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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion molecules involved in leukocyte recruitment and lymphocyte recirculation impact on several aspects of tumor biology--the primary host response, the delivery of effective adoptive immunotherapy and the hematogenous spread of malignant cells. Common to all three processes are receptor-mediated adhesive interactions between circulating cells and the vessel wall. Recruitment of circulating lymphocytes, monocytes and natural killer cells is essential for an effective host response or successful adoptive immunotherapy. Thus poor induction or blockade of leukocyte binding sites on the microvasculature of tumor implants may help malignancies evade natural defenses. In addition, perturbation of adhesion receptor function during ex vivo expansion may alter the behavior of infused cells in adoptive immunotherapy protocols. Finally, circulating malignant cells may utilize receptors normally involved in recruitment and recirculation. This paper reviews the function and regulation of adhesion molecules involved in normal leukocyte trafficking. The evidence implicating specific adhesion receptors in the spread of lymphoid malignancies through the bloodstream is then discussed.
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PMID:Adhesion molecules involved in the trafficking of normal and malignant leukocytes. 139 99

Local spinal cord lesions are often greatly enlarged by secondary damage, a process which leads to massive additional cell death. This process is poorly understood. In order to investigate which types of cells could play a role in increasing the size of the lesion, we have analysed the events occurring at rat spinal cord lesion sites from 1 h to 3 months after partial transection using cell type-specific markers. One hour after transection, the lesion site was small and corresponded to the zone of primary mechanical damage. Extravasation of blood and an opening of the blood-brain barrier occurred. Rapidly thereafter, at 3 and 6 h, an area of secondary cell death developed around the zone of the primary lesion. This secondary cell death, which was probably largely of the necrotic type, affected neurons, macroglia and microglial cells indiscriminately. It was virtually complete at 12 h. Recruitment of inflammatory cells followed a time course which lagged behind that of secondary cell death. Adhesion of neutrophils to the inside of blood vessels was observed at 3 h. They appeared in large numbers at 6 h at the site of the primary lesion, but not yet in the area of secondary cell death. They were numerous throughout the lesion site at 24 h and then disappeared rapidly. Proliferation and recruitment of macrophages and microglial cells became predominant 2 days after injury. Their density was highest within the lesion site between 4 and 8 days. Very few astrocytes were present in the lesion site during the first week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secondary cell death and the inflammatory reaction after dorsal hemisection of the rat spinal cord. 807 16

Recruitment and activation of inflammatory cells such as neutrophils, lymphocytes, and macrophages are important events in the pathogenesis of chronic obstructive pulmonary disease (COPD). Adhesion molecules play an central role in these processes. Several clinical investigations have demonstrated that the expression of ICAM-1 on the bronchial epithelium and E-selectin on bronchial mucosal vessels was increased in the patients with COPD. These findings suggested that adhesion molecules are involved in the pathogenesis of COPD.
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PMID:[Role of adhesion molecules in the pathogenesis of COPD]. 1049 91

Adhesion of inflammatory cells to vascular endothelium is mediated by specific cell adhesion receptors on both leukocytes and endothelial cells. One of the adhesion molecules on the endothelium is P-selectin. Decreased vascular P-selectin expression has been associated with tumor progression in melanoma patients. We now report on the expression of endothelial P-selectin in colorectal cancer (CRC). We studied a colorectal tissue specimen series ranging from normal colorectal tissue via unmetastasized primary tumors to tumors with the same depth of invasion at the primary site but with liver metastases. Moreover, P-selectin expression levels in liver metastases were determined. The number of P-selectin positive vessels as a fraction of the total number of vessels, both intra- and peritumorally, was determined by staining for CD62P and CD34, respectively. Furthermore, by immunostaining for leukocytes (CD45) and macrophages (CD68), it was evaluated whether levels of P-selectin expression influenced infiltrate density and composition. The results showed that levels of peritumoral P-selectin expression were reciprocal to the degree of progression in CRC. This relation was even more pronounced intratumorally: in metastasized primary tumors and in the metastatic lesions, P-selectin expression was virtually absent. This distribution pattern was reflected in the numbers of leukocytes that accumulated in the various tissues, since in the primary tumors with metastases, and in the metastatic lesions, hardly any infiltrating cells were observed. In these lesions, leukocytes were present in the peritumoral zone, but seemed unable to enter the tumor tissue. In primary tumors without metastasis, the intratumoral leukocyte infiltration density was significantly higher. Recruitment levels of macrophages remained constant throughout the different tissues. We suggest that downregulation of endothelial P-selectin expression is a mechanism by which CRC lesions evade inflammatory regression and, thereby, progress to a more advanced stage of malignancy.
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PMID:Progressive loss of endothelial P-selectin expression with increasing malignancy in colorectal cancer. 1564 Aug 34

