Diethylstilbestrol Exposure in Neonatal Mice Induces Changes in the Adulthood in the Immune Response toTaenia crassicepswithout Modifications of Parasite Loads

Industrial growth has increased the exposition to endocrine disruptor compounds (EDC’s), which are exogenous agents with agonist or antagonist action of endogenous steroid hormones that may affect the course of parasite infections. We wanted to determine if the exposure to diethylstilbestrol (DES), an estrogen agonist, to both male and female mice affected the immune response and their susceptibility toT. crassicepscysticercosis. In all infected groups, females showed higher parasite loads than males, and neonatal DES administration did not modify this pattern. In the spleen, noninfected mice showed sex-related differences in the percentage of the CD8+ subpopulation, but DES decreased the percentage of CD3+, CD19+, and CD8+ subpopulations in infected mice. In the mesenteric lymphatic node (MNL), DES showed a dimorphic effect in the percentage of CD19+ cells. Regarding estrogen receptor alpha (ER-α) expression, DES treatment induced a reduction in the expression of this receptor in both noninfected female and male mice in the spleen, which was decreased only in males in CD3+ and CD8+ lymphocytes in MNL cell subpopulations. Our study is the first one to demonstrate that DES neonatal treatment in male and female mice affects the immune cell percentage, without effect on the susceptibility toT. crassicepscysticercosis.

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Effects of an estrogen receptor alpha agonist on agonistic behaviour in intact and gonadectomized male and female mice

Psychoneuroendocrinology ◽

10.1016/j.psyneuen.2010.12.010 ◽

2011 ◽

Vol 36 (7) ◽

pp. 981-995 ◽

Cited By ~ 34

Author(s):

Amy E. Clipperton-Allen ◽

Anne Almey ◽

Ashley Melichercik ◽

Craig P. Allen ◽

Elena Choleris

Keyword(s):

Estrogen Receptor ◽

Estrogen Receptor Alpha ◽

Agonistic Behaviour ◽

Male And Female ◽

Receptor Alpha ◽

Female Mice ◽

Alpha Agonist

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Characterization of the immune response in male and female mice following lipopolysaccharide‐induced systemic inflammation (1096.10)

The FASEB Journal ◽

10.1096/fasebj.28.1_supplement.1096.10 ◽

2014 ◽

Vol 28 (S1) ◽

Author(s):

Nina Bubalo ◽

Peter Nguyen ◽

Tuan Nguyen ◽

Tzvia Abramson ◽

Katherine Wilkinson

Keyword(s):

Immune Response ◽

Systemic Inflammation ◽

Male And Female ◽

Female Mice

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A Quantitative Difference in the Immune Response between Male and Female Mice

Experimental Biology and Medicine ◽

10.3181/00379727-127-32768 ◽

1968 ◽

Vol 127 (3) ◽

pp. 664-667 ◽

Cited By ~ 74

Author(s):

G. Terres ◽

S. L. Morrison ◽

G. S. Habicht

Keyword(s):

Immune Response ◽

Quantitative Difference ◽

Male And Female ◽

Female Mice

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Endogenous and Therapeutic Estrogens: Maestro Conductors of the Microenvironment of ER+ Breast Cancers

Cancers ◽

10.3390/cancers13153725 ◽

2021 ◽

Vol 13 (15) ◽

pp. 3725

Author(s):

Linda A. Schuler ◽

Fern E. Murdoch

Keyword(s):

