Circulating ICAM-1 isoforms: diagnostic prospects for inflammatory and immune disorders

Seth, Ram; Raymond, Frank D.; Makgoba, M. W.

doi:10.1016/0140-6736(91)90077-3

Cited by 363 publications

(159 citation statements)

References 8 publications

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“…Alternatively, sICAM-1 could be produced as a secreted splice variant of ICAM-l lacking the intramembrane and intracellular domains, however no corresponding spliced mRNA has yet been identified (Budnik et al, 1996). Several circulating forms differing in molecular weight have been observed, suggesting that molecules might assemble to complexes and/or experience a cell type-dependent glycosylation Seth et al, 1991 (Martin et al, 1993;Welder et al, 1993;Woska et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Elevated serum levels of sICAM-1 have been identified in various inflammatory, infectious and malignant diseases Seth et al, 1991;Tsujisaki et al, 1991), including pancreatic carcinoma (Santarosa et al, 1995 Gearing and Newman, 1993), malignant melanoma (Harning et al, 1991), breast cancer (Klein et al, 1995) and lymphomas (Gruss et al, 1993;Christiansen et al, 1996). They are associated with an unfavourable prognosis in chronic lymphatic leukaemia and Hodgkin's disease (Christiansen et al, 1994(Christiansen et al, , 1995.…”

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confidence: 99%

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Serum levels of soluble intercellular adhesion molecule-1 (ICAM-1, CD54) in patients with non-small-cell lung cancer: correlation with histological expression of ICAM-1 and tumour stage

Grothey¹,

Heistermann²,

Philippou³

et al. 1998

Br J Cancer

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Summary The expression of the intercellular adhesion molecule-1 (ICAM-1, CD54) seems to have an influence on the metastatic behaviour of tumour cells via immunological mechanisms. Recently, a soluble form of ICAM-1 was identified in physiological fluids. We analysed the serum levels of sICAM-1 in patients with non-small-cell lung cancer (NSCLC) and healthy individuals using a sandwich ELISA technique. Sera from 51 patients with NSCLC were tested for sICAM-1 (46 male, five female; age 38-81 years, median 64 years), 29 of whom presented with localized and 26 with metastatic disease. The control group consisted of 40 healthy individuals (20 smokers, 20 non-smokers). Immunohistochemical analysis of ICAM-1 in tumour cells was performed in 20 cases. Patients with NSCLC had significantly higher serum levels of sICAM-1 compared with healthy non-smokers (P = 0.00001) and smokers (P = 0.0328). Metastatic disease was associated with higher sICAM-1 than localized tumours (P = 0.0013). Only 11 out of 23 patients with localized NSCLC had sICAM-1 levels >300 ng ml-1, compared with 25 out of 28 patients with metastatic disease. Histological expression of ICAM-1 was positively correlated with serum sICAM-1 (P = 0.0399). No difference was observed between histological tumour types with regard to sICAM-1 or NSCLC expression of ICAM-1. In sequential analysis (13 patients), rising sICAM-1 levels predicted a short-term fatal outcome (P = 0.0054) but, overall, sICAM-1 levels did not correlate with prognosis. In the control group, smokers showed significantly higher levels than non-smokers (P = 0.0016). In contrast to patients with NSCLC, sICAM-1 in the control group was correlated to the leucocyte count (r = 0.580, P = 0.003). In conclusion, serum levels of sICAM-1 seem to be associated with tumour burden and histological expression of ICAM-1 in patients with NSCLC. However, the (patho-) physiological role of ICAM-1 in NSCLC remains to be determined.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Serum levels of soluble intercellular adhesion molecule-1 (ICAM-1, CD54) in patients with non-small-cell lung cancer: correlation with histological expression of ICAM-1 and tumour stage

Grothey¹,

Heistermann²,

Philippou³

et al. 1998

Br J Cancer

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“…To ensure the reality of an absence of E-selectin and VCAM-1 expression on vascular endothelium, we measured levels of their soluble forms in biologic fluids, especially BALF. Indeed, a first explanation for the absence of detection of these two molecules could be related to a shedding from the EC surface [16], but as soluble ICAM-1 was only detected in BALF, the hypothesis of an impaired expression of E-selectin and VCAM-1 appeared more convincing. This phenomenon could be related to the chronic inflammatory reaction observed in pneumoconiotic lung.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, activation of these different cell types leads to the release of soluble forms of these molecules (sE-selectin, sICAM-1, sVCAM-1) from cell membranes. Their detection in biological fluids may reflect EC activation, and so the severity of the inflammatory reaction [15,16].…”

Section: Introductionmentioning

confidence: 99%

Expression of leucocyte–endothelial adhesion molecules is limited to intercellular adhesion molecule-1 (ICAM-1) in the lung of pneumoconiotic patients: role of tumour necrosis factor-alpha (TNF-α)