Elevated cholesterol levels promote proinflammatory and prothrombogenic responses in venules and impaired endothelium-dependent arteriolar dilation. Although NAD(P)H oxidase-derived superoxide has been implicated in the altered vascular responses to hypercholesterolemia, it remains unclear whether this oxidative pathway mediates the associated arteriolar dysfunction and platelet adhesion in venules. Platelet and leukocyte adhesion in cremasteric postcapillary venules and arteriolar dilation responses to acetylcholine were monitored in wild-type (WT), Cu,Zn-superoxide dismutase transgenic (SOD-TgN), and NAD(P)H oxidase-knockout (gp91(phox-/-)) mice placed on a normal (ND) or high-cholesterol (HC) diet for 2 weeks. HC elicited increased platelet and leukocyte adhesion in WT mice versus ND. Cytosolic subunits of NAD(P)H oxidase (p47phox and p67phox) were expressed in platelets. This was not altered by hypercholesterolemia; however, platelets and leukocytes from HC mice exhibited elevated generation of reactive oxygen species compared to ND mice. Hypercholesterolemia-induced leukocyte recruitment was attenuated in SOD-TgN-HC and gp91(phox-/-)-HC mice. Recruitment of platelets derived from WT-HC mice in venules of SOD-TgN-HC or gp91(phox-/-)-HC recipients was comparable to ND levels. Adhesion of SOD-TgN-HC platelets paralleled the leukocyte response and was attenuated in SOD-TgN-HC recipients, but not in WT-HC recipients. However, gp91(phox-/-)-HC platelets exhibited low levels of adhesion comparable to those of WT-ND in both hypercholesterolemic gp91(phox-/-) and WT recipients. Arteriolar dysfunction was evident in WT-HC mice, compared to WT-ND. Overexpression of SOD or, to a lesser extent, gp91(phox) deficiency restored arteriolar vasorelaxation responses toward WT-ND levels. These findings reveal a novel role for platelet-associated NAD(P)H oxidase in producing the thrombogenic phenotype in hypercholesterolemia and demonstrate that NAD(P)H oxidase-derived superoxide mediates the HC-induced arteriolar dysfunction.
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PMID:Platelet-associated NAD(P)H oxidase contributes to the thrombogenic phenotype induced by hypercholesterolemia. 1756 Oct 90

Epithelial ovarian cancer cells metastasize by implanting onto the peritoneal mesothelial surface of the abdominal cavity. Adhesive molecules that lead to this implantation remain unclear. The aim of our study was to focus on the role of vitronectin (Vn) and its receptors, alpha(v) integrins and urokinase plasminogen activator receptor (uPAR), in the interactions of ovarian adenocarcinoma cells (IGROV1 and SKOV3 cell lines) with mesothelial cells (MeT-5A cell line and primary cultures). For all cell lines, immunofluorescence staining disclosed the presence of Vn over the whole cell surface and in thin continuous deposits underlining the cell periphery. Recruitment of Vn receptors to cell-cell contact sites was also revealed. We developed two distinct methods for the evaluation of in vitro cell-cell adhesion using cocultures of the tumor and mesothelial cells. Both adhesion assays revealed a strong ability of ovarian cancer cells to adhere preferentially to mesothelial intercellular junctions. Adhesion of ovarian carcinoma cells to mesothelial cells was significantly inhibited using anti-Vn-, -alpha(v)-integrin- and -uPAR-blocking antibodies or cyclic peptide cRGDfV. These results evidence the ability of ovarian carcinoma cells to bind to peritoneal mesothelium in vitro and strongly suggest that Vn and its receptors contribute to this crucial event.
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PMID:Vitronectin and its receptors partly mediate adhesion of ovarian cancer cells to peritoneal mesothelium in vitro. 1878 Oct 95

Recruitment of specific leukocyte subpopulations at the site of inflammation requires a series of cell adhesion molecules (CAMs)-mediated interactions. The major CAMs, viz., intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin are expressed on endothelium in response to various cytokines. Caffeic acid (CA), a natural phenolic compound from herbs and other sources, has been shown to prevent cardiovascular diseases. We investigated the effect of CA on the expression of CAMs by human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor (TNF-alpha). Adhesion of monocytes to CA-treated HUVECs was evaluated by co-culture experiments using 2,7-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethylester (BCECF-AM) labeling of U937 cells. The expression of adhesion and chemoattractant molecules was evaluated by Western blot and reverse transcription-polymerase chain reaction (RT-PCR), respectively. CA significantly inhibited the TNF-alpha-induced increase in U937 monocyte adhesion to HUVECs as well as decreased the protein and mRNA expression levels of CAMs on HUVECs. CA also inhibited the mRNA expression of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). The involvement of nuclear factor (NF)-kappaB in the transcriptional control of CAMs protein was assessed by degradation of inhibitory (I)kappaB and nuclear translocation of NF-kappaB using Western blotting and immunofluorescence staining. CA attenuated TNF-alpha-induced IkappaB degradation and NF-kappaB translocation from cytosol to the nucleus. In conclusion, TNF-alpha-induced NF-kappaB-DNA complex formation was inhibited by CA. CA reduced TNF-alpha-induced endothelial adhesiveness to HUVECs by inhibiting transcription factor activation, and CAMs expression suggesting its potential role in atherosclerosis diseases.
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PMID:Effect of caffeic acid on tumor necrosis factor-alpha-induced vascular inflammation in human umbilical vein endothelial cells. 1965 76

Crohn's disease can affect any part of the gastrointestinal tract, but terminal ileum is the most frequent localization. The reason why Crohn's disease is primarily located in the distal part of the ileum remains unexplained. In this article it has been attempted to provide a compelling explanation why Crohn's disease usually occurs in terminal ileum. Recent data indicate that some individuals are genetically predisposed to develop ileal Crohn's disease. Two genetic alterations, the polymorphism of Caspase Associated Recruitment Domain (CARD15) and Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 (CEACM6), favour the colonization of terminal ileum by entero adherent-invasive Escherichia coli (AIEC). The adhesion of these bacteria to epithelial intestinal cells depends on Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 expression in ileal epithelial cells and on the reduced ileal defensins expressed in a CARD15 dependent manner. Genetic defects in Authophagy-related 16-like gene (ATG16L1) and Immunity-related Guanosine Triphospatase (IRGM) recently found in ileal CD patients lead to a reduction of bacterial killing by macrophages and consequent continuous immunological upstimulation, cytokine secretion, chronic inflammation of the ileum and tissue injury. On the basis of all these data Crohn's disease of the ileum seems to be a subset of the disease mainly genetically determined.
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PMID:Why does Crohn's disease usually occur in terminal ileum? 2117 38