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)

Adhesion molecules such as ICAM-1 and E-selectin have been shown to play important roles in the production of allergic inflammation. In the present study, we measured serum soluble ICAM-1 (sICAM-1) and soluble E-selectin (sE-selectin) levels by ELISA in 42 patients with bronchial asthma (22 atopic and 20 non-atopic) during asthma attacks and in stable conditions in order to assess the state of ICAM-1 and E-selectin in allergic inflammation. Both serum sICAM-1 levels and serum sE-selectin levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These findings were observed regardless of atopic status. To examine the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels, serum tumour necrosis factor-alpha (TNF-alpha) levels were measured by ELISA. TNF-alpha levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. There was a correlation between the nature of change in serum TNF-alpha levels and the nature of change in serum sICAM-1 levels or serum sE-selectin levels, though serum TNF-alpha levels did not correlate with serum sICAM-1 levels or serum sE-selectin levels. These results suggest that higher levels of sICAM-1 and sE-selectin during asthma attacks may reflect the up-regulation of ICAM-1 and E-selectin expression in allergic inflammation, and that the soluble form of these adhesion molecules may be useful markers for the presence of allergic inflammation. TNF-alpha is shown to enhance the expression and release of ICAM-1 and E-selectin in vitro, however; the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels remains to be clarified.
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PMID:Elevation of serum soluble intercellular adhesion molecule-1 (sICAM-1) and sE-selectin levels in bronchial asthma. 751 4

Adhesion of Plasmodium falciparum-infected erythrocytes to vascular endothelium is in part mediated by ICAM-1 and ELAM-1 (E-selectin), which can be induced via the 55-kDa TNF-receptor (TNF-R55kDa). We have studied serum levels of soluble ICAM-1 (sICAM-1), ELAM-1 (sELAM-1), and soluble TNF-R55kDa (sTNF-R55kDa) in 37 patients with uncomplicated P. falciparum infection and in 17 control subjects in Bangkok, Thailand. The serum levels of sICAM-1 were markedly elevated in patients prior to treatment (601 +/- 239 ng/ml versus 160 +/- 47 ng/ml in healthy controls). In addition, elevated levels of sELAM-1 (53.6 +/- 23.1 ng/ml versus 21.5 +/- 10.1 ng/ml) and sTNF-R55kDa (4.7 +/- 3.2 ng/ml versus 1.0 +/- 0.4 ng/ml) were observed (P < 0.05 for all). Soluble ELAM-1 reached normal levels on Day 3, and sTNF-R55kDa on Day 14, while sICAM-1 was still significantly elevated 28 days after treatment was started (P < 0.05 for all). A correlation between sTNF-R55kDa (P < 0.05) and sELAM-1 (P < 0.05), respectively, with parasitemia prior to antimalarial treatment was found. These results suggest that a TNF-mediated expression of adhesion molecules induced by the asexual stage of malaria parasites serves as an immune-evasion mechanism.
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PMID:Soluble intercellular adhesion molecule-1 (ICAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1), and tumor necrosis factor receptor (55 kDa TNF-R) in patients with acute Plasmodium falciparum malaria. 751 38

Adhesion receptors on endothelial cells are considered to be important for cellular influx in tissue. In this regard, skin constitutes a specialised environment for migration of leukocytes during inflammation. Using immuno-enzymatic staining techniques, we compared the in situ expression of ICAM-1, E-selectin, and VCAM-1 on endothelial cells and inflammatory infiltrates in both lesional and non-lesional biopsied skin from two immuno-inflammatory diseases, viz. psoriasis and contact dermatitis. The results were compared with those in skin specimens obtained from normal healthy individuals free from any history of skin disease. Our results show that ICAM-1 and ELAM-1 are upregulated in psoriatic non-lesional and lesional skin. On the other hand, in non-lesional biopsy from contact dermatitis patients, all three AR molecules are sparsely present, similar to the situation in normal skin although they are overtly expressed in the lesional sites. Moreover, VCAM-1 was found to be significantly increased on endothelial cells in the lesional sites of contact dermatitis as compared with biopsied psoriatic specimens. Interestingly VCAM-1 was also found to be present on some T-cells and Langerhans cells in contact dermatitis alone. The present data suggest that in different inflammatory dermatitis, varying adhesion receptor-ligand interactions involving endothelial cells and leukocytes are involved, which may be due to the differing cytokine profiles of perivascularly located T-cells.
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PMID:Differential expression of ICAM-1, E-selectin and VCAM-1 by endothelial cells in psoriasis and contact dermatitis. 752 Nov 4

