Amount of pollen has an effect on the systemic and local levels of soluble ICAM-1 in patients with seasonal allergic rhinitis

We investigated whether the amount of antigen has an effect on the systemic and local levels of soluble ICAM-1 (sICAM-1) in patients with pollinosis, and assessed its biologic significance. The levels of subjective symptoms and sICAM-1 in sera and nasal epithelial lining fluids (ELF) from 14 subjects with pollinosis (allergic group) and eight healthy subjects (control group) were measured from pre- to postseason in 1993 (total pollen count: 10854/cm²) and 1994 (total pollen count: 415/cm²), and the results were compared with each other among the four groups. The levels of subjective symptoms and sICAM-1 in ELF from the allergic group significantly increased during the season in both 1993 and 1994. However, there was a significant difference ( P < 0.01) between the levels of those in 1993 and those in 1994 during the season. The levels of sICAM-1 in sera from the allergic group were significantly upregulated during the seasons and postseasons only in 1993, and there was a significant difference ( P < 0.05) between the levels in 1993 and those in 1994 during the postseason. We conclude that amount of pollen has an influence on the local and systemic levels of sICAM-1, as well as the scores of subjective symptoms, in patients with seasonal allergic rhinitis.     

Elevation of serum soluble intercellular adhesion molecule-1 (sICAM-1) and sE-selectin levels in bronchial asthma.

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.     

Elevated levels of soluble ICAM-1 in sera from patients with bronchial asthma

We measured the levels of soluble intercellular adhesion molecule-1 (sICAM-1) in sera from patients with bronchial asthma. sICAM-1 levels in sera from atopic asthmatic patients in stable conditions were higher than in normal control subjects. Furthermore, the sICAM-1 levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These results suggest that higher levels of sICAM-1 in sera reflect the upregulation of ICAM-1 expression in allergic inflammation.     

Soluble intercellular adhesion molecule-1 (sICAM-1) in sera of patients with Graves' ophthalmopathy and thyroid diseases.

Intercellular adhesion molecule, a ligand for the leucocyte integrins CD11a/CD18 (LFA-1) and CD11b/CD18 (Mac-1), that plays an important role in a variety of inflammatory and immune-mediated mechanisms, is strongly expressed in retroocular connective tissue from patients with Graves' ophthalmopathy (GO) and involved in lymphocyte attachment to cultured retroocular fibroblasts via the ICAM-1/LFA-1-mediated pathway. Here, we report the detection and functional activity of a soluble form of the ICAM-1 molecule (sICAM-1) in sera from patients with GO and other thyroid diseases. Serum concentrations for sICAM-1 were determined using a highly sensitive ELISA. Compared with normal controls, patients with hyperthyroid or euthyroid GO and patients with Riedel's invasive fibrous thyroiditis revealed markedly elevated sICAM-1 serum concentrations (all P < 0.0001). In patients with Graves' disease (GD) without clinical GO and in patients with Hashimoto's thyroiditis (HT), sICAM-1 levels were elevated to a lesser degree (both P < 0.001). sICAM-1 serum levels in patients with non-autoimmune hyperthyroidism due to a toxic adenoma were not significantly different from normal controls. In a separate group of 12 patients with severe inflammatory GO, sICAM-1 serum levels markedly declined (P < 0.0001) within 3 months of glucocorticoid therapy in nine patients who responded to this form of treatment with a decrease in periorbital inflammation. In contrast, sICAM-1 serum levels remained unchanged in three patients with poor response to steroids and persistent inflammatory periorbital disease. When tested in a cell adhesion assay, GO sera containing elevated concentrations of sICAM-1 were found to enhance the attachment of peripheral blood mononuclear cells (PBMC) to interferon-gamma (IFN-gamma)-treated retroocular fibroblasts in a dose-dependent manner, up to a maximal stimulation of approximately 5.5-fold (P < 0.001). This effect was abolished by preabsorption of sera with a MoAb against ICAM-1 and inhibited, in a dose-dependent manner, by coincubation with increasing concentrations of purified sICAM-1. In conclusion, sICAM-1 concentrations are markedly elevated in sera from patients with GO, and changes in sICAM-1 serum levels during glucocorticoid therapy closely parallel changes in the degree of inflammation. Given the capacity of sICAM-1 to modulate the adhesion of lymphocytes to retroocular fibroblasts in vitro, sICAM-1 may play a role in the ongoing immune process within the connective tissue in GO.     

