Steroid sex hormones regulate the release of tumor necrosis factor by macrophages

Tzu Chieh Chao; Pierson J. Van Alten; John A. Greager; Robert J. Walter

doi:10.1016/0008-8749(95)80007-6

Steroid sex hormones regulate the release of tumor necrosis factor by macrophages

Tzu Chieh Chao^*
, Pierson J. Van Alten
, John A. Greager
, Robert J. Walter

^*Corresponding author for this work

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

131 Scopus citations

Abstract

Generally, females have been found to have a heightened immune response and a concomitantly higher incidence of autoimmune diseases compared to males. We have used male rat peritoneal macrophages (Mφ) to study the effect of female sex hormones on tumor necrosis factor (TNF) release. The amount of TNF released by macrophages (Mφ) exposed to 10^-2 and 10^-3 ng/ml of 17β-estradiol (E₂) (35.1 ± 7.3 and 23.2 ± 2.5 units/ml, respectively) was significantly (P < 0.05; n = 9) greater than that released by untreated Mφ. Progesterone (P) also significantly (P < 0.05; n = 8) stimulated a maximal TNF release (24.4 ± 2.8 units/ml TNF) at 10^-2 ng/ml. On the other hand, the amount of TNF released by Mφ exposed to E₂ or P at concentrations greater than 10^-1 or less than 10^-4 ng/ml was significantly (P < 0.05) reduced compared to untreated controls. In contrast, testosterone did not significantly affect TNF release at any concentration. Within the physiological range of E₂ and P concentrations, TNF release from Mφ is finely regulated and dramatically affected by relatively small changes in hormone concentrations.

Original language	English
Pages (from-to)	43-49
Number of pages	7
Journal	Cellular Immunology
Volume	160
Issue number	1
DOIs	https://doi.org/10.1016/0008-8749(95)80007-6
State	Published - 01 1995
Externally published	Yes

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title = "Steroid sex hormones regulate the release of tumor necrosis factor by macrophages",

abstract = "Generally, females have been found to have a heightened immune response and a concomitantly higher incidence of autoimmune diseases compared to males. We have used male rat peritoneal macrophages (Mφ) to study the effect of female sex hormones on tumor necrosis factor (TNF) release. The amount of TNF released by macrophages (Mφ) exposed to 10-2 and 10-3 ng/ml of 17β-estradiol (E2) (35.1 ± 7.3 and 23.2 ± 2.5 units/ml, respectively) was significantly (P < 0.05; n = 9) greater than that released by untreated Mφ. Progesterone (P) also significantly (P < 0.05; n = 8) stimulated a maximal TNF release (24.4 ± 2.8 units/ml TNF) at 10-2 ng/ml. On the other hand, the amount of TNF released by Mφ exposed to E2 or P at concentrations greater than 10-1 or less than 10-4 ng/ml was significantly (P < 0.05) reduced compared to untreated controls. In contrast, testosterone did not significantly affect TNF release at any concentration. Within the physiological range of E2 and P concentrations, TNF release from Mφ is finely regulated and dramatically affected by relatively small changes in hormone concentrations.",

author = "Chao, \{Tzu Chieh\} and \{Van Alten\}, \{Pierson J.\} and Greager, \{John A.\} and Walter, \{Robert J.\}",

year = "1995",

month = jan,

doi = "10.1016/0008-8749(95)80007-6",

language = "英语",

volume = "160",

pages = "43--49",

journal = "Cellular Immunology",

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publisher = "Academic Press Inc.",

number = "1",

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TY - JOUR

T1 - Steroid sex hormones regulate the release of tumor necrosis factor by macrophages

AU - Chao, Tzu Chieh

AU - Van Alten, Pierson J.

AU - Greager, John A.

AU - Walter, Robert J.

PY - 1995/1

Y1 - 1995/1

N2 - Generally, females have been found to have a heightened immune response and a concomitantly higher incidence of autoimmune diseases compared to males. We have used male rat peritoneal macrophages (Mφ) to study the effect of female sex hormones on tumor necrosis factor (TNF) release. The amount of TNF released by macrophages (Mφ) exposed to 10-2 and 10-3 ng/ml of 17β-estradiol (E2) (35.1 ± 7.3 and 23.2 ± 2.5 units/ml, respectively) was significantly (P < 0.05; n = 9) greater than that released by untreated Mφ. Progesterone (P) also significantly (P < 0.05; n = 8) stimulated a maximal TNF release (24.4 ± 2.8 units/ml TNF) at 10-2 ng/ml. On the other hand, the amount of TNF released by Mφ exposed to E2 or P at concentrations greater than 10-1 or less than 10-4 ng/ml was significantly (P < 0.05) reduced compared to untreated controls. In contrast, testosterone did not significantly affect TNF release at any concentration. Within the physiological range of E2 and P concentrations, TNF release from Mφ is finely regulated and dramatically affected by relatively small changes in hormone concentrations.

AB - Generally, females have been found to have a heightened immune response and a concomitantly higher incidence of autoimmune diseases compared to males. We have used male rat peritoneal macrophages (Mφ) to study the effect of female sex hormones on tumor necrosis factor (TNF) release. The amount of TNF released by macrophages (Mφ) exposed to 10-2 and 10-3 ng/ml of 17β-estradiol (E2) (35.1 ± 7.3 and 23.2 ± 2.5 units/ml, respectively) was significantly (P < 0.05; n = 9) greater than that released by untreated Mφ. Progesterone (P) also significantly (P < 0.05; n = 8) stimulated a maximal TNF release (24.4 ± 2.8 units/ml TNF) at 10-2 ng/ml. On the other hand, the amount of TNF released by Mφ exposed to E2 or P at concentrations greater than 10-1 or less than 10-4 ng/ml was significantly (P < 0.05) reduced compared to untreated controls. In contrast, testosterone did not significantly affect TNF release at any concentration. Within the physiological range of E2 and P concentrations, TNF release from Mφ is finely regulated and dramatically affected by relatively small changes in hormone concentrations.

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U2 - 10.1016/0008-8749(95)80007-6

DO - 10.1016/0008-8749(95)80007-6

M3 - 文章

C2 - 7842485

AN - SCOPUS:0028954432

SN - 0008-8749

VL - 160

SP - 43

EP - 49

JO - Cellular Immunology

JF - Cellular Immunology

IS - 1

ER -

Steroid sex hormones regulate the release of tumor necrosis factor by macrophages

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