Estrogens ameliorate remote organ inflammation induced by burn injury in rats

Özveri, Emel; Bozkurt, Ayhan; Haklar, Goncagül; Çetınel, Şule; Arbak, Serap; Yeğen, Cumhur; Yeğen, Berrak Ç.

doi:10.1007/pl00000238

Cited by 65 publications

(42 citation statements)

References 33 publications

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“…In addition to a decrease in MPO, estrogen treatment significantly reduced burn-induced innate cell infiltration in the liver and lung. The androgen receptor blocker, cyproterone acetate, reduced MPO levels but not as effectively as estrogen treatment but this may be due to a suboptimal blockade of the androgen receptor [47]. These and other studies show that both testosterone and estrogen play a role in leukocyte recruitment and effector function.…”

Section: Neutrophilsmentioning

confidence: 67%

“…This enzyme is often used as an index of neutrophil activation or content. MPO activity induced by burn injury was significantly reduced following castration of male mice [47]. In addition to a decrease in MPO, estrogen treatment significantly reduced burn-induced innate cell infiltration in the liver and lung.…”

Section: Neutrophilsmentioning

confidence: 89%

“…Other studies have shown that estrogen reduces neutrophil invasion into tissues, while testosterone has an opposite effect [47][48][49]. MPO and elastase are two of the soluble toxic mediators in a neutrophil's arsenal used to kill bacterial and fungal pathogens.…”

Section: Neutrophilsmentioning

confidence: 99%

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Sex differences and estrogen modulation of the cellular immune response after injury

Bird¹,

Karavitis²,

Kovacs³

2008

Cellular Immunology

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Cell-mediated immunity is extremely important for resolution of infection and for proper healing from injury. However, the cellular immune response is dysregulated following injuries such as burn and hemorrhage. Sex hormones are known to regulate immunity, and a well-documented dichotomy exists in the immune response to injury between the sexes. This disparity is caused by differences in immune cell activation, infiltration, and cytokine production during and after injury. Estrogen and testosterone can positively or negatively regulate the cellular immune response either by aiding in resolution or by compounding the morbidity and mortality. It is apparent that the hormonal dysregulation is dependent not only on the type of injury sustained but also the amount of circulating hormones. Therefore, it may be possible to design sex-specific therapies to improve immunological function and patient outcome.

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Section: Neutrophilsmentioning

confidence: 67%

Section: Neutrophilsmentioning

confidence: 89%

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Sex differences and estrogen modulation of the cellular immune response after injury

Bird¹,

Karavitis²,

Kovacs³

2008

Cellular Immunology

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“…[53] Accordingly, in another study, diminishing TNF-a expression significantly reduced ischemia-induced renal fibrosis and inflammation and improved renal functions. [54] On the other hand, the administration of E 2 depressed elevations in serum TNF-a levels following burn-injury [22] or trauma-hemorrhage. [55] In addition, E 2 inhibited the production of TNF-a by the unstimulated and hydrogen peroxide-stimulated macrophages from males and females.…”

Section: Discussionmentioning

confidence: 99%

“…We have previously reported that 17b-estradiol (E 2 ) protects the liver and intestines against sepsis-induced damage, [20] improves the healing of gastric and colonic injury, [21] and ameliorates burn-induced liver and lung injury in rats. [22] However, the effect of E 2 treatment on the oxidative complications of CRF has not (to our knowledge) been previously addressed.…”

Section: Introductionmentioning

confidence: 94%

Estrogen Protects against Oxidative Multiorgan Damage in Rats with Chronic Renal Failure

et al. 2009

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The impact of sex dimorphism on chronic renal failure (CRF)-induced oxidative multiorgan damage and the effects of estradiol (E 2 ) loss and E 2 supplementation on the progress of CRF were studied. Sprague-Dawley rats underwent 5/6 nephrectomy (CRF), and a group of female rats had bilateral ovariectomy (OVX), while the sham-operated rats had no nephrectomy or OVX. Rats received either estradiol propionate (50 μg/kg/day) or vehicle for six weeks. Serum BUN levels were elevated in both male and female CRF groups treated with vehicle, while creatinine level was not significantly changed in the female CRF group. CRF-induced elevation in serum TNF-a of male rats was abolished when the animals were treated with E 2 , while OVX exaggerated TNF-a response. In OVX and male rats with CRF, E 2 treatment reversed the malondialdehyde elevations in all the studied tissues (kidney, heart, lung, ileum, brain, liver, and gastrocnemius muscle), while depletion of glutathione in these tissues was prevented by E 2 treatment. Similarly, increased levels of myeloperoxidase activity, lucigenin chemiluminescence, and collagen in most of the tissues were reversed by E 2 treatment. The findings show that the extent of tissue injuries was relatively less in females, while ovariectomy exacerbated all the indices of oxidative injury. Moreover, the administration of E 2 , with its potent anti-oxidant and anti-inflammatory effects, markedly improved CRF-induced systemic inflammatory outcomes in both male and female rats by depressing tissue neutrophil infiltration and modulating the release of inflammatory cytokines.

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Aromatase (CYP19) promoter gene polymorphism and risk of nonviral hepatitis‐related hepatocellular carcinoma

Koh

Yuan

Wang

et al. 2011

Cancer

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BACKGROUND: Experimental studies suggest that sex hormones may induce or promote the development of hepatocellular carcinoma (HCC). Androgens are converted to estrogens by the CYP19 gene product, aromatase. Hepatic aromatase level and activity have been shown to be markedly elevated in HCC. Aromatase expression in liver tumors is driven by a promoter upstream of CYP19 exon I.6. METHODS: First, the authors identified an A/C polymorphism in the exon I.6 promoter of the CYP19 gene. To determine whether allelic variants in the CYP19 I.6 promoter differ in their ability to drive gene expression, we carried out an in vitro reporter gene assay. Then, the authors studied the association between this polymorphism and HCC risk in 2 complementary case‐control studies: 1 in high‐risk southern Guangxi, China, and another in low‐risk US non‐Asians of Los Angeles County. RESULTS: Transcriptional activity was 60% higher for promoter vectors carrying the rs10459592 C allele compared with those carrying an A allele (P = .007). In both study populations, among subjects negative for at‐risk serologic markers of hepatitis B or C, there was a dose‐dependent association between number of high activity C allele and risk of HCC (Ptrend = .014). Risk of HCC was significantly higher (odds ratio [OR], 2.25; 95% confidence interval (CI), 1.18‐4.31) in subjects homozygous for the C allele compared with those homozygous for the A allele. CONCLUSIONS: This study provides epidemiologic evidence for the role of hepatic aromatization of androgen into estrogen in the development of nonviral hepatitis‐related HCC. Cancer 2011. © 2011 American Cancer Society.

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Estrogens ameliorate remote organ inflammation induced by burn injury in rats

Abstract: We propose that treatment with estrogens or antiandrogens might be applicable in clinical situations to ameliorate systemic inflammation induced by burn.

Cited by 65 publications

References 33 publications

Sex differences and estrogen modulation of the cellular immune response after injury

Sex differences and estrogen modulation of the cellular immune response after injury

Estrogen Protects against Oxidative Multiorgan Damage in Rats with Chronic Renal Failure

Aromatase (CYP19) promoter gene polymorphism and risk of nonviral hepatitis‐related hepatocellular carcinoma

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