Salicylate inhibited the response of human peripheral lymphocytes to phytohemagglutinim (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), and X-irradiated allogeneic lymphocytes. In addition, salicylate suppressed the generation of cytotoxic lymphocytes (CL) in vitro. The effect was dose dependent with over 90% inhibition at 48 mg%. Once CL were generated, however, the drug had little effect on their ability to lyse target cells. Sodium salicylate also suppressed the proliferative response of parental mouse thymocytes adoptively transferred into lethally irradiated F1 hybrid recipients as assessed by splenic uptake of [125I] iododeoxyuridine. High-dose, chronic treatment of both thymocyte donors and recipients was necessary to effect a 20-60% suppression. Similar chronic treatment of mice depressed the number of splenic plaque-forming cells by 48-72% when assayed 4 days after primary challenge with sheep erythrocytes. On the contrary, we could find no effect of phenobarbital on the response to PHA, mixed lymphocyte culture, or on the generation of CL.

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Effects of salicylate and phenobarbital on lymphocyte proliferation and function

Abstract

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