Intercellular adhesion molecule 1 and tumor necrosis factor alpha in asthma and persistent allergic rhinitis: relationship with disease severity.

BACKGROUND: Tumor necrosis factor alpha (TNF-alpha) is involved in the up-regulation of intercellular adhesion molecule 1 (ICAM-1). Allergic rhinitis is often associated with bronchial hyperresponsiveness. OBJECTIVE: We investigated the relationship between allergic airway disease severity and serum concentrations of soluble ICAM-1 (sICAM-1) and TNF-alpha and nasal expression of ICAM-1. METHODS: Serum concentrations of TNF-alpha and sICAM-1 were investigated in 85 adults with persistent rhinitis and 90 patients with asthma. Seventy patients with rhinitis were challenged with methacholine. Nasal biopsy for ICAM-1 expression was performed in 6 patients with moderate-severe rhinitis and in 6 patients with mild rhinitis. RESULTS: In patients with rhinitis, serum sICAM-1 concentrations were as follows: group without bronchial hyperresponsiveness (n = 29), 206.85 ng/mL; group with bronchial hyperresponsiveness but without asthma symptoms (n = 20), 233.39 ng/mL; and group with newly recognized asthma (n = 21), 260.06 ng/mL. The sICAM-1 level was significantly lower in patients with mild rhinitis (216.21 ng/mL) than in patients with moderate-severe rhinitis (244.08 ng/mL). Nasal ICAM-1 expression was significantly higher in the moderate-severe rhinitis group than in the mild rhinitis group. In patients with asthma, serum concentrations of sICAM-1 were as follows: patients with mild asthma, 272.8 ng/mL; patients with moderate asthma, 340.16 ng/mL; patients with severe asthma without oral corticosteroids therapy, 426.74 ng/mL; and patients with severe asthma with oral corticosteroids therapy, 314 ng/mL. The serum TNF-alphaa concentration differed between patients with rhinitis (n = 15) (1.065 pg/mL) and patients with asthma (n = 12) (3.46 pg/mL). Among patients with asthma, TNF-alpha concentrations were similar in all groups classified according to the disease severity. CONCLUSIONS: sICAM and ICAM-1 expression correlates with airways diseases severity.     

Elevated soluble tumor necrosis factor receptor levels in seasonal allergic rhinitis patients

In this study, we examined the symptom scores and tumor necrosis factor-alpha (TNF-alpha), p55 soluble tumor necrosis factor receptor (sTNFR1), and p75 soluble tumor necrosis factor receptor (sTNFR2) levels in the sera and nasal epithelial lining fluids (ELF) of 20 patients with Japanese cedar pollinosis from the pre- to the postseason period, and compared the results with those of 10 nonallergic control subjects. The symptom scores of the allergic subjects were significantly (P<0.01) higher than those of the nonallergic subjects during the early stage and mid-stage of the season. There were no statistical differences between the allergic and nonallergic subjects in the TNF-alpha levels in sera and ELF from the pre- to the postseason. In the allergic subjects, however, the levels of sTNFR1 and sTNFR2 in ELF were significantly elevated during the early stage (P<0.05) and mid-stage (P<0.01) of the season, whereas those in sera did not change from the pre- to the post-season period. The levels of TNF-alpha in ELF were more than 10 times higher than those in sera, whereas the levels of sTNFR1 and sTNFR2 in ELF were less than half of those in sera in the allergic and nonallergic subjects. These results suggest that sTNFR1 and sTNFR2 may play a role in the pathogenesis of nasal allergic reaction.     

CD11a expression and soluble ICAM-1 levels in peripheral blood in high-risk and overt type 1 diabetes subjects.

