Sex differences in arachidonate cyclo-oxygenase products in elicited rat peritoneal macrophages

Du, Julie T.; Vennos, Elizabeth; Ramey, Estelle R.; Ramwell, Peter W.

doi:10.1016/0005-2760(84)90153-x

Cited by 19 publications

(8 citation statements)

References 20 publications

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“…This arachidonic acid metabolite is a very powerful immune suppressant that suppresses T-cell mitogenesis, IL-2 production, and IL-2 receptor expression (Faist et al 1996). Numerous studies have also demonstrated that estrogen upregulates macrophage-derived PGE 2 production (Du et al 1984, Chang 1989 and that PGE 2 , in turn, can enhance IL-6 production (Miller & Baker 1979, Fukushima et al 1994. Therefore, E 2 may be suppressing cell-mediated immune function in female mice at 10 days post burn through increasing circulating concentrations of both PGE 2 and IL-6 during the post-burn period.…”

Section: Discussionmentioning

confidence: 99%

Estrogen mediates the sex difference in post-burn immunosuppression

Gregory

Duffner²,

Faunce³

et al. 2000

Journal of Endocrinology

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Previous studies in our laboratory have demonstrated that cell-mediated immune function was suppressed in female, but not male, mice at 10 days after burn injury and was mediated, in part, by increased production of interleukin-6 (IL-6). Because 17 -estradiol (E 2 ) influences immune function after trauma and the hormone is known to regulate IL-6 production, the effect of E 2 on immune function after thermal injury was examined. Increased circulating concentrations of E 2 corresponded with suppressed delayed-type hypersensitivity (DTH) and splenocyte-proliferative responses, and increased circulating concentrations of IL-6 in female mice after burn.Ovariectomy restored the suppressed DTH response and decreased IL-6 concentrations, and administration of exogenous E 2 to both ovariectomized females and intact male mice resulted in a suppressed DTH response. In addition, in vitro treatment with E 2 suppressed splenocyte proliferation in a macrophage-dependent manner and enhanced macrophage production of IL-6. These results strongly suggest that the sex difference in cell-mediated immunity 10 days after burn injury is mediated by altered concentrations of E 2 , which in turn modulate key macrophage-derived immunoregulatory cytokines.

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Section: Discussionmentioning

confidence: 99%

Estrogen mediates the sex difference in post-burn immunosuppression

Gregory

Duffner²,

Faunce³

et al. 2000

Journal of Endocrinology

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“…Among humans and lizards, the phagocytic activity of neutrophils and macrophages is higher in females than males (50,51). Following parasitic or antigenic stimulation, the production and release of prostaglandin E 2 , thromboxane B 2 , and nitric oxide is reportedly higher in females than males (50,52,53). Other studies, however, demonstrate that plasma concentrations of several pro‐inflammatory cytokines, including IL‐6 and TNFα, are higher in males following trauma (54).…”

Section: Immunological Differences Between the Sexesmentioning

confidence: 99%

Hormonal and immunological mechanisms mediating sex differences in parasite infection

Klein

2004

Parasite Immunology

592

489

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The prevalence and intensity of infections caused by protozoa, nematodes, trematodes, cestodes, and arthropods is higher in males than females. The primary thesis of this review is that immunological differences exist between the sexes that may underlie increased parasitism in males compared to females. Several field and laboratory studies link sex differences in immune function with circulating steroid hormones; thus, the roles of sex steroids, including testosterone, oestradiol, and progesterone, as well as glucocorticoids will be discussed. Not only can host hormones affect responses to infection, but parasites can both produce and alter hormone concentrations in their hosts. The extent to which changes in endocrine-immune interactions following infection are mediated by the host or the parasite will be considered. Although males are more susceptible than females to many parasites, there are parasites for which males are more resistant than females and endocrine-immune interactions may underlie this sex reversal. Finally, although immunological differences exist between the sexes, genetic and behavioural differences may explain some variability in response to infection and will be explored as alternative hypotheses for how differences between the sexes contribute to dimorphic responses to parasites.

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“…For example, in vitro and experimental animal models have demonstrated elevated production of immunosuppressive factors (e.g. prostaglandins and interleukin‐10) that function to counterbalance the progression of inflammation in women compared with men .…”

Section: Sex Steroids Modulate the Immune Systemmentioning

confidence: 99%

Influence of sex steroids on inflammation and bone metabolism

Shiau¹,

Aichelmann-Reidy²,

Reynolds³

2013

Periodontology 2000

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Sex steroids are central to sexual development and reproduction, exerting pleiotropic effects on multiple tissues and organs throughout the lifespan of humans. Sex steroids are fundamental to skeletal development, bone homeostasis and immune function. The composite effect of sex-specific genetic architecture and circulating levels of sex-steroid hormones closely parallels differences in the immune response and may account for corresponding sex-related differences in risk for chronic periodontitis, with men exhibiting greater susceptibility than women. Age-associated reductions in sex steroids also provide insight into apparent temporal increases in susceptibility to periodontitis and alveolar bone loss, particularly among women. Chronic infection and inflammatory conditions, such as periodontal disease, provide a unique platform for exploring the interface of sex steroids, immunity and bone metabolism.

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Sex differences in arachidonate cyclo-oxygenase products in elicited rat peritoneal macrophages

Cited by 19 publications

References 20 publications

Estrogen mediates the sex difference in post-burn immunosuppression

Estrogen mediates the sex difference in post-burn immunosuppression

Hormonal and immunological mechanisms mediating sex differences in parasite infection

Influence of sex steroids on inflammation and bone metabolism

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