Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progesterone has been reported to have an antiinflammatory as well as immunosuppressive effect, and may prevent adhesion formation. In this study, nine treated and seven control rabbits were randomly selected for either pre- and postoperative progesterone treatment or no treatment. All rabbits underwent hysterectomy, focal peritoneal denudation, and intraabdominal instillation of suspended talc. Adhesion formation was evaluated 1 month postoperatively during repeat exploratory laparotomy. Progesterone-treated and control rabbits did not show any significant difference overall in the incidence of adhesion formation. Subgrouping of adhesion formation into adhesions formed by major surgical tissue trauma or minor peritoneal damage revealed a beneficial effect of progesterone in the reduction of only minor adhesion formation.
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PMID:Effects of progesterone on postoperative adhesion formation in hysterectomized rabbits. 289 53

Findings from our previous studies revealed a correlation between the level of adherence in vitro of Candida albicans to human exfoliated vaginal epithelial cells (VEC) and the hormonal status of the cell donors. In the present study we investigated the effect of the sex hormones estradiol, estriol, progesterone, and testosterone on the binding of the yeasts to HeLa cell lines and VEC in vitro. Monolayers of HeLa cells were exposed to the hormones and yeasts under controlled conditions. The number of adherent yeasts per square millimetre of HeLa cell monolayers and the percentage of VEC with adherent yeasts was estimated by microscopic counts. The results showed that the tested sex hormones affected at various degrees the adhesion of yeasts to HeLa cells or VEC. Progesterone had the most marked effect, leading to a significant increase in the number of adherent yeasts to HeLa cells or in the percentage of adhesion of VEC. In addition, VEC were separated on Percoll gradients into the two cell types: superficial (S) and intermediate (I), cell types which appear physiologically under increased serum levels of estradiol or progesterone, respectively. Adhesion assays with the separated cell populations revealed an increased binding capacity of the I cells. The finding that progesterone increased the adherence of yeasts to genital mucosa and that VEC of the I type have a higher capacity to adhere the yeasts is compatible with our previous observation that increased numbers of I cells, appearing under high level of progesterone, are found in situations known to have predisposition to vaginal candidiasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction of Candida albicans with genital mucosa: effect of sex hormones on adherence of yeasts in vitro. 304 21

Progesterone (P) has been shown to have antiinflammatory and immunosuppressive properties. This study was designed to evaluate these effects on operative adhesion formation. Forty guinea pigs received standardized injuries to their uterine horns. Four groups were examined. Normal saline was used as an irrigant in the first, or control, group. Aqueous P (50 mg or 1 ml) was dripped over the injured site and instilled intraperitoneally in the second group. The third group received intramuscular aqueous P (3.3 mg/kg body weight) 1 day postoperatively, the day of surgery, and either 6 or 13 days postoperatively until reexploration. In the fourth group 1 ml of 32% dextran 70 (Hyskon) was administered in the same manner as aqueous P in the second group. The animals in all groups were reexplored 1 or 2 weeks after the initial surgical procedure, and the adhesions were scored. Adhesion formation was significantly reduced (P less than 0.001) in all treatment groups when compared with the control group. Aqueous P may have a role in the prevention of adhesion formation associated with pelvic surgery and, in particular, microscopic tubal and ovarian surgery.
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PMID:The effect of aqueous progesterone on operative adhesion formation. 618 3

Adhesion of leukocytes to endothelial cells is a critical step in the development of acute and chronic inflammatory lesions. We report here that estradiol treatment of cultured human umbilical vein endothelial cells stimulated up to a twofold increase in TNF-induced adhesion of both polymorphonuclear leukocytes and PMA-activated peripheral blood mononuclear cells. This effect was more evident (threefold increase) when endothelial cells were cultured on the basement membrane glycoprotein laminin. Progesterone, but not testosterone, had a similar stimulatory effect. Estradiol also promoted a slight increase in interferon gamma-stimulated endothelial cell adherence for peripheral blood mononuclear cells, but no effect of estradiol was observed when adhesion of leukocytes to endothelial cells was stimulated with IL-1 or IL-4. The estradiol-induced increase in leukocyte binding to human umbilical vein endothelial cells was partially blocked by antibodies to the adhesion molecules E-selectin, intercellular adhesion molecule type 1 (ICAM-1), and vascular cell adhesion molecule type 1 (VCAM-1). Indirect immunofluorescence techniques showed that estradiol produces an increase in TNF-induced cell surface expression of these molecules. Northern blot analysis demonstrated a transient increase in TNF-induced expression of mRNA for E-selectin, ICAM-1, and VCAM-1 in endothelial cells treated with estradiol. Our data demonstrate that estradiol has important regulatory functions in promoting leukocyte-endothelial cell interactions that might contribute to the observed predominance in females of some autoimmune inflammatory diseases.
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PMID:Estradiol enhances leukocyte binding to tumor necrosis factor (TNF)-stimulated endothelial cells via an increase in TNF-induced adhesion molecules E-selectin, intercellular adhesion molecule type 1, and vascular cell adhesion molecule type 1. 750 11

Adhesion of mature Plasmodium falciparum parasitized erythrocytes to microvascular endothelial cells or to placenta contributes directly to the virulence and severe pathology of P falciparum malaria. Whereas CD36 is the major endothelial receptor for microvasculature sequestration, infected erythrocytes adhering in the placenta bind chondroitin sulfate A (CSA) but not CD36. Binding to both receptors is mediated by different members of the large and diverse protein family P falciparum erythrocyte membrane protein-1 (PfEMP-1) and involves different regions of the molecule. The PfEMP-1-binding domain for CD36 resides in the cysteine-rich interdomain region 1 (CIDR-1). To explore why CSA-binding parasites do not bind CD36, CIDR-1 domains from CD36- or CSA-binding parasites were expressed in mammalian cells and tested for adhesion. Although CIDR-1 domains from CD36-adherent strains strongly bound CD36, those from CSA-adherent parasites did not. The CIDR-1 domain has also been reported to bind CSA. However, none of the CIDR-1 domains tested bound CSA. Chimeric proteins between CIDR-1 domains that bind or do not bind CD36 and mutagenesis experiments revealed that modifications in the minimal CD36-binding region (M2 region) are responsible for the inability of CSA-selected parasites to bind CD36. One of these modifications, mapped to a 3-amino acid substitution in the M2 region, ablated binding in one variant and largely reduced binding of another. These findings provide a molecular explanation for the inability of placental sequestered parasites to bind CD36 and provide additional insight into critical residues for the CIDR-1/CD36 interaction.
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PMID:Modifications in the CD36 binding domain of the Plasmodium falciparum variant antigen are responsible for the inability of chondroitin sulfate A adherent parasites to bind CD36. 1134 58