A pair of correspondent adhesion molecules: LFA-1 (CD11aCD18) and ICAM-1 (CD54) was shown to be involved in autoimmune insulitis in animal models. Anti-LFA-1 or anti-ICAM-1 monoclonal antibodies administered in vivo had a very strong preventive effect on the development of spontaneous diabetes with a marked reduction of insulitis. On the other hand elevated levels of the soluble form of ICAM-1 (sICAM-1) were documented in subjects at risk for type 1 diabetes. Recently sICAM-1 was shown to play an immunoregulatory role as an inhibitor of islet insulitis. The aim of the present study was to evaluate CD11a + mononuclear cells (lymphocytes and monocytes) and soluble sICAM-1 levels in the peripheral blood of subjects with preclinical and overt type 1 diabetes to assess their role in the development of the autoimmune process and their possible associations with the humoral autoimmune markers. The study was carried out in three groups of subjects: 26 first degree relatives of type 1 diabetes patients (prediabetics) with the combinations of autoantibodies against pancreatic B cells (ICA, GADA, IA-2A, IAA), 22 patients with a recent onset of type 1 diabetes and age and sex-matched 24 healthy volunteers (control group). We observed an increased fluorescence intensity of CD11a on mononuclear cells in overt diabetes subjects and a positive correlation between CD11a fluorescence intensity on monocytes and ICA titre. The highest sICAM-1 levels we obtained in the peripheral blood in the prediabetics in comparison to patients with clinical diabetes and the healthy controls. We found a positive correlation between slCAM-1 and values of ICA, GADA and a total number of antibodies present. In conclusion our study suggests that LFA-1 and sCAM-1 play an important role in the pathogenesis of type 1 diabetes. The assessment of the CD11a bearing monocytes and sICAM-1 levels are potential markers of the preclinical stage of the autoimmune diabetes, but further prospective studies in high risk diabetes type 1 subjects are needed.     

Soluble Intercellular Adhesion Molecule-1 (ICAM-1) Antigen in Patients with Rheumatoid Arthritis

Intercellular adhesion molecule-1 (ICAM-1), a member of the immunoglobulin supergene family, is known to play an important role in inflammatory diseases. Using a previously developed enzyme-linked immunosorbent assay (ELISA) with two monoclonal antibodies (MoAbs) against human ICAM-1, levels of soluble ICAM-1 (sICAM-1) were measured in sera from patients with collagen diseases and in synovial fluids (SF) from patients with rheumatoid arthritis (RA). Although the results did not demonstrate that RA and other collagen diseases, as a group, had significantly higher levels of sICAM-1 in sera as compared with healthy controls, 21 of 138 cases (15%) with collagen diseases and 11 out of 57 patients (19%) with RA clearly showed higher levels of sICAM-1 in the sera. Comparisons between RA patients of radiological stages I and II and between stage I and other stages showed significantly higher levels of sICAM-1 in the sera of patients in the latter stages. RA patients with vasculitis and/or pneumonitis showed significantly higher levels of sICAM-1 than those without vasculitis or pneumonitis. Significant correlations were demonstrated between sICAM-1 and the factors IgG-RF, IgM-RF, erythrocyte sedimentation rate (ESR) and TNF-α in sera of RA patients. In addition, it was noted that the levels of sICAM-1 in SF were as high as those in the sera of patients with RA.     

Reduction of soluble ICAM-1 levels in nasal secretion by H1-blockers in seasonal allergic rhinitis

ICAM-1, a transmembrane glycoprotein promoting adhesion in immunologic and inflammatory reactions, was found to be increased on nasal epithelial cells of patients with allergic rhinitis. Loratadinae, an H₁-Mocker, was found to reduce in vitro the expression of ICAM-1 on nasal epithelial cells. A double-blind, parallel-group study was carried out during the pollen season to compare the effect of two H₁-blockers, cetiraizine (10 mg OD) and loratadine (10 mg OD), on the release of soluble ICAM-1 in nasal secretions. A group of untreated patients was used as a control group. sICAM-1 was measured by enzyme immunoassay before and after 2 weeks of treatment. Symptoms were significantly decreased in the actively treated groups. sICAM-1 levels were unchanged in the control group but were significantly reduced in the two treated groups ( P <0.015, Wilcoxon's W test). This study shows that two H₁-blockers, loratadine and cetirizinae, have a similar effect on sICAM-1 released in nasal secretions during the pollen season.     

