Distribution Of Intercellular Adhesion Molecule-1 Research Articles

Atherosclerotic Lesions Grow Through Recruitment and Proliferation of Circulating Monocytes in a Murine Model

Macrophage-derived foam cells in developing atherosclerotic lesions may potentially originate either from recruitment of circulating monocytes or from migration of resident tissue macrophages. In this study, we have determined the source of intimal macrophages in the apoE-knockout mouse flow-cessation/hypercholesterolemia model of atherosclerosis using a bone marrow transplantation approach. We also examined the time course and spatial distribution of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression to assess whether endothelial adhesion molecules were involved in recruitment of either circulating monocytes or resident macrophages. We used allelic variants of the mouse common leukocyte antigen (CD45) to distinguish host-derived and donor-derived white blood cells (WBCs) both in blood and in macrophage-rich carotid lesions. We found that the distribution of CD45 isoforms in lesions is similar to that of circulating WBCs, whereas the host-type CD45 isoform is more prevalent in resident adventitial macrophages. These data indicate that macrophage-derived foam cells in the lesion derive mainly from circulating precursors rather than from resident macrophages. The corresponding time course of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression suggests that recruitment of circulating WBCs by endothelial adhesion molecules is likely to be more important during lesion initiation than during the later phase of rapid lesion growth.

Quantitative analysis of inflammatory cells infiltrating the cystic fibrosis airway mucosa.

Airway inflammation represents a hallmark of the cystic fibrosis (CF) disease. However, the mucosal distribution of immune cells along the CF airways has not been clearly defined, particularly in intermediate bronchi and distal bronchioles. We analysed lung tissues collected at the time of transplantation from homozygous DeltaF508+/+CF patients versus non-CF donors. Using immunohistochemistry, the distribution of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin, polymorphonuclear neutrophils (PMN), mast cells, CD3+ T cells, including the CD4+ and CD8+ subsets, CD20+ B cells, CD38+ plasma cells and CD68+ macrophages, was analysed at lobar, segmental and distal levels of the bronchial tree. Using image cytometry, the number of cells per mm2 was assessed in the depth of the bronchial wall. In CF airways, alterations mainly consisted in lesions of the surface epithelium. Numerous immune cells were heterogeneously distributed all along the bronchial tree and mainly located in the mucosa, beneath the surface epithelium. Compared to non-CF donors, the lymphoid aggregates formed by B cells were significantly larger all along the CF airways (P = 0.001). The number of T lymphocytes was higher at the CF distal level (P = 0.035), where we observed an intense tissue damage. PMN preferentially accumulated (P = 0.033) in the CF surface epithelium, which overexpressed ICAM-1 but not VCAM-1 and E-selectin. These results highlight the nature of the inflammatory infiltrate in the CF airway mucosa and emphasize a prominent implication of PMN, B and T lymphocytes in the CF disease.

Three-Dimensional Distribution of Intercellular Adhesion Molecule-1 on Lymphocytes in the High Endothelial Venule Analyzed by Backscatter Electron Imaging

The intercellular adhesion molecule-1 (ICAM-1) is a ligand for the β2 integrin. It is present on the vascular endothelium and plays an important role in cell to cell interaction in lymphocyte recirculation. ICAM-1 is expressed not only on the endothelium but also on other cells, especially lymphocytes adhering to the endothelium, B cells and mitogen-stimulated T cells. To define the functional role of ICAM-1 in lymphocytes, the three-dimensional distribution of ICAM-1 on the surface of lymphocytes in the rat mesenteric lymph node HEV was investigated by immunoscanning electron microscopy. ICAM-1 expression was closely associated with variations in surface structures of lymphocytes, which showed a cap-like structure, membrane ruffles and slender microvilli. ICAM-1 was preferentially localized on the cell surface including membrane ruffles (about 90% of all counted gold particles), but rarely on the microvilli (10%). The results suggest that activated lymphocytes with variations in surface structures demonstrate moderate expression and preferential localization of ICAM-1. This seems to enable a three-dimensional interaction of the microvilli of one lymphocyte with the surface membrane of another cell and might be a prerequisite for cluster formation between them, as seen in antigen presentation.

