scholarly journals Immunohistochemical localization of P-glycoprotein in adult human ovary and female genital tract of patients with benign gynecological conditions.

1990 ◽  
Vol 38 (11) ◽  
pp. 1677-1681 ◽  
Author(s):  
C L Finstad ◽  
P E Saigo ◽  
S C Rubin ◽  
M G Federici ◽  
D M Provencher ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Ovarian Surface Epithelium ◽  
Cytotoxic Agents ◽  
Surface Epithelium ◽  
Positive Staining ◽  
Multidrug Resistance Gene ◽  
P Glycoprotein ◽  
Female Genital

The multidrug-resistance gene, MDR1, encodes a plasma membrane glycoprotein termed P-glycoprotein, which mediates active cellular efflux of certain cytotoxic agents. Two mouse monoclonal antibodies (MAb), C219 and JSB-1, were used to identify P-glycoprotein in frozen tissue from the female genital tract of 14 women with benign gynecological conditions; multiple samples from several sites in the genital tract were available from seven patients. P-glycoprotein was detected in the ovarian surface epithelium in four of 14 cases, in the Fallopian tube in three of five cases, in occasional epithelial cells of the endometrial glands in two of five cases, in some endocervical glandular epithelium in three of five cases, in ectocervical squamous epithelium in one of the two cases, and in luteinized cells of the eight cases in which a corpus luteum was present in the specimen. Positive staining with these two MAb was also observed in some endothelial cells in the cortex of the ovary and in the stromal tissue of the myometrium, endometrium, and endocervix. These studies suggest that, if epithelial ovarian cancers are derived from the surface epithelial cells of the ovary, a small proportion of the cancers might be expected to retain the phenotype found in non-cancerous cells and to express P-glycoprotein.

scholarly journals Mechanisms of Endogenous HIV-1 Reactivation by Endocervical Epithelial Cells

2020 ◽  
Vol 94 (9) ◽  
Author(s):  
Germán G. Gornalusse ◽  
Rogelio Valdez ◽  
Gabriella Fenkart ◽  
Lucia Vojtech ◽  
Lamar M. Fleming ◽  
...  
Keyword(s):  
T Cells ◽  
Herpes Simplex ◽  
Epithelial Cells ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Tnf Α ◽  
Simplex Virus ◽  
Herpes Simplex Virus 2 ◽  
Hiv 1 ◽  
Female Genital

ABSTRACT Pharmacological HIV-1 reactivation to reverse latent infection has been extensively studied. However, HIV-1 reactivation also occurs naturally, as evidenced by occasional low-level viremia (“viral blips”) during antiretroviral treatment (ART). Clarifying where blips originate from and how they happen could provide clues to stimulate latency reversal more effectively and safely or to prevent viral rebound following ART cessation. We studied HIV-1 reactivation in the female genital tract, a dynamic anatomical target for HIV-1 infection throughout all disease stages. We found that primary endocervical epithelial cells from several women reactivated HIV-1 from latently infected T cells. The endocervical cells’ HIV-1 reactivation capacity further increased upon Toll-like receptor 3 stimulation with poly(I·C) double-stranded RNA or infection with herpes simplex virus 2 (HSV-2). Notably, acyclovir did not eliminate HSV-2-induced HIV-1 reactivation. While endocervical epithelial cells secreted large amounts of several cytokines and chemokines, especially tumor necrosis factor alpha (TNF-α), CCL3, CCL4, and CCL20, their HIV-1 reactivation capacity was almost completely blocked by TNF-α neutralization alone. Thus, immunosurveillance activities by columnar epithelial cells in the endocervix can cause endogenous HIV-1 reactivation, which may contribute to viral blips during ART or rebound following ART interruption. IMPORTANCE A reason that there is no universal cure for HIV-1 is that the virus can hide in the genome of infected cells in the form of latent proviral DNA. This hidden provirus is protected from antiviral drugs until it eventually reactivates to produce new virions. It is not well understood where in the body or how this reactivation occurs. We studied HIV-1 reactivation in the female genital tract, which is often the portal of HIV-1 entry and which remains a site of infection throughout the disease. We found that the columnar epithelial cells lining the endocervix, the lower part of the uterus, are particularly effective in reactivating HIV-1 from infected T cells. This activity was enhanced by certain microbial stimuli, including herpes simplex virus 2, and blocked by antibodies against the inflammatory cytokine TNF-α. Avoiding HIV-1 reactivation could be important for maintaining a functional HIV-1 cure when antiviral therapy is stopped.