Effect of glucocorticosteroids on tumour necrosis factor-α-induced intercellular adhesion molecule-1 expression in cultured primary human nasal epithelial cells

OBJECTIVE: In order to confirm the direct effect of glucocorticosteroids on epithelial intercellular adhesion molecule-1 (ICAM-1) expression, we examined ICAM-1 expression on primary cultured human nasal epithelial cells (HNECs) at both protein and mRNA levels. MATERIAL AND METHODS: HNECs were stimulated with recombinant human TNF-alpha (20 pg/mL-20 ng/mL) for specified time periods (0, 12, 24, and 48 h) and ICAM-1 mRNA and the soluble ICAM-1 (sICAM-1) concentrations were measured by quantitative RT-PCR and ELISA, respectively. We also evaluated surface expression of ICAM-1 by flow cytometry 48 h after stimulation and determined the effect of dexamethasone (DEX) on TNF-alpha-induced ICAM-1 expression. RESULTS: Significant increases in ICAM-1 gene expression in HNECs were initially detected at 24 h, peaking at 48 h after the stimulation. The TNF-mediated-ICAM-1 mRNA and ICAM-1 surface expression at 48 h was significantly inhibited by co-incubation with human recombinant soluble TNF receptor I. Similarly, TNF-alpha-induced release sICAM-1 occurred in a time- and concentration-dependent manner. DEX 10(-6) M attenuated the TNF-alpha-induced ICAM-1 expression at mRNA and protein levels. CONCLUSIONS: Our finding suggests a potential role for topical steroids in allergic rhinitis in suppressing inflammatory reactions in the nasal mucosa by regulating ICAM-1 expression on nasal epithelium.     

Soluble intercellular adhesion molecules in human schistosomiasis: correlations with disease severity and decreased responsiveness to egg antigens.

Granuloma formation, the principal pathologic consequence of infection with Schistosoma mansoni, is a complex process involving intricate cell-cell interactions in which intercellular adhesion molecules are likely to participate. To examine this possibility, sera of schistosomiasis patients in various clinical groups were assayed for the presence of soluble intercellular adhesion molecule 1 (sICAM-1) and soluble E-selectin (sE-selectin). Comparisons were made between groups with different infection intensities (as predicted by fecal egg count) as well as between groups with severe (hepatosplenic) or milder (intestinal) pathology. All groups had elevated levels of sICAM-1 compared with controls. Also, patients in the high egg-excreting and hepatosplenic groups had significantly higher levels of serum sICAM-1 than patients in the low-egg-excreting and intestinal groups, respectively. The levels of sE-selectin were significantly elevated in the sera of all patients except those in the hepatosplenic group compared with controls. Patients in the intestinal group had significantly higher levels of sE-selectin in their sera than did hepatosplenic group patients, but serum sE-selectin levels of high- and low-egg-excreting patients were comparable. A striking finding of this study was the inverse correlation observed between sICAM-1 levels and peripheral blood mononuclear cell responses to schistosome soluble egg antigens (SEA) but not with responses to other schistosome antigens, purified protein derivative, or mitogen. Because ICAM-1 can perform a costimulatory function in antigen-presenting cell-T cell interactions, it is possible that shedding of ICAM-1 in the granuloma microenvironment interrupts proper costimulation, leading to unresponsive SEA-specific T cells. In this way, sICAM-1 could be one factor contributing to the observed modulation of cellular responses to SEA in chronic human schistosomiasis.     

Mechanism of topical glucocorticoid treatment of hay fever: IL-5 and eosinophil activation during natural allergen exposure are suppressed, but IL-4, IL-6, and IgE antibody production are unaffected

BACKGROUND: Allergic rhinitis is traditionally defined as an IgE- and mast cell-mediated hypersensitivity reaction. Allergen challenge models suggest that cytokines and eosinophil mediators may also play roles. However, the causal relationship among inflammatory cells, their products, and patients' symptoms during natural allergen exposure has not been established. OBJECTIVE: We sought to elucidate the mechanisms of seasonal allergic rhinitis and the beneficial effects of topical glucocorticoids. METHODS: Thirty patients with ragweed-induced hay fever and a strongly positive serologic test response for ragweed IgE antibody received budesonide nasal spray or placebo in a randomized, parallel, double-blind study. Nasal wash fluids and sera were collected before and during the hay fever season. The levels of inflammatory mediators and allergen-specific immunoglobulins were measured by immunoassay. The activation markers on blood eosinophils were quantitated by flow cytometry. RESULTS: Compared with placebo-treated patients, budesonide-treated patients had strikingly reduced symptoms. In the placebo group, nasal symptoms correlated with nasal lavage fluid eosinophil-derived neurotoxin and IL-5 levels. At the season peak, the budesonide-treated group had significantly lower nasal fluid eosinophil-derived neurotoxin, IL-5, and soluble intracellular adhesion molecule-1 levels. In the treated group eosinophil expression of CD11b was suppressed at the season peak. In contrast, levels of IL-4 and IL-6 in nasal fluid and the seasonal increases in serum ragweed-specific IgE and nasal fluid IgA antibodies did not differ between groups. CONCLUSION: Eosinophilic inflammation plays a critical role in seasonal allergic rhinitis symptoms. One of the therapeutic effects of glucocorticoids is to suppress this inflammation.     