Immunohistochemical analysis of intercellular adhesion molecule-1 expression in human gastric adenoma and adenocarcinoma

In this study, we examined the distribution of intercellular adhesion molecule-1 (ICAM-1) in gastric adenomas and carcinomas immunohistochemically at the light and electron microscopic levels. ICAM-1 was expressed on tumour cells in 12 of 28 gastric carcinomas and in 3 of 11 adenomas but not on most normal gastric epithelial cells. ICAM-1 was localized on luminal sites of neoplastic glands in adenomas and in intestinal-type carcinomas, and rarely on the surface of tumour cells of diffuse carcinomas. Expression of ICAM-1 on the tumour cells was more frequent in intestinal-type than diffuse carcinomas (P < 0.005). At the ultrastructural level, ICAM-1 was present prominently on the apical membrane and weakly on the lateral surface of the tumour cells of the intestinal-type carcinoma and also localized on the perinuclear membrane and the membrane of the endoplasmic reticulum of cancer cells. There was no significant association between ICAM-1 expression and HLA antigen expression or the number of infiltrating lymphocyte subsets. These results may implicate the synthesis of ICAM-1 by gastric cancer cells, but the expression is infrequent and may not be sufficient for host immune surveillance of the tumour cell.

Distribution of intercellular adhesion molecule-1 on leukocytes and corneal endothelium after endotoxin stimulation in rats

After stimulation with Salmonella typhimurium endotoxin, the intercellular adhesion molecule-1 (ICAM-1) was studied on the corneal endothelium and associated leukocytes in rats using immunoscanning electron microscopy. Two hundred micrograms of the endotoxin was injected in Lewis rats. The corneae were excised at 0-h and 16-h-postinjection time (n = 5, respectively). The corneae were prepared in hypothermic University of Wisconsin (UW) solution for immunoscanning electron microscopy. Histotopographical examination visualized ICAM-1 antigen on cytoplasmic processes of the corneal endothelium, arranged along microfolds, especially at the peaks. In the leukocytes, ICAM-1 was located primarily in morphologically non-specialized domains of the cell body surface, and only rarely scattered on the surface of microvillar projections. We concluded that the endotoxin stimulation can increase ICAM-1 in both corneal endothelium and associated leukocytes. Increased ICAM-1 may be an important factor for the leukocytes to form clustering and adhering to the corneal endothelium.

Immunohistochemical study of the distribution of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in chronic type B hepatitis

The expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) in the livers of 11 patients with chronic hepatitis B was studied immunohistochemically by light and electron microscopy to clarify the role of these adhesion molecules in tissue damage in chronic hepatitis B. On hepatocytes, ICAM-1 expression was confined to the bile canalicular surface when the liver inflammation was mild. In contrast, when the liver inflammation was severe, ICAM-1 was distributed on the entire surface of the hepatocyte, including the sinusoidal and lateral membranes; lymphocytes which were mostly positive for LFA-1, were often observed invading deeply among these hepatocytes. The degree of ICAM-1 expression on the hepatocytes was also related to the expression of HLA class 1 antigen. In liver showing diffuse expression of ICAM-1 on the hepatocytes, strong expression of HLA class 1 antigen was observed, and amounts of HBV in the liver were decreased. Diffuse expression of ICAM-1 and HLA class 1 antigen was mostly observed after acute exacerbation of liver inflammation. These results suggest that the ICAM-1/LFA-1 pathway is involved in the immunological mechanism responsible for liver cell damage in chronic hepatitis B.

Leukocyte adhesion molecules in rejected corneal allografts.

Leukocyte adhesion molecules are believed to play a key role in the selective recruitment of different leukocyte populations to inflammatory sites. In this study, we investigated the presence and distribution of intercellular adhesion molecule-1 (ICAM-1), E-selectin (endothelial leukocyte adhesion molecule-1) and vascular cell adhesion molecule-1 (VCAM-1) in 12 rejected corneal allografts and compared the presence of these adhesion molecules with the composition of the associated inflammatory infiltrates. ICAM-1 was focally expressed on corneal epithelial cells and its expression was increased on keratocytes, corneal and vascular endothelial cells particularly at the site of dense infiltration with mononuclear leukocytes. E-selectin was present on endothelial cells of vessels in the stroma of rejected corneal allografts which were characterized by dense infiltration with T cells and macrophages. VCAM-1 was predominantly expressed on inflammatory cells of the macrophage/monocyte lineage, but only sporadically on vascular endothelial cells in the stroma of vascularized rejected corneal allografts. Our results suggest that ICAM-1, E-selectin and VCAM-1 may all be involved in the pathogenesis of corneal allograft rejection, particularly in the generation of the inflammatory infiltrates.

