Gender Differences in Adrenal and Gonadal Responses to Inflammatory Aggression

Silva, José António Pereira da; Pinto, Alberto; Cutolo, Maurizio; Porto, Armando

doi:10.1111/j.1749-6632.1999.tb07632.x

Cited by 7 publications

(4 citation statements)

References 9 publications

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“…These findings can be explained by previously mentioned results of Dasilva et al. , 37 who mentioned that there was altered sex hormone balance in RA synovial fluid, resulting in lower immunosuppressive androgens and higher immuno‐enhancing estrogens, and this might provide a favorable condition for the development of immune‐mediated RA synovitis. Vanttinen et al.…”

Section: Discussionsupporting

confidence: 51%

“…These findings can be explained by previously mentioned results of Dasilva et al, 37 who mentioned that there was altered sex hormone balance in RA synovial fluid, resulting in lower immunosuppressive androgens and higher immuno-enhancing estrogens, and this might provide a favorable condition for the development of immune-mediated RA synovitis. Vanttinen et al 38 stated that the activin A/inhibin A system might have a significant role in the regulation of glucocorticoids and androgen production and apoptotic cell death in the human adrenal cortex.…”

Section: Discussionsupporting

confidence: 51%

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Value of serum and synovial fluid activin A and inhibin A in some rheumatic diseases

El-Gendi¹,

Moniem²,

Tawfik³

et al. 2010

Int J of Rheum Dis

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Section: Discussionsupporting

confidence: 51%

Section: Discussionsupporting

confidence: 51%

Value of serum and synovial fluid activin A and inhibin A in some rheumatic diseases

El-Gendi¹,

Moniem²,

Tawfik³

et al. 2010

Int J of Rheum Dis

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“…Down-modulation of Eselectin and IL-6 gene expression by estrogen may have contributed to a reduction in the cellular infiltration seen in a model of acute anterior uveitis (32). Several reports of risk factors associated with AHR have noted a higher level of responsiveness in female compared with male subjects (6,23,(33)(34)(35), implicating that sex hormones play a role in altered airway responsiveness. However, the specific mechanisms responsible for the development of AHR were unclear.…”

Section: Discussionmentioning

confidence: 98%

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Matsubara

Swasey

Loader

et al. 2008

Am J Respir Cell Mol Biol

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The female hormone estrogen is an important factor in the regulation of airway function and inflammation, and sex differences in the prevalence of asthma are well described. Using an animal model, we determined how sex differences may underlie the development of altered airway function in response to allergen exposure. We compared sex differences in the development of airway hyperresponsiveness (AHR) after allergen exposure exclusively via the airways. Ovalbumin (OVA) was administered by nebulization on 10 consecutive days in BALB/c mice. After methacholine challenge, significant AHR developed in male mice but not in female mice. Ovariectomized female mice showed significant AHR after 10-day OVA inhalation. ICI182,780, an estrogen antagonist, similarly enhanced airway responsiveness even when administered 1 hour before assay. In contrast, 17b-estradiol dose-dependently suppressed AHR in male mice. In all cases, airway responsiveness was inhibited by the administration of a neurokinin 1 receptor antagonist. These results demonstrate that sex differences in 10-day OVAinduced AHR are due to endogenous estrogen, which negatively regulates airway responsiveness in female mice. Cumulatively, the results suggest that endogenous estrogen may regulate the neurokinin 1-dependent prejunctional activation of airway smooth muscle in allergen-exposed mice.Keywords: estrogen; sex; airway hyperresponsiveness; EFS; neuronal activation Sex differences have been described to play a role in various diseases, including atherosclerosis (1), osteoporosis (2), and certain neurologic disorders (3). Accumulating evidence suggests that hormonal factors are important in the expression of such sex differences at the phenotypic and genotypic levels. A number of epidemiologic and experimental reports suggest that the female hormone estrogen is an important factor in the regulation of airway function and inflammation. Estrogen can prevent cholinergic constriction of asthmatic tracheal rings in vitro (4), and estrogen treatment decreases airway responsiveness to acetylcholine in ovariectomized rats (5). On the other hand, female mice may be more susceptible than male mice to allergen-induced airway inflammation (6-8). The role of estrogen on sex differences in asthma has been the subject of much discussion (9, 10).There are many animal protocols for investigating allergeninduced airway hyperresponsiveness (AHR) and inflammation, with the majority using initial sensitization to allergen together with an adjuvant such as alum. Using this sensitization approach, some mouse studies have suggested a female superiority in the development of allergic airway inflammation (6-8). We examined the development of AHR after allergen exposure exclusively via the airways for 10 consecutive days in the absence of any adjuvant. Although AHR to inhaled methacholine (MCh) was not detected in female mice after 10-day ovalbumin (OVA) inhalation in vivo, electrical field stimulation (EFS) in vitro detected altered airway responsiveness. In large part, this EFS respon...

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“…Our results with PKCε‐null mice support this notion, in that absence of PKCε was associated with decreased epinephrine‐induced hyperalgesia only in male PKCε‐null mice. The finding of a more prominent role for female sex hormone in epinephrine‐induced hyperalgesia is consistent with gender differences observed in inflammation‐induced pain (Angele et al ., 1999; Da Silva et al ., 1999) and pain produced by formalin (Aloisi et al ., 1994; Aloisi et al ., 1995; Nayebi & Ahmadiani, 1999).…”

Section: Discussionmentioning

confidence: 99%

Sex hormones regulate the contribution of PKCε and PKA signalling in inflammatory pain in the rat

Dina

Aley

Isenberg

et al. 2001

Eur J of Neuroscience

110

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We have evaluated the contribution of differences in second messenger signalling to sex differences in inflammatory pain and its control by sex hormones. In normal male but not female rats, epinephrine-induced mechanical hyperalgesia was antagonized by inhibitors of protein kinase Cepsilon (PKCepsilon), protein kinase A (PKA) and nitric oxide synthetase (NOS). Similarly, in PKCepsilon knockout mice, a contribution of PKCepsilon to epinephrine-dependent mechanical hyperalgesia occurred in males only. In contrast, hyperalgesia induced by prostaglandin E2, in both females and males, was dependent on PKA and NO. In both sexes, inhibitors of mitogen-activated protein kinase/extracellular-signal related kinase kinase (MEK) inhibited epinephrine hyperalgesia. In gonadectomized females, the second messenger contributions to epinephrine hyperalgesia demonstrated the pattern seen in males. Administration of oestrogen to gonadectomized females fully reconstituted the phenotype of the normal female. These data demonstrate gender differences in PKCepsilon, PKA and NO signalling in epinephrine-induced hyperalgesia which are oestrogen dependent and appear to be exerted at the level of the beta-adrenergic receptor or the G-protein to which it is coupled.

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Gender Differences in Adrenal and Gonadal Responses to Inflammatory Aggression

Cited by 7 publications

References 9 publications

Value of serum and synovial fluid activin A and inhibin A in some rheumatic diseases

Value of serum and synovial fluid activin A and inhibin A in some rheumatic diseases

Estrogen Determines Sex Differences in Airway Responsiveness after Allergen Exposure

Sex hormones regulate the contribution of PKCε and PKA signalling in inflammatory pain in the rat

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