Stromal Cells ◽

Estrogen Receptor Alpha ◽

Immune Cell ◽

Disease Recurrence ◽

Target Cells ◽

Breast Cancers ◽

Cancer Subtypes ◽

Treatment And Prevention ◽

Immune Cell Subpopulations ◽

Cell Subpopulations

Estrogen receptor alpha (ERα) marks heterogeneous breast cancers which display a repertoire of somatic genomic mutations and an immune environment that differs from other breast cancer subtypes. These cancers also exhibit distinct biological behaviors; despite an overall better prognosis than HER2+ or triple negative breast cancers, disseminated dormant cells can lead to disease recurrence decades after the initial diagnosis and treatment. Estrogen is the best studied driver of these cancers, and antagonism or reduction of estrogen activity is the cornerstone of therapeutic approaches. In addition to reducing proliferation of ERα+ cancer cells, these treatments also alter signals to multiple other target cells in the environment, including immune cell subpopulations, cancer-associated fibroblasts, and endothelial cells via several distinct estrogen receptors. In this review, we update progress in our understanding of the stromal cells populating the microenvironments of primary and metastatic ER+ tumors, the effects of estrogen on tumor and stromal cells to modulate immune activity and the extracellular matrix, and net outcomes in experimental and clinical studies. We highlight new approaches that will illuminate the unique biology of these cancers, provide the foundation for developing new treatment and prevention strategies, and reduce mortality of this disease.

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Environmental Pollution as a Risk Factor in Testicular Tumour Development: Focus on the Interaction between Bisphenol A and the Associated Immune Response

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph16214113 ◽

2019 ◽

Vol 16 (21) ◽

pp. 4113 ◽

Cited By ~ 1

Author(s):

Karen Elizabeth Nava-Castro ◽

Ricardo Ramírez-Nieto ◽

Lucía Angélica Méndez-García ◽

Manuel Iván Girón-Pérez ◽

Mariana Segovia-Mendoza ◽

...

Keyword(s):

Immune Response ◽

Bisphenol A ◽

Tumour Growth ◽

Immune Cell ◽

Breast Cancer Incidence ◽

Pregnant Female ◽

Male Offspring ◽

Testicular Tumour ◽

Female Mice ◽

Tnf Α

Bisphenol A (BPA) is an endocrine disruptor to which animals and humans are highly exposed. Many reports have established a relationship between BPA exposure and breast cancer incidence, especially during critical periods of development. However, its effects on the immune response in testicular tumour growth have not yet been described. Thus, we wanted to analyse the effect of perinatal BPA exposure in pregnant female mice and the immune response modulation and tumour growth in an intratesticular cancer model in offspring male mice. Pregnant female mice were exposed to a dose of 250 mg/kg/day/body weight of BPA in their drinking water. In adulthood, male offspring underwent intrascrotal inoculation with 4T1 cancer cells. On day 21 after inoculation, mice were euthanised, and serum was obtained to measure BPA levels using HPLC coupled to mass spectrometry. The percentages of immune cell populations in peripheral lymph nodes (PLN), the spleen and tumours were evaluated by flow cytometry. In addition, the tumour expression of IL-10, TNF-α and TGF-β was analysed by RT-PCR. Of note, we found detectable circulating levels of BPA in the offspring of mothers exposed to it while pregnant. Remarkably, BPA treatment promoted tumour growth by about 75% compared to mice coming from female mice that did not receive the compound. Perinatal exposure to BPA modulated the percentages of different immune cells in the spleen and PLN. In addition, the expression of inflammatory-related cytokines (IL-10 and TNF-α) in the tumours was significantly enhanced compared to control and vehicle groups. In conclusion, the perinatal BPA administration in pregnant female mice modulated different cellular and molecular immune components that resulted in outstanding testicular tumour size in male offspring.

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Augmenting Renal Lymphatic Density Prevents Angiotensin II-Induced Hypertension in Male and Female Mice

American Journal of Hypertension ◽

10.1093/ajh/hpz139 ◽

2019 ◽

Vol 33 (1) ◽

pp. 61-69 ◽

Cited By ~ 4

Author(s):

Dakshnapriya Balasubbramanian ◽

Catalina A Lopez Gelston ◽

Alexandra H Lopez ◽

Geina Iskander ◽

Winter Tate ◽

...