Intercellular adhesion molecule-1 expression on the alveolar epithelium and its modification by hyperoxia.

The distribution of intercellular adhesion molecule-1 (ICAM-1) on alveolar epithelial cells and the effects of exposure to 100% O2 on ICAM-1 expression in mouse lungs were studied by EM immunocytochemistry and immunoblot analysis. Cryoultrathin sections from mouse lungs exposed to air or 100% O2 for 84 h were labeled with a monoclonal rat anti-mouse ICAM-1 antibody. In the normal lung, abundant ICAM-1 expression was found on the alveolar surface of type I epithelial cells. Furthermore, ICAM-1 is highly concentrated on the surfaces near cell junctions. ICAM-1 was also found on the capillary surface of endothelial cells and alveolar surface of type II cells at densities considerably lower than that found on type I epithelial cells. After exposure to O2, the labeling density of ICAM-1 on the central surface of type I epithelial cells was not changed significantly. However, the gradient of ICAM-1 on the surfaces near cell junctions was nearly abolished. ICAM-1 labeling on the capillary surface of endothelial cells remained low. ICAM-1 was also markedly induced on the alveolar surface of type II epithelial cells after hyperoxic exposure. These results show that ICAM-1 is expressed primarily on type I epithelial cell surfaces near cell junctions. Exposure to hyperoxia causes a dramatic change in the distribution pattern of ICAM-1 on alveolar type I epithelial cells and induces expression of ICAM-1 on alveolar type II epithelial cells. These hyperoxia-induced changes may influence the associated neutrophil invasion/retention in the alveolar air spaces or alveolar walls.

Expression of Intercellular Adhesion Molecule-1 (ICAM-1) in the Skin of Patients with Systemic Scleroderma

The expression and tissue distribution of intercellular adhesion molecule-1 (ICAM-1) in skin biopsies from 12 patients with systemic (SSc) and localized (LS) scleroderma was studied and compared to the biopsies from patients with lupus erythematosus (LE) and normal individuals. In normal human skin ICAM-1 expression was restricted to the vascular endothelium, infiltrating mononuclear cells (MNC), and to few individual keratinocytes. In the inflammatory stage of SSc, however, the expression of ICAM-1 was dramatically increased at the site of MNC infiltrates and could also be detected on fibroblast-like cells lying well apart from these infiltrates in the deep dermis. In contrast, in LS ICAM-1 was expressed mainly at the sites of MNC infiltrates. In LE ICAM-1 expression was confined to the keratinocytes, endothelial cells, and mononuclear cells in the upper parts of the dermis. Analysis of serial tissue sections from patients with SSc demonstrated also colocalization of staining of ICAM-1 around blood vessels with LFA-1-positive lymphocytes. Increased expression of ICAM-1 in the dermis of patients with SSc may represent an important mechanism by which MNC become localized and retained at a site of connective tissue inflammation, leading to the activation of fibroblasts.

Modulation of leucocyte adhesion molecules, a T-cell chemotaxin (IL-8) and a regulatory cytokine (TNF-α) in allergic contact dermatitis (rhus dermatitis)

To understand the molecular events which are important in leucocyte trafficking in cutaneous inflammation, poison ivy/oak extract was applied topically to the skin, and the simultaneous assessment of a variety of clinical and immunopathological parameters performed. The clinical response of subjects was divided into three main groups: I, 2-24h after application, before the onset of erythema; II, 48 h-1 week after application during maximal clinical changes; III, 2-3 weeks after application when the inflammation had subsided. Six different biopsies per subject were evaluated over the study period and the density of dermal cellular infiltrate, and the distribution of intercellular adhesion molecule-1, (ICAM-1), endothelial leucocyte adhesion molecule-1, (ELAM-1), vascular cell adhesion molecule-1, (VCAM-1), interleukin 8 (IL-8) and tumour necrosis factor-alpha (TNF-alpha), determined. Eight hours after exposure, before lymphocytes and monocytes had entered the dermal interstitium or epidermis, the keratinocytes expressed TNF-alpha and ICAM-1, whilst the endothelial cells expressed ELAM-1, VCAM-1 and ICAM-1. Group II biopsies revealed increasing keratinocyte expression of TNF-alpha and ICAM-1 with the appearance of IL-8, which correlated with the onset of epidermal T-cell trafficking. The endothelium was strongly positive for ELAM-1 and VCAM-1, but there was no influx of neutrophils. Group III biopsies showed a decrease in the expression of ICAM-1, VCAM-1 and ELAM-1 by both keratinocytes and endothelium with a reduction in epidermal/dermal inflammation, although the endothelial cell staining of VCAM-1 and ELAM-1 did not completely disappear. These results suggest that on exposure to poison ivy/oak, keratinocytes rapidly produce TNF-alpha which leads to an early autoinduction of ICAM-1, and later IL-8. There is also a paracrinemediated induction and augmentation of underlying endothelial cell ELAM-1, VCAM-1 and ICAM-1.