Adhesion molecules such as selectins and integrins are known to mediate leukocyte attachment and transmigration through activated vascular endothelium. However, the molecules that mediate subsequent leukocyte entry into nonvascular spaces such as the abdominal cavity during states of peritoneal inflammation have not been identified. Because the peritoneal mesothelial lining represents the final barrier to leukocyte migration into the abdomen, it is likely that adhesion molecules expressed by mesothelial cells are involved in this process. We have developed an in vitro binding assay using confluent layers of normal human mesothelial cells to determine which adhesion molecules might be involved in T lymphocyte-mesothelial recognition. Normal peripheral blood T lymphocytes exhibit low-level specific binding to mesothelium (mean 13% specific binding, n = 4), which is enhanced by phorbol myristate acetate (PMA) treatment (mean 38% specific binding, n = 4). This binding is significantly inhibited in the combined presence of antibodies reactive with CD29 and CD18, suggesting a role for beta 1 and beta 2 integrins, respectively, in this interaction. Interestingly, cultured human mesothelial cells were shown to express vascular cell adhesion molecule-1 (VCAM-1), suggesting that this molecule might function as a counter-receptor for alpha 4 beta 1 expressed by T lymphocytes. Mesothelial cells were also noted to express ICAM-1, CD29, and CD44, but not CD18 or selectins. VCAM-1 expression was not a constitutive property of freshly obtained mesothelial cells but was inducible upon culture in the presence of either interleukin-1 (IL-1), tumor necrosis factor (TNF), or PMA. Neutralizing antibodies reactive with either alpha 4, VCAM-1, or CD29 were all equally capable of inhibiting the binding of activated leukocytes to mesothelial cells (in the presence of anti-CD18 antibody). Mesothelial VCAM-1 was found to have a molecular mass of 110 kD and an mRNA transcript of approximately 3.2 kb, consistent with the predominant VCAM-1 species found in activated endothelium. These data suggest that functional VCAM-1 is expressed on activated mesothelial cells and may play a role in the distal arm of leukocyte trafficking to the abdominal cavity.
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PMID:Vascular cell adhesion molecule-1 expressed by peritoneal mesothelium partly mediates the binding of activated human T lymphocytes. 752 88

Adhesion molecules facilitate infiltration of leukocytes into the central nervous system (CNS) of mice with experimental allergic encephalomyelitis (EAE). Expression of the adhesion molecules ICAM-1 (CD54), VCAM-1 (CD106), L-selectin (CD62L), and leukosialin (CD43) was analyzed via immunocytochemistry 4-28 days after the injection of encephalitogen into EAE-susceptible SWXJ mice. Constitutive ICAM-1 expression on large-diameter CNS vessels was upregulated on post-injection days 8, 11, 14 and 18 (concurrent with de novo expression on smaller capillaries and glial cells), partially downregulated by day 23, and back to control levels by day 28. Constitutive VCAM-1 expression was upregulated by day 14 and back to control levels by day 28. Upregulation of ICAM-1 temporally coincided with the immigration of CD4+ lymphocytes and L-selectin+ leukocytes into the CNS, while downregulation coincided with their emigration. The infiltration of CD43+ leukocytes also coincided with the upregulation of vascular adhesion molecules, but CD43+ cells remained in the CNS after ICAM-1 and VCAM-1 had returned to control levels. Cellular infiltration and adhesion-molecule expression preceded EAE clinical symptoms by a minimum of 3 days, suggesting a causal role of adhesion molecules in the initiation of CNS inflammation. However, prophylactic injections of monoclonal antibodies against either ICAM-1, L-selectin, or CD43, did not ameliorate the clinical severity of EAE in this model.
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PMID:Expression of ICAM-1, VCAM-1, L-selectin, and leukosialin in the mouse central nervous system during the induction and remission stages of experimental allergic encephalomyelitis. 752 43

