Induction of adhesion molecule expression on blood vessels and keratinocytes in recurrent oral ulceration

Adhesion molecules are known to play a crucial role in the recruitment of inflammatory cells to sites of inflammation. In this study endothelial cell and keratinocyte adhesion molecule expression in recurrent oral ulcers (ROU) ( n =13) was compared with that found in normal oral mucosa (NOM) ( n =11) and experimentally induced ulcers (EIU) ( n =5) by using immunohistochemistry. Significantly greater expression of both vascular cell adhesion molecule-1 (VCAM-1) and E-selectin was demonstrated on vasculature in ROU compared with that found in both NOM and EIU. Induction of keratinocyte intercellular adhesion molecule-1 (ICAM-1) was also a prominent feature of ROU. The expression of VCAM-1 and E-selectin on blood vessels in ROU is likely to be important in the accumulation of lymphocytes that characterise early aphthous lesions. The induction of keratinocyte ICAM-1 may facilitate lymphocyte invasion of the epithelium in ROU, which may ultimately result in ulcer formation.     

The role of LFA-1 in osteoclast development induced by co-cultures of mouse bone marrow cells and MC3T3-G2/PA6 cells

Interactions between leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) influence the development of osteoclasts. However, little is known about how these adhesion molecules are involved in the process of osteoclast development. This study evaluated the role of LFA-1 and its ligands in osteoclast development and bone resorption. Co-cultures of bone marrow cells from LFA-1-deficient mice and MC3T3-G2/PA6 (PA6) cells were cultured in the presence of 1alpha,25(OH)2D3 and dexamethasone for 7 days. The number of TRAP-positive cells that were generated by bone marrow cells from LFA-1-deficient mice was smaller than that generated by bone marrow cells from wild-type mice. In addition, the bone-resorbing activity of osteoclast-like cells that were generated from LFA-1-deficient mice was lower than that generated by osteoclast-like cells from wild-type mice. Immunofluorescence flow cytometry showed that osteoclast stromal PA6 cells expressed the cell adhesion molecules, ICAM-1 and VCAM-1. When monoclonal antibodies to mice VCAM-1, CD11b or CD18 were added separately to the co-culture system, the number of TRAP-positive cells that were generated from LFA-1-deficient mice was 20-30% smaller than that generated from wild-type mice. The formation of TRAP-positive cells from both LFA-1 deficient and wild-type mice was especially inhibited by anti-CD18 antibody, in comparison to the addition of normal IgG serum. These results suggest that LFA-1 adhesion molecules play a role in osteoclast development by affecting adhesion between stromal cells and osteoclast progenitors before the occurrence of ODF-ODF receptor signaling. CD18 appears to be a key adhesion molecule in cell-to-cell contacts during the early stage of osteoclast development.     

Immune-activation in recurrent oral ulcers (ROU).

Tissue specimens from eight patients with recurrent oral ulcers (ROU) were analyzed for possible signs of active lymphocyte involvement. A total of 13 specimens were analyzed, eight (8) taken at the ulcer site and five (5) from clinically unaffected mucosa at a site opposite the ulcer. Monoclonal antibodies or heterologous antisera were applied using the avidin-biotin-peroxidase complex (ABC) or peroxidase-antiperoxidase complex (PAP) methods to visualize cell-activation-associated marker proteins. In specimens from the ulcer area, approximately 43 +/- 18% of all inflammatory cells were positive for the MHC locus II coded Ia antigen. Furthermore, markers for cycling cells, interleukin-2 (CD25, 13 +/- 6%) and transferrin (CD71, 23 +/- 14%) receptors, were frequent in the specimens studied. Staining for CD1 (5 +/- 2%) disclosed dendritic intraepithelial cells in diseased and in clinically unaffected mucosa. Mobilization of such cells is suggested by their presence in submucosa in ROU specimens, but not in clinically unaffected mucosa. The presence of CD1 cells, presumably denoting their identity as potent antigen-presenting Lagerhans' cells, and the rich presence of Ia suggest that local conditions are favorable for induction of T-cell-mediated responses. The simultaneous presence in such infiltrates of activation marker positive T-cells suggests activation de facto. This together with the rarity of activated B-cells, i.e. plasmablasts/cells containing cytoplasmic immunoglobulin, suggests active involvement of the local cells of the T-lymphocyte lineage in the pathogenesis of ROU.     

Cellular adhesion molecules on periodontal lymphocytes

T cell induced differentiation of B cells has been shown to be dependent on the CD2/LFA-3 and LFA-1/ICAM-1 pathways. Flow cytometric analysis was used to examine these adhesion molecules on T and B cells extracted from gingival tissues before and after stimulation with the putative periodon-topathic bacteria, Porphyromonas gingivalis and Fusobacterium nucleatum. Adhesion molecule expression on peripheral blood cells from healthy adults was used as a control. Approximately 50 per cent of B cells extracted from gingival tissues expressed LFA-3 and ICAM-1 compared with 30 per cent positive peripheral blood B cells. Around 50 per cent of gingival T cells expressed CD2 relative to 76 per cent positive peripheral blood T cells. However, 40–50 per cent of both gingival and peripheral blood T cells expressed LFA-1. There was no difference in the expression of adhesion molecules on T and B cells extracted from health/marginal gingivitis or adult periodontitis lesions. After stimulation of gingival cells in vitro , the per cent CD2 positive T cells and LFA-3 and ICAM-1 positive B cells remained relatively stable over the six-day culture period, although P. gingivalis and F. nucleatum appeared to induce an increase in the percentage of gingival T cells expressing LFA-1. In contrast to the gingival lymphocytes, stimulation of peripheral blood cells resulted in an increase in the per cent CD2 positive T cells, LFA-3 and ICAM-1 positive B cells, with a decrease in LFA-1 positive T cells. The results therefore demonstrated that gingival T and B cells express adhesion molecules in vivo. Stimulation of these cells with periodontopathy bacteria failed to increase expression, suggesting not only that these cells are already activated in vivo , but also that their phenotype is consistent with cell-cell contact occurring in the gingival tissues. Whether or not this cell-cell contact is also antigen specific remains to be determined.     

Oral lichen planus: immunohistology of mucosal lesions.

BACKGROUND: Current evidence suggests that immunological mechanisms are involved in oral lichen planus (OLP) pathogenesis. The events implicate activated epithelia that comprise antigen-presenting Langerhans cells, immunocompetent keratinocytes and subepithelial inflammatory infiltrate. Also, the presence of a high density of leucocyte cells may occur for the expression of a variety of adhesion molecules. The aim of this study was to analyse the immunoexpression of some adhesion molecules as well as lymphocytic markers in order to determine the disease pathogenesis in a Venezuelan population. METHODS: The 18 OLP and 10 normal oral mucosa biopsies were immunostained for CD4, CD8, CD1a, LFA-1, VCAM-1 and ICAM-1. RESULTS: The results showed an increased number of CD4+, CD8+, CD1a+ cells in OLP. Serial sections showed CD4+ and CD8+ cells also expressed