Expression of Intercellular Adhesion Molecule-1 (CD54) on Hematopoietic Progenitors

Abstract The distribution of intercellular adhesion molecule-1 (ICAM-1), a ligand for lymphocyte function antigen-1, on hematopoietic tissue was determined using the anti-ICAM-1 monoclonal antibody CL203.4 with flow cytometry and short-term semi-solid hematopoietic progenitor cultures. After timed incubation in media with fetal bovine serum, 29% of erythroid burst-forming units (BFU-E), 24% of erythroid colony-forming units (CFU-E), and 52% of granulocyte-macrophage colony-forming units (CFU-GM) bone marrow progenitors expressed ICAM-1. This finding, which is consistent with the detection of ICAM-1 on acute non-lymphoblastic leukemic blasts, is at variance with recent reports. ICAM-1 was also detected on bone marrow blasts, proerythroblasts, promyelocytes, and cells of monocyte/macrophage lineage, but was not detected on erythroblasts, normoblasts, neutrophilic myelocytes, metamyelocytes, bands, or on most lymphocytes. These results indicate that maturation of cells of the erythroid and myeloid lineage is associated with loss of ICAM-1. The distribution of ICAM-1 on bone marrow progenitors, early precursor cells, and accessory cells in conjunction with the function of this molecule in cell-cell interactions suggests that ICAM-1 may play a role in the cell-cell and cell-stromal interactions that regulate hematopoiesis.

Expression of intercellular adhesion molecule-1 (CD54) on hematopoietic progenitors

The distribution of intercellular adhesion molecule-1 (ICAM-1), a ligand for lymphocyte function antigen-1, on hematopoietic tissue was determined using the anti-ICAM-1 monoclonal antibody CL203.4 with flow cytometry and short-term semi-solid hematopoietic progenitor cultures. After timed incubation in media with fetal bovine serum, 29% of erythroid burst-forming units (BFU-E), 24% of erythroid colony-forming units (CFU-E), and 52% of granulocyte-macrophage colony-forming units (CFU-GM) bone marrow progenitors expressed ICAM-1. This finding, which is consistent with the detection of ICAM-1 on acute non-lymphoblastic leukemic blasts, is at variance with recent reports. ICAM-1 was also detected on bone marrow blasts, proerythroblasts, promyelocytes, and cells of monocyte/macrophage lineage, but was not detected on erythroblasts, normoblasts, neutrophilic myelocytes, metamyelocytes, bands, or on most lymphocytes. These results indicate that maturation of cells of the erythroid and myeloid lineage is associated with loss of ICAM-1. The distribution of ICAM-1 on bone marrow progenitors, early precursor cells, and accessory cells in conjunction with the function of this molecule in cell-cell interactions suggests that ICAM-1 may play a role in the cell-cell and cell-stromal interactions that regulate hematopoiesis.

Distribution of intercellular-adhesion molecule-1 (ICAM-1) and lymphocyte-function-associated antigen-1 (LFA-1) in epidermal tumours

The cutaneous distributions of intercellular‐adhesion molecule‐1 (ICAM‐1) and lymphocyte‐function‐associated antigen‐1 (LFA‐1) in epidermal tumours were studied.

Distribution of intercellular adhesion molecule-1 (ICAM-1) in inflammatory liver disease

Distribution of intercellular adhesion molecule-1 (ICAM-1) in inflammatory liver disease