Vanhée

Molet

Gosset

et al. 1996

Clinical and Experimental Immunology

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SUMMARYCoal workers' pneumoconiosis (CWP) is characterized by a chronic inflammatory lung reaction associated with macrophage accumulation in alveolar spaces. In this study, we investigated in CWP the implication of adhesion molecules such as E-selectin, ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1) and the role of TNF-® which is one of the cytokines inducing their expression. Adhesion molecule expression was analysed by immunohistochemistry on lung biopsies from patients with CWP and from healthy subjects. In parallel, soluble adhesion molecules were detected in bronchoalveolar lavage fluids (BALF) from patients by specific ELISA. The involvement of TNF in the induction of these adhesion molecules was measured (i) by immunohistochemistry on sections from lung fragments, and (ii) by evaluating in vitro the expression of adhesion molecules on endothelial cells and on alveolar epithelial cells in the presence of alveolar macrophage supernatants. In control subjects, a weak staining of ICAM-1 was detected only in alveolar walls, while E-selectin and VCAM-1 were undetectable. In pneumoconiotic patients, ICAM-1 was expressed at a high level by endothelium, by alveolar and bronchial epithelial cells and by alveolar macrophages. E-selectin and VCAM-1 expression remained undetectable. Measurement of soluble adhesion molecule showed that only the concentration of sICAM-1 was significantly increased in BALF from patients with CWP compared with controls. The involvement of TNF in this ICAM-1 expression was shown by the in vitro effect of alveolar macrophage supernatants on adhesion molecule expresssion by endothelial cells and epithelial cells (this effect was neutralized by anti-TNF antibodies) and by the increased production of TNF in the lung of pneumoconiotic patients. These data provide evidence for the involvement of ICAM-1, induced at least in part by alveolar macrophage-derived TNF, in the development of the inflammatory reaction in CWP.

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“…Constitutive levels of a soluble form of ICAM-I (sICAM-1) have been identified in the serum of healthy subjects (Rothlein et al, 1991;Seth et al, 1991), and elevated amounts are detectable in inflammatory (Seth et al, 1991;Jones et al, 1995) and autoimmune (Schopf et al, 1993;Sharief et al, 1993) disorders. Furthermore, high levels of sICAM-1 are detectable in malignancies of different histotype and correlate with disease progression (Tsujisaki et al, 1991;Altomonte et al, 1992;Banks et al, 1993;Pui et al, 1993).…”

mentioning

confidence: 99%

Tumour-derived interleukin 1α (IL-1α) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells

Fonsatti

Altomonte²,

Coral³

et al. 1997

Br J Cancer

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Summary Levels of circulating soluble intercellular adhesion molecule-1 (sICAM-1) are elevated in patients affected by solid malignancies; however, the cellular sources generating high levels of sICAM-1 remain to be characterized. Using conditioned media (CM) from seven ICAM-1-positive or -negative neoplastic cells, we demonstrate that tumour-derived interleukin 1a (IL-1 a) significantly (P < 0.05) up-regulates the release of sICAM-1 by human umbilical vein endothelial cells. The intensity of the effect correlated with the amounts of IL-la detectable in CM. Levels of ICAM-1 mRNA were also up-regulated by tumour-secreted IL-i a. The up-regulation of the shedding of sICAM-1 and of its expression at protein and mRNA level were completely reversed by the addition of anti-IL-i a neutralizing antibodies. Consistent with the in vitro data, tumour endothelia were strongly stained for ICAM-1 compared with autologous normal tissue endothelia. Taken altogether, our observations reveal an IL-la-mediated tumour-endothelium relationship sustaining the shedding of sICAM-1 by endothelial cells. This is a general phenomenon in solid malignancies that correlates with the ability of neoplastic cells to secrete IL-1a rather than with their expression of ICAM-1 and/or histological origin. sICAM-1 has been previously shown to inhibit LFA-1/ICAM-1-mediated cell-cell interactions; therefore, the ability of neoplastic cells to secrete IL-1a is likely to represent a mechanism for their escape from immune interaction.

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Circulating ICAM-1 isoforms: diagnostic prospects for inflammatory and immune disorders

Cited by 363 publications

References 8 publications

Serum levels of soluble intercellular adhesion molecule-1 (ICAM-1, CD54) in patients with non-small-cell lung cancer: correlation with histological expression of ICAM-1 and tumour stage

Serum levels of soluble intercellular adhesion molecule-1 (ICAM-1, CD54) in patients with non-small-cell lung cancer: correlation with histological expression of ICAM-1 and tumour stage

Expression of leucocyte–endothelial adhesion molecules is limited to intercellular adhesion molecule-1 (ICAM-1) in the lung of pneumoconiotic patients: role of tumour necrosis factor-alpha (TNF-α)

Tumour-derived interleukin 1α (IL-1α) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells

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