scholarly journals Inflammatory Myofibroblastic Tumor in Female Genital Tract

2018 ◽  
Vol 143 (1) ◽  
pp. 122-129 ◽  
Author(s):  
Pratibha Sharma Shukla ◽  
Khushbakhat Mittal
Keyword(s):  
Smooth Muscle ◽  
Genital Tract ◽  
Inflammatory Myofibroblastic Tumor ◽  
Abdominal Cavity ◽  
Female Genital Tract ◽  
High Recurrence Rate ◽  
Positive Staining ◽  
Molecular Features ◽  
Mesenchymal Neoplasm ◽  
Female Genital

Context.— Inflammatory myofibroblastic tumor is a mesenchymal neoplasm of low malignant potential. It was first described in lung, but is known to occur in many extrapulmonary sites including female genital organs, most commonly the uterus. It has a high recurrence rate and a low risk for metastasis. A more recently described aggressive variant, epithelioid myofibroblastic sarcoma with a predilection for the abdominal cavity of males, has also been recently reported to occur in the ovary. This tumor is composed of spindled and epithelioid myofibroblasts in a variably myxoid stroma and commonly shows a fascicular growth pattern with positive staining for desmin, smooth muscle actin, and CD10, which may mimic a smooth muscle or endometrial stromal neoplasm. In the female genital tract it has the potential for being misdiagnosed as a leiomyoma, endometrial stromal tumor, or as a myxoid leiomyosarcoma, resulting in undertreatment or overtreatment. It harbors rearrangements in the ALK gene, resulting in abnormal expression of ALK protein. Immunostaining for ALK is a helpful diagnostic tool. Objective.— To provide a brief review of clinical, histologic, immunohistochemical, and molecular features of inflammatory myofibroblastic tumor with emphasis on possible diagnostic pitfalls in the female genital tract. Data Sources.— Review of pertinent literature on inflammatory myofibroblastic tumor occurring in the female genital tract and personal experience of the authors. Conclusions.— Inflammatory myofibroblastic tumor in the female genital tract can mimic other more common benign and malignant tumors like leiomyoma, leiomyosarcoma, and endometrial stromal sarcoma. Familiarity with clinical and histologic features and use of ALK immunostaining can be critical for correct diagnosis.

scholarly journals Distinct Proinflammatory Host Responses to Neisseria gonorrhoeae Infection in Immortalized Human Cervical and Vaginal Epithelial Cells

2001 ◽  
Vol 69 (9) ◽  
pp. 5840-5848 ◽  
Author(s):  
Raina Nakova Fichorova ◽  
Pragnya Jasvantrai Desai ◽  
Frank C. Gibson ◽  
Caroline Attardo Genco
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Genital Tract ◽  
Fluorescent Protein ◽  
Female Genital Tract ◽  
Host Responses ◽  
Intercellular Adhesion Molecule ◽  
Epithelial Cell Lines ◽  
Female Genital

ABSTRACT In this study we utilized immortalized morphologically and functionally distinct epithelial cell lines from normal human endocervix, ectocervix, and vagina to characterize gonococcal epithelial interactions pertinent to the lower female genital tract. Piliated, but not nonpiliated, N. gonorrhoeae strain F62 variants actively invaded these epithelial cell lines, as demonstrated by an antibiotic protection assay and confocal microscopy. Invasion of these cells by green fluorescent protein-expressing gonococci was characterized by colocalization of gonococci with F actin, which were initially detected 30 min postinfection. In all three cell lines, upregulation of interleukin 8 (IL-8) and IL-6, intercellular adhesion molecule 1 (CD54), and the nonspecific cross-reacting antigen (CD66c) were detected 4 h after infection with piliated and nonpiliated gonococci. Furthermore, stimulation of all three cell lines with gonococcal whole-cell lysates resulted in a similar upregulation of IL-6 and IL-8, confirming that bacterial uptake is not essential for this response. Increased levels of IL-1 were first detected 8 h after infection with gonococci, suggesting that the earlier IL-8 and IL-6 responses were not mediated through the IL-1 signaling pathway. The IL-1 response was limited to cultures infected with piliated gonococci and was more vigorous in the endocervical epithelial cells. The ability of gonococci to stimulate distinct proinflammatory host responses in these morphologically and functionally different compartments of the lower female genital tract may contribute directly to the inflammatory signs and symptoms characteristic of disease caused by N. gonorrhoeae.

scholarly journals Protective Effect of Probiotic Bacteria and Estrogen in Preventing HIV-1-Mediated Impairment of Epithelial Barrier Integrity in Female Genital Tract