Expression of ICAM-1 on conjunctival epithelium and ECP in tears and serum from children with allergic conjunctivitis.

BACKGROUND: Conjunctival eosinophilia may be considered to be an indicator of conjunctival allergic disease. The absence of eosinophils on conjunctival scraping, however, cannot rule out the diagnosis of allergic conjunctivitis because eosinophil infiltration may be deeper in conjunctival tissue. Eosinophil cationic protein (ECP) is a toxic product secreted by activated eosinophil as a marker of eosinophil activation. Eosinophil cationic protein concentrations in body fluids correlate with the severity of some allergic diseases. ICAM-1 promotes adhesion of leukocytes to epithelium, endothelium, and upregulates inflammation. Expression of adhesion can be modified by many extracellular and intracellular variables such as proinflammatory cytokines, extracellular matrix proteins, and viral infection. OBJECTIVE: We investigated whether local eosinophils are only activated in conjunctival epithelium or circulating activated eosinophils are involved in peripheral blood during allergic reaction of the eye. We also demonstrated the possible expression of ICAM-1 on epithelial cells from conjunctival scraping and compared them with soluble ICAM-1 values of serum and tears in children with allergic conjunctivitis and healthy children. METHODS: Seventeen subjects were selected on the basis of clinical manifestations, history, skin prick test, and total serum IgE. A microcapillary tube was used to collect the tears from the inner canthus. Conjunctival epithelia were obtained by scraping the upper tarsal conjunctiva. The level of ECP was measured by the CAP system, soluble ICAM-1 was measured by ELISA, and ICAM-1 on conjunctival epithelial cells were expressed by the avidine-biotin peroxide complex procedure. RESULTS: Serum IgE and the eosinophil count were increased in 10 out of 17 patients, positive skin prick tests were positive in 11 patients (Dermatophagoides pternyssinus; 9, Dermatophagoides farinae: 8), and eosinophilia in conjunctival epithelium was in 11 patients (4 patients: >3/HPF, 7 patients: 1-3/HPF). The ECP levels in tears were significantly increased in the patient group (12.0+/-8.0 versus 3.9+/-3.8 microg/mL, P = .01), but not in serum (52.5+/-43.1 versus 28.3+/-25.9 microg/mL). There is significant correlation between the eosinophil count in peripheral blood and on conjunctival epithelium (P = .007, r = .62; n = 25). The ICAM-1 expression score on conjunctival epithelial cells was significantly different between the patient group and controls (patient group: 1.77+/-1.25 versus control: 0.13+/-0.35 ng/mL, P = .002). There was a significant correlation between ICAM-1 expression on conjunctival epithelial cells and the ECP levels of tears (P = .01, r = .58; n = 25). Soluble ICAM-1 levels in serum and tears showed no significant difference between the patient group and controls, and also, there was no correlation between sICAM-1 levels in the serum and tears. CONCLUSION: Eosinophil cationic protein in tears and ICAM-1 expression scores on conjunctival epithelium showed a significant difference between children with allergic conjunctivitis and the healthy controls, but circulating ECP and sICAM-1 in serum were not significantly different between the two groups. These results may suggest that ICAM-1 is locally upregulated in inflammation, mediating eosinophil activation and migration to conjunctival epithelium, but is not involved as inflammatory mediators in peripheral blood during allergic response in children with allergic conjunctivitis.     

Effect of cytokine-induced soluble ICAM-1 from human synovial cells on synovial cell-lymphocyte adhesion.