Keyword(s):

Angiotensin Ii ◽

Lymphatic Vessel ◽

Immune Cell ◽

Peritoneal Macrophages ◽

Lymphatic Endothelial Cells ◽

Male And Female ◽

Female Mice ◽

Induced Hypertension ◽

Lymphatic Density

Abstract BACKGROUND Renal inflammation and immune cell infiltration are characteristic of several forms of hypertension. Our laboratory has previously demonstrated that renal-inflammation-associated lymphangiogenesis occurs in salt-sensitive and nitric-oxide-inhibition-induced hypertension. Moreover, enhancing renal lymphatic density prevented the development of these two forms of hypertension. Here, we investigated the effects of angiotensin II-induced hypertension on renal lymphatic vessel density in male and female mice. METHODS Wild-type and genetically engineered male and female mice were infused with angiotensin II for 2 or 3 weeks. Isolated splenocytes and peritoneal macrophages from mice, and commercially available mouse lymphatic endothelial cells were used for in vitro studies. RESULTS Compared to vehicle controls, angiotensin II-infused male and female mice had significantly increased renal lymphatic vessel density in association with pro-inflammatory immune cells in the kidneys of these mice. Direct treatment of lymphatic endothelial cells with angiotensin II had no effect as they lack angiotensin II receptors; however, angiotensin II treatment of splenocytes and peritoneal macrophages induced secretion of the lymphangiogenic growth factor VEGF-C in vitro. Utilizing our genetic mouse model of inducible renal lymphangiogenesis, we demonstrated that greatly augmenting renal lymphatic density prior to angiotensin II infusion prevented the development of hypertension in male and female mice and this was associated with a reduction in renal CD11c+F4/80- monocytes. CONCLUSION Renal lymphatics play a significant role in renal immune cell trafficking and blood pressure regulation, and represent a novel avenue of therapy for hypertension.

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FOXO3, estrogen receptor alpha, and androgen receptor impact tumor growth rate and infiltration of dendritic cell subsets differentially between male and female mice

Cancer Immunology Immunotherapy ◽

10.1007/s00262-017-1972-4 ◽

2017 ◽

Vol 66 (5) ◽

pp. 615-625 ◽

Cited By ~ 8

Author(s):

Matthew G. Thompson ◽

Daniel S. Peiffer ◽

Michelle Larson ◽

Flor Navarro ◽

Stephanie K. Watkins

Keyword(s):

Growth Rate ◽

Estrogen Receptor ◽

Androgen Receptor ◽

Dendritic Cell ◽

Tumor Growth ◽

Estrogen Receptor Alpha ◽

Tumor Growth Rate ◽

Male And Female ◽

Female Mice ◽

Dendritic Cell Subsets

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Systemic Markers of Adaptive and Innate Immunity Are Associated with COPD Severity and Spirometric Disease Progression

10.1101/193920 ◽

2017 ◽

Author(s):

Eitan Halper-Stromberg ◽

Jeong H. Yun ◽

Margaret M. Parker ◽

Ruth Tal Singer ◽

Amit Gaggar ◽

...

Keyword(s):

Immune Response ◽

Lung Function ◽

Immune Cell ◽

Critical Role ◽

Cell Immune Response ◽

Cell Type ◽

Cross Sectional ◽

Cell Counts ◽

Immune Cell Subpopulations ◽

Cell Subpopulations

ABSTRACTThe progression of chronic obstructive pulmonary disease (COPD) is associated with marked alterations in circulating immune cell populations, but no studies have characterized alterations in these cell types across the full spectrum of lung function impairment in current and former smokers. In 6,299 subjects from the COPDGene and ECLIPSE studies, we related Coulter blood counts and proportions to cross-sectional FEV1 adjusting for current smoking status. We also related cell count measures to three-year change in FEV1 in ECLIPSE subjects. In a subset of subjects with blood gene expression data, we used cell type deconvolution methods to infer the proportions of immune cell subpopulations, and we related these to COPD clinical status. We observed that FEV1 levels are positively correlated with lymphocytes and negatively correlated with myeloid populations such as neutrophils and monocytes. In multivariate models, absolute cell counts and proportions were associated with cross-sectional FEV1, and lymphocytes, monocytes, and eosinophil counts were predictive of three-year change in lung function. Using cell type deconvolution to study immune cell subpopulations, we observed that subjects with COPD had a lower proportion of CD4+ resting memory cells and naive B cells compared to non-COPD smokers. Alterations in circulating immune cells in COPD support a mixed pattern of lymphocyte suppression and an enhanced myeloid cell immune response. Cell counts and proportions contribute independent information to models predicting lung function suggesting a critical role for immune response in long-term COPD outcomes. Cell type deconvolution is a promising method for immunophenotyping in large cohorts.

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