Adhesion receptors and their ligands play a vital role in the immune system. We studied the expression of different adhesion receptors, using single- and double-staining immunohistochemical techniques, in both lesional and non-lesional skin specimens from seven psoriasis patients and in skin biopsy specimens from eight normal healthy controls. Our results showed an overall increased expression of several adhesion receptors in both lesional and non-lesional psoriatic skin. We consistently found an increased expression in particular of ICAM-1 and E-selectin on endothelial cells, and ICAM-1 on T cells and Langerhans cells. In contrast, a weak expression of VCAM-1 was found on endothelial cells and mononuclear cells in lesional psoriatic skin specimens alone. Interestingly, LFA-1 was also expressed on Langerhans cells, with a greater frequency in skin from lesional than from non-lesional sites, but was never expressed in skin from normal healthy individuals. Furthermore, significantly increased numbers of Langerhans cells and T cells with a positive reactivity for MAb HECA-452 were found in both lesional and non-lesional psoriatic skin. We hypothesize that the enhanced expression of adhesion receptors on migrating immunocompetent cells and endothelial cells of psoriatic skin in general facilitates the increased influx of activated T lymphocytes and other immunocomponent cells into the skin, and thus underscores the generalized character of the disease.
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PMID:Increased expression of adhesion receptors in both lesional and non-lesional psoriatic skin. 752 4

Adhesion of parasitized red blood cells to vascular endothelium contributes to the ischaemic pathology of severe falciparum malaria. One of the endothelial cytoadhesion receptors, CD36, is also expressed by platelets. We have studied adhesion of flowing parasitized cells to a surface coated with immobilized, activated platelets, both as a model for CD36-mediated adhesion and because interaction with platelets might play a direct role in thrombotic complications of malaria. Parasitized cells were able to bind firmly to platelets over a range of shear stress (up to 0.3 Pa) close to those found in the microcirculation. The binding was largely abolished by treatment of platelets with antibody to CD36, with only a small effect by antibody to ICAM-1. Binding showed pH sensitivity consistent with previous reports of CD36-mediated cytoadhesion. Fixation of the platelet surface with formaldehyde preserved adhesion and its antibody sensitivity, while fixation with glutaraldehyde greatly reduced adhesion and increased the sensitivity to antibody against ICAM-1. Thus CD36-mediated binding is inhibited by glutaraldehyde--but not formaldehyde--fixation, while ICAM-1 can mediate adhesion after either form of fixation. We conclude that platelet-coated surfaces (with or without fixation) represent a practically simple model for studying malarial cytoadhesion and that platelets are likely to be able to bind parasitized cells in vivo and could thus promote vascular occlusion.
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PMID:Plasmodium falciparum: characterization of adhesion of flowing parasitized red blood cells to platelets. 752 16

T cell induced differentiation of B cells has been shown to be dependent on the CD2/LFA-3 and LFA-1/ICAM-1 pathways. Flow cytometric analysis was used to examine these adhesion molecules on T and B cells extracted from gingival tissues before and after stimulation with the putative periodontopathic bacteria, Porphyromonas gingivalis and Fusobacterium nucleatum. Adhesion molecule expression on peripheral blood cells from healthy adults was used as a control. Approximately 50 per cent of B cells extracted from gingival tissues expressed LFA-3 and ICAM-1 compared with 30 per cent positive peripheral blood B cells. Around 50 per cent of gingival T cells expressed CD2 relative to 76 per cent positive peripheral blood T cells. However, 40-50 per cent of both gingival and peripheral blood T cells expressed LFA-1. There was no difference in the expression of adhesion molecules on T and B cells extracted from health/marginal gingivitis or adult periodontitis lesions. After stimulation of gingival cells in vitro, the per cent CD2 positive T cells and LFA-3 and ICAM-1 positive B cells remained relatively stable over the six-day culture period, although P. gingivalis and F. nucleatum appeared to induce an increase in the percentage of gingival T cells expressing LFA-1. In contrast to the gingival lymphocytes, stimulation of peripheral blood cells resulted in an increase in the per cent CD2 positive T cells, LFA-3 and ICAM-1 positive B cells, with a decrease in LFA-1 positive T cells. The results therefore demonstrated that gingival T and B cells express adhesion molecules in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cellular adhesion molecules on periodontal lymphocytes. 754 Mar 89

