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

Cellular adhesion molecules are crucial determinants of the migration of immune effector cells to the tissues. In chronic inflammatory diseases, upregulation of the expression of these molecules may contribute to the persistent inflammatory process. The aim of this study was to determine whether there is evidence of adhesion molecule expression in chronically inflamed lung. Soluble adhesion molecules in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunoassay in 54 patients with chronic interstitial lung diseases and 16 normal controls. Adhesion molecule expression in fibrosing alveolitis (FA) lung and in control lung was assessed using immunohistology and reverse transcription-polymerase chain reaction (RT-PCR) amplification. Soluble intercellular adhesion molecule-1 (ICAM-1) was detected in all but two subjects. There was no difference in ICAM-1 concentration between disease groups and normal subjects. In contrast, soluble E-selectin was detected in 17 of the 70 subjects and was significantly associated with the presence of lung disease (p=0.0173). Furthermore, the presence of soluble E-selectin was associated with a raised lymphocyte percentage in BALF (p=0.0069). Soluble VCAM was only detected in five of the 70 subjects (two normals, three patients). There was no difference in adhesion molecule expression in lung parenchyma between FA and controls assessed by immunohistology and RT-PCR. The most striking finding of our study was the universal expression of intercellular adhesion molecule-1 in both normal and diseased lung, emphasizing the important role of the lung in immune function. Upregulation of E-selectin may contribute to inflammatory cell accumulation in chronic interstitial lung diseases.
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PMID:Adhesion molecule expression in the lung: a comparison between normal and diffuse interstitial lung disease. 954 76

Invasive lung disease caused by Aspergillus species is a potentially fatal infection in immunocompromised patients. The adhesion of Aspergillus fumigatus conidia to proteins in the basal lamina is thought to be an initial step in the development of invasive aspergillosis. The purpose of this study was to determine the mechanism of adhesion of A. fumigatus conidiospores to basal-lamina proteins and to determine whether conidia possess unique adhesins which allow them to colonize the host. We compared conidia from different Aspergillus species for the ability to bind to purified fibronectin and intact basal lamina. Adhesion assays using immobilized fibronectin or type II pneumocyte-derived basal lamina showed that A. fumigatus conidia bound significantly better than those of other Aspergillus species to both fibronectin and intact basal lamina. Neither desialylation nor complete deglycosylation of fibronectin decreased the binding of A. fumigatus conidia to fibronectin, suggesting that oligosaccharides on fibronectin were not involved in conidiospore binding. Further evidence for this hypothesis came from experiments using purified fragments of fibronectin; A. fumigatus conidia preferentially bound to the nonglycosylated 40-kDa fragment which contains the glycosaminoglycan (GAG) binding domain. Negatively charged carbohydrates, including dextran sulfate and heparin, as well as high-ionic-strength buffers, inhibited binding of A. fumigatus conidia to both fibronectin and intact basal lamina, suggesting that negatively charged carbohydrates on the surface of the conidium may bind to the GAG binding domain of fibronectin and other basal-lamina proteins. These data provide evidence for a novel mechanism of conidial attachment whereby adherence to fibronectin and other basal-lamina proteins is mediated via negatively charged carbohydrates on the conidial surface.
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PMID:Adhesion of Aspergillus species to extracellular matrix proteins: evidence for involvement of negatively charged carbohydrates on the conidial surface. 1081 88

Platelet Endothelial Cell Adhesion Molecule (PECAM) is an adhesion and signaling molecule used for leukocyte extravasation. We have generated two strains of PECAM-deficient mouse, one in the original C57BL/6 and a second by backcrossing nice generations into the FVB/n strain. The FVB/n strain has reduced responses in models of acute inflammation. We show here that this strain is also susceptible to a chronic pneumonia which leads to pulmonary fibrosis. In contrast, PECAM-deficient C57BL/6 mice do not develop this lung disease and have normal responses in acute models of inflammation. This demonstrates that PECAM-dependent and -independent mechanisms are found in both acute and chronic inflammation. Further, the PECAM-deficient FVB/n strain has many pathologic similarities to the human disease Idiopathic Pulmonary Fibrosis, suggesting that similar molecular mechanisms may play a role in human disease.
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PMID:Different susceptibilities of PECAM-deficient mouse strains to spontaneous idiopathic pneumonitis. 1645 10