The present study was designed to establish (i) the effects of cytokines on soluble ICAM-1 (sICAM-1) production by human synovial cells (SC) and ICAM-1 expression on these cells, and (ii) the effects of sICAM-1 on lymphocyte-SC adhesion. sICAM-1 production was enhanced in parallel with ICAM-1 expression by IL-1 beta, TNF-alpha and IFN-gamma. IL-4 showed no effects on ICAM-1 expression. In contrast with the transient elevation of cell-associated ICAM-1 by IL-1 beta, which peaked 36 h after stimulation and declined thereafter, sICAM-1 continued to accumulate in culture supernatants even after 48 h. Purified sICAM-1 was obtained from a 48 h culture synovial cell supernatant by affinity chromatography using ICAM-1 monoclonal antibody. The purified sICAM-1 significantly inhibited adhesion of lymphocytes and monocytes to cytokine-stimulated synovial cells. These results suggest that sICAM-1 may modulate chronic synovitis by inhibiting ICAM-1-mediated cell-to-cell adhesion.     

Soluble intercellular adhesion molecule-1 (ICAM-1) in sera and bronchoalveolar lavage (BAL) fluids of extrinsic allergic alveolitis.

ICAM-1 plays an important role in inflammatory diseases. We analysed ICAM-1 expression on BAL fluid cells and measured soluble ICAM-1 (sICAM-1) concentrations in sera and BAL fluids from patients with extrinsic allergic alveolitis (EAA). We found significantly increased cellular ICAM-1 expression on BAL fluid lymphocytes and alveolar macrophages, and significantly increased values of circulating and BAL fluid sICAM-1 in EAA patients compared with controls. Successive measurement showed prompt decrease of both sICAM-1 values in EAA patients during periods when antigen exposure was prevented. In BAL fluids from EAA patients, sICAM-1 values significantly correlated to neutrophil and ICAM-1+ lymphocyte counts. In EAA patients, circulating and BAL fluid sICAM-1 values has significant negative correlations to values of carbon monoxide diffusing capacity and to time intervals between last episode and sample collection. However, these values had significant positive correlation to values of alveolar-arterial oxygen pressure difference. In EAA, antigen exposure appears to induce cellular ICAM-1 expression on BAL fluid cells, and also appears to up-regulate shedding of ICAM-1 in the alveolar lining fluid and in the circulation. The sICAM values appear to reflect disease activity of EAA.     

Relationship between IL-18 and sICAM-1 serum levels in patients affected by coeliac disease: preliminary considerations

OBJECTIVES: Cytokine production from activated T cells play a pathogenetic role in mucosal lesions of coeliac disease (CD). Active interleukin (IL)-18 is expressed in the small intestinal mucosa in CD but not in healthy controls. IL-18 enhances intercellular adhesion molecule-1 (ICAM-1) expression. We analyzed IL-18 serum levels in CD patients before and after gluten-free diet and the possible correlation with soluble ICAM-1 (sICAM-1) serum levels. METHODS: The study comprises ten CD patients before and after gluten free diet and ten healthy controls. Serum IL-18 and sICAM-1 levels were assayed by immunoenzymatic methods. RESULTS: Serum IL-18 and sICAM-1 levels were significantly higher in patients with CD before diet with respect to healthy controls (P<0.05), with a highly significant correlation between the two parameters (Rho=0.800, P=0.0167). Gluten free diet significantly reduces IL-18 and sICAM-1. CONCLUSION: Our findings show that IL-18 serum concentrations correlated with the clinical status of CD patients suggesting a role for this cytokine in the pathophysiology of this disease.     

Inhibition of adhesion molecules by budesonide on a human epithelial cell line (lung carcinoma)

Inhaled corticosteroids in the treatment of asthma have been shown to produce marked reductions in the number of inflammatory cells (mainly mast cells and eosinophils) and their products at bronchial level (such as cytokines). Recently, it has been demonstrated that epithelial cells express ICAM-1/CD54 in allergic patients both during natural allergen exposure and after allergen challenge. We have previously demonstrated that deflazacort (a systemic steroid) reduces the expression of ICAM-1 on conjunctival epithelial cells. The present study aimed to evaluate the effects exerted by budesonide on adhesion molecule expression by a human epithelial cell line (lung carcinoma: DM) and on soluble ICAM-1. Budesonide was added at concentrations corresponding to 10⁻⁸, 10⁻⁷, and 10⁻⁶ mol/1 in cultured epithelial cells, either in the absence of any stimulus or in the presence of interferon-gamma (IFN-y) at 500 U/ml. After 24 h of incubation, cytofluorometric analysis was performed for ICAM-1 and CD29/VLAP1. The 24–h supernatants of the same cultures were collected and then evaluated for soluble ICAM-1 (sICAM-1). The results showed that budesonide inhibits ICAM-1 and CD29 basal expression on the cells studied (P<0.05): budesonide was effective in a dose-dependent manner. In addition, budesonide reduced surface ICAM-1 upregulation induced by IFN-γ at 500 U/ml (p<0.05). Finally, cell cultures with budesonide showed decreased levels of soluble ICAM-1 in basal condition, but not after IFN-γ stimulation.     

Soluble intercellular adhesion molecule-1 in sera of children with bronchial asthma exacerbation.

Previous studies have suggested that intercellular adhesion molecule-1 (ICAM-1; CD54) may be involved in the pathogenesis of asthma. In addition, a soluble form of intercellular adhesion molecule-1 (sICAM-1) has been detected in increased concentrations in the sera from adult patients with certain inflammatory, immune, or malignant diseases. To determine whether bronchial asthma exacerbation in children is associated with increased levels of serum sICAM-1 and to investigate the effect of the severity of exacerbation on these levels, the concentrations of sICAM-1 were measured in sera of 20 healthy control children and 45 asthmatic children (15 with mild, 15 with moderate, and 15 with severe asthma exacerbation) using an immunoenzymatic assay. Assessment of the severity of asthma exacerbation was based on clinical and physiological parameters. The mean (+/- SD) level of serum sICAM-1 for asthmatic children (390.0+/-108.3 ng/ml) was significantly higher than that for healthy (193.2+/-33.95 ng/ml; p = 0.000). We have also found a differential rise of serum sICAM-1 level which correlates well with the severity of asthma exacerbation. The elevated concentrations of serum sICAM-1 in acute bronchial asthma may reflect the extensive inflammatory response occurring in the airways during acute exacerbation of the disease with airway obstruction. The results of this study suggest that serum sICAM-1 is a promising serological marker of the severity of inflammation in bronchial asthma in children and it would not only facilitate staging of inflammation but also allow the monitoring of therapy and intervention.     

Levels of soluble ICAM-1 in atopic dermatitis A new marker for monitoring the clinical activity?

Levels of soluble intercellular adhesion molecule-1 (sICAM-1) were measured in sera from patients with an acute exacerbation of their atopic dermatitis (AD) ( n = 16) on admission to and discharge from our department of dermatology. At admission, the sICAM-1 levels in sera from patients with AD were slightly higher than those of the blood donors ( n = 100) and dropped at discharge significantly ( P = 0.014) after improvement of the skin conditions. Therefore, sICAM-1 may be, together with soluble interleukin-2 receptor (sIL-2), eosinophilic cationic protein (ECP), and CD14, another marker for monitoring AD.     

Graves''病患者外周血ICAM-1水平与疾病免疫状态间的关系

目的探讨Graves'病患者外周血细胞间粘附分子-1（ICAM-1） 水平与机体免疫状态间的关系。方法用流式细胞术测定34例Graves'病（ GD）患者治疗前外周血淋巴细胞膜上细胞间粘附分子-1（CD54 ）、CD4 、CD3 、CD 8 、CD19 、CD25 （可溶性白介素-2受体）的表达水平，用ELISA 方法测定其血清 中可溶性细胞间粘附分子-1（sICAM-1）的浓度，同时测定该病患者的其它体液免疫指标(TsAb、TGAb、TpoAb），并和22例正常对照人群进行各指标间的比较；细胞间粘附分子-1水平与机体其它免疫指标间做相关分析。结果Graves'病患者血 清可溶性细胞间粘附分子-1水平明显高于对照人群(P<0.001)，与细胞免疫指标中 的CD4 水平呈负相关(n=34,r=-0.503,P<0.005)；但与其它细胞免疫指标和 体液免疫指标间无相关关 系 ，外周血淋巴细胞膜上细胞间粘附分子-1的表达水平和正常对照组间无差异。结论 sICAM-1在未治疗的GD病患者中是升高的，其升高与体液免疫指标不相关，与细 胞免疫指标有一定关系。因此，sICAM-1可能是不同于体液免疫指标的一项新型免疫指标， 它不同程度地反映着细胞免疫水平。