Adhesion molecules appear on leukocytes and endothelial cells mediating the localization and migration of leukocytes to sites of inflammation. Rejecting kidney grafts have shown an increased expression of these molecules. Recent reports have detected in serum soluble forms of adhesion molecules that could play a role in regulating inflammation. We have measured by ELISA the circulating serum levels of ICAM-1, VCAM-1 and E-selectin in: 23 controls, 33 chronic renal failure patients (CRF), 20 hemodialysis patients (HD), 17 samples from 6 patients with stable kidney graft function (STx), 25 samples from 8 patients with steroid-responsive rejection proven by biopsy, and 28 samples from 9 patients with steroid-resistant rejection and good response to OKT3. There was not a rise in cICAM-1 or cE-selectin levels during rejection compared with the steady phase before and after rejection. In the case of cVCAM-1, only the OKT3 group showed increased rejection levels (P < 0.05) that were maintained after rejection. For ICAM-1, CRF and HD groups had higher levels than the remaining groups. cVCAM-1 levels were elevated in all groups when compared with control, furthermore, OKT3 and HD groups had higher levels than the STx, CRF, or steroid-responsive groups. For cE-selectin, we only found differences between the CRF and both rejection groups. Serum creatinine correlated significantly with c-ICAM-1 and cVCAM-1 R = 0.30 and R = 0.22), but not with cE-selectin. We conclude that soluble adhesion molecules levels are not valuable markers for rejection. Patients with chronic renal failure have increased levels of adhesion molecules, which could reflect an impaired elimination.
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PMID:Circulating adhesion molecules during kidney allograft rejection. 754 76

Human fetal livers contain progenitor cells that become mast cells after 4 weeks of culture with recombinant human stem cell factor. Expression of cell surface CD29 (beta 1), CD18 (beta 2), CD61 (beta 3), and beta 5 integrins was investigated on such cells by flow cytometry and adhesion measurements. High surface expression of CD49e, CD51, and CD61 along with kit was apparent by 4 weeks of culture, whereas expression of each at day 0 was low to undetectable. CD29 and CD49d were detected on cells from day 0 to 4 weeks of culture; CD49b, CD49c, CD49f, CD18, and CD54 expression was negligible. The fetal liver-derived mast cells spontaneously adhered to vitronectin. No evidence for degranulation was found during vitronectin-dependent adhesion. Adhesion occurred in part through the CD61/CD51 receptor. No evidence for adhesion to vitronectin through CD29 and beta 5 integrins was obtained. Almost all of the vitronectin-adherent cells expressed CD51, CD61, kit, and tryptase, and exhibited metachromasia with toluidine blue. Thus, among the fetal liver-derived cells, developing mast cells were selectively adherent to vitronectin. These mast cells and the other cell types present also adhere spontaneously to fibronectin and to laminin, this adhesion being partially inhibited by antibodies against CD61 and CD29 integrins. In conclusion, human mast cells acquire functional vitronectin receptors as they develop from fetal liver progenitors under the influence of rhSCF. This may be important for the recruitment, localization, and retention of developing mast cells.
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PMID:Human mast cells derived from fetal liver cells cultured with stem cell factor express a functional CD51/CD61 (alpha v beta 3) integrin. 754 4


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