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1120 ◽  
Author(s):  
Sara Dizzell ◽  
Aisha Nazli ◽  
Gregor Reid ◽  
Charu Kaushic
Keyword(s):  
Epithelial Cells ◽  
Protective Effect ◽  
Sex Hormones ◽  
Proinflammatory Cytokines ◽  
Barrier Function ◽  
Genital Tract ◽  
Female Genital Tract ◽  
Probiotic Lactobacilli ◽  
Hiv 1 ◽  
Female Genital

Approximately 40% of global HIV-1 transmission occurs in the female genital tract (FGT) through heterosexual transmission. Epithelial cells lining the FGT provide the first barrier to HIV-1 entry. Previous studies have suggested that certain hormonal contraceptives or a dysbiosis of the vaginal microbiota can enhance HIV-1 acquisition in the FGT. We examined the effects of lactobacilli and female sex hormones on the barrier functions and innate immune responses of primary endometrial genital epithelial cells (GECs). Two probiotic strains, Lactobacillus reuteri RC-14 and L. rhamnosus GR-1, were tested, as were sex hormones estrogen (E2), progesterone (P4), and the hormonal contraceptive medroxyprogesterone acetate (MPA). Our results demonstrate that probiotic lactobacilli enhance barrier function without affecting cytokines. Treatment of GECs with MPA resulted in reduced barrier function. In contrast, E2 treatment enhanced barrier function and reduced production of proinflammatory cytokines. Comparison of hormones plus lactobacilli as a pre-treatment prior to HIV exposure revealed a dominant effect of lactobacilli in preventing loss of barrier function by GECs. In summary, the combination of E2 and lactobacilli had the best protective effect against HIV-1 seen by enhancement of barrier function and reduction in proinflammatory cytokines. These studies provide insights into how probiotic lactobacilli in the female genital microenvironment can alter HIV-1-mediated barrier disruption and how the combination of E2 and lactobacilli may decrease susceptibility to primary HIV infection.

scholarly journals PBX1 intracellular localization is independent of MEIS1 in epithelial cells of the developing female genital tract

2005 ◽  
Vol 49 (7) ◽  
pp. 851-858 ◽  
Author(s):  
Agnes Dintilhac ◽  
Rejane Bihan ◽  
Daniel Guerrier ◽  
Stephane Deschamps ◽  
Heloise Bougerie ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Genital Tract ◽  
Intracellular Localization ◽  
Female Genital Tract ◽  
Female Genital

LOCAL IMMUNOLOGICAL RESPONSE IN THE VAGINA, CERVIX AND ENDOMETRIUM

1975 ◽  
Vol 80 (2_Suppl) ◽  
pp. S281-S305 ◽  
Author(s):  
J.-P. Vaerman ◽  
J. Férin
Keyword(s):  
Epithelial Cells ◽  
Genital Tract ◽  
Plasma Cells ◽  
Specific Binding ◽  
Female Genital Tract ◽  
Secretory Component ◽  
Secretory Iga ◽  
Local Synthesis ◽  
Female Genital

ABSTRACT The mechanism of the local excretion of secretory IgA (SIgA) in exocrine secretions has been reviewed. Numerous local IgA-plasma cells, in the lamina propria of the glandular mucosa, synthesize dimeric IgA with J-chain. Free secretory component (FSC) is synthesized and accumulated in the Golgi area of the columnar epithelial cells. It is then supposed to get onto their cell membranes. Dimeric IgA (and some IgM) reaches the spaces between and under the epithelial cells. There, a specific binding occurs between dimeric IgA (and some IgM) and the FSC located in the cell-membrane, whereby SIgA is formed. The complex becomes mobilized and is transported toward the apical part of the cell, where it will be excreted into the mucous coat covering the epithelium. In the female genital tract, the cervical mucosa appears to be better adapted to achieve a local secretory immune system. The endometrium seems less suitable, being normally short of local plasma cells. The vaginal wall appears almost incompatible with the proposed mechanism of local antibody secretion. Criteria for establishing a local immune response in the female genital tract comprise: 1) a lack of correlation between antibody titers in secretions and serum; 2) the demonstration that the secretory antibodies are mainly of IgA class and 3) that they are SIgA molecules, possessing bound secretory component. However, the best criterion would be 4) the observation that antibody is actually synthesized in samples of mucosa, by in vitro culture or immunohistology. Reviewing the literature, relatively few examples were found where SIgA antibodies were demonstrated, and unambiguous evidence for their local synthesis is almost non-existent. In addition, the authors were unable to detect antibody-containing cells in cervical and endometrial biopsies of women locally "immunized" with horse spleen ferritin and bovine serum albumin. The need for further investigation with simple antigens and adequate immunological reagents is stressed.

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