Physiological concentration of estradiol inhibits polymorphonuclear leukocyte chemotaxis via a receptor mediated system

Ito, Izumi; Hayashi, Toshio; Yamada, Kazuyoshi; Kuzuya, Masafumi; Naito, Michitaka; Iguchi, Akihisa

doi:10.1016/0024-3205(95)00214-q

Cited by 77 publications

(39 citation statements)

References 16 publications

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“…In transwell migration assays, E2 treatment inhibited human neutrophil chemotaxis toward N-formylmethionylleucyl-phenylalanine-methylester in a dose-dependent manner, whereas pretreatment with clomiphene or tamoxifen eliminated the inhibitory effect of E2 on migration and restored neutrophil chemotaxis to control levels. 35 Similarly, extracts of E2-treated HUVECs that had been stimulated with TNF-␣ expressed reduced levels of MCP-1 and IL-8 compared with untreated controls and produced less U-937 monocyte chemotaxis in a transwell migration assay than did extracts of untreated HUVECs. 33 Measurement of neutrophil (and other leukocyte) chemotactic activity of extracts from injured vessels provides a useful bioassay of the effects of E2 and other potential modulators of inflammation in the setting of acute vascular injury.…”

Section: Discussionmentioning

confidence: 97%

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

et al. 2004

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Background-We have previously shown that estrogen (17␤-estradiol; E2) inhibits neointima formation and migration of leukocytes, particularly neutrophils, into rat carotid arteries after acute endoluminal injury. This study tested the hypothesis that E2 inhibits expression of adhesion molecules, chemokines, and proinflammatory cytokines in rat carotid arteries in the early hours after balloon injury, thus attenuating the stimulus for leukocyte entry and negatively modulating the injury response. Methods and Results-Ovariectomized (OVX) rats were randomly assigned to treatment with E2 or vehicle (V) and subjected to balloon injury of the right carotid artery. After 2, 6, and 24 hours, rats were euthanized, and both carotid arteries were processed for real-time reverse transcription-polymerase chain reaction (2 and 24 hours), ELISA (6 hours), or neutrophil chemotaxis assay (24 hours). Expression of mRNA for adhesion molecules (P-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1), chemoattractants (cytokine-induced neutrophil chemoattractant [CINC]-2␤ and monocyte chemoattractant protein [MCP]-1), and proinflammatory cytokines (interleukin [IL]-1 and IL-6) was markedly increased (2 to 5000 times) in injured arteries of OVXϩV rats at 2 hours and was reduced by 24 hours. E2 significantly attenuated expression of the proinflammatory mediators (by 60% to 80%) at 2 hours. ELISA confirmed injury-induced upregulation of neutrophil and monocyte/macrophage chemoattractants (CINC-2␣, MCP-1) in OVXϩV arteries and E2-induced inhibition of CINC-2␣ expression. E2 significantly (by 65%) inhibited neutrophil chemotactic activity of arterial homogenates. Conclusions-E2 attenuates the early vascular injury response, at least in part, by negatively modulating proinflammatory mediator expression and the resultant chemotactic activity of injured vessels for neutrophils.

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Section: Discussionmentioning

confidence: 97%

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

et al. 2004

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“…15 In vitro evidence has demonstrated an ER-dependent mechanism for inhibition of neutrophil chemotaxis. 16 In a modified Boyden chamber, physiological levels of E 2 inhibited neutrophil migration to N-formylmethionyl-leucylphenylalanine-methyl ester in a dose-dependent manner, whereas the hormonally inert 17␣-estradiol had no effect. Furthermore, the ER antagonists clomiphene and tamoxifen blocked the inhibitory effect of E 2 , providing evidence of its ER dependence.…”

Section: Discussionmentioning

confidence: 99%

Estradiol and Progestins Differentially Modulate Leukocyte Infiltration After Vascular Injury

et al. 2004

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Background-Inflammation plays an important role in the response to endoluminal vascular injury. Estrogen (17␤-estradiol, E 2 ) inhibits neointima formation in animal models, and the progestin medroxyprogesterone acetate (MPA) blocks this effect. This study tested the hypothesis that E 2 inhibits the migration of inflammatory cells, particularly granulocytes, into the rat carotid arteries after acute endoluminal injury and that MPA blocks this effect. Methods and Results-Ovariectomized rats were randomly divided into subgroups and treated with E 2 , MPA, E 2 ϩMPA, or vehicle and subjected to balloon injury of the right carotid artery. After 1, 3, or 7 days, rats were euthanized, and carotid arteries (injured and control) were analyzed for inflammatory cells by flow cytometry. At 1 day, granulocytes (HIS48 ϩ and CD45 ϩ ), monocyte/macrophages (Mar1 ϩ and CD45 ϩ ), and T lymphocytes (CD3 ϩ and CD45 ϩ ) were increased 26-fold, 12-fold, and 3-fold, respectively, in injured compared with contralateral control arteries of vehicle-treated rats. Granulocytes and monocyte/macrophages decreased markedly by 3 days. E 2 reduced the granulocyte and monocyte/macrophage populations of injured vessels by Ϸ50% and increased T lymphocytes. MPA had no independent effect on inflammatory cells but completely blocked the effect of E 2 . Immunohistochemical examination verified these findings and localized inflammatory cells to the adventitial and periadventitial domains of injured vessels. Conclusions-E 2 may limit the neointimal response to endoluminal vascular injury, at least in part, by limiting leukocyte entry from adventitial/periadventitial tissues into injured vessels early in the injury response.

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“…We and other authors previously observed that 17β-estradiol decreases migration of PMN of bovine and human origin [14,16,21]. In order to gain insight into the molecular mechanism by which 17β-estradiol affects PMN migration, the influence of 17β-estradiol on the expression of molecules important in PMN migration [18,26,32], was evaluated.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, studies report a negative influence of 17β-estradiol on the migration of human [14,21] and bovine PMN [16] whereas the influence of progesterone is less clear. In order to gain insight into the suppressive effect of 17β-estradiol on PMN migration, its influence on the expression of CD11b, CD18 and CD47 should be evaluated.…”

Section: Introductionmentioning

confidence: 99%

Influence of sex steroids on the viability and CD11b, CD18 and CD47 expression of blood neutrophils from dairy cows in the last month of gestation

et al. 2006

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-In the period around parturition, cows experience an increased susceptibility for the development of Escherichia coli mastitis. This increased susceptibility has been correlated with a decreased functionality of neutrophils. In the current study, it is suggested that the decreased neutrophil functionality may be induced by the extensive alterations in sex steroid levels occurring around parturition. It was first hypothesized that 17β-estradiol and progesterone influence the viability, apoptosis and necrosis of blood neutrophils from cows in their last month of gestation. Subsequently, it was hypothesized that 17β-estradiol modulates the expression of CD11b, CD18 or CD47 thereby explaining its influence on the migration of bovine neutrophils. Neither 17β-estradiol nor progesterone significantly influenced viability, apoptosis or necrosis in spontaneous apoptosis conditions. However, when apoptosis was induced with TNF-α and gliotoxin, progesterone exerted a survival effect (P < 0.05). In addition, 17β-estradiol treatment of bovine blood neutrophils significantly decreased the expression of CD47 (P < 0.05) but not of CD11b or CD18. It can be concluded that 17β-estradiol and progesterone do not affect spontaneous apoptosis of bovine blood neutrophils while a survival effect was observed for progesterone on induced neutrophils apoptosis. Moreover, our results concerning the influence of 17β-estradiol on the CD11b, CD18 and CD47 expression extend previous demonstrations of the suppressive effect of 17β-estradiol on neutrophils migration and indicate that the altered expression of CD47 may contribute to this phenomenon. sex steroid / β 2 -integrin / CD47 / viability / polymorphonuclear neutrophil leukocyte

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Physiological concentration of estradiol inhibits polymorphonuclear leukocyte chemotaxis via a receptor mediated system

Cited by 77 publications

References 16 publications

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

Estrogen Modulates Inflammatory Mediator Expression and Neutrophil Chemotaxis in Injured Arteries

Estradiol and Progestins Differentially Modulate Leukocyte Infiltration After Vascular Injury

Influence of sex steroids on the viability and CD11b, CD18 and CD47 expression of blood neutrophils from dairy cows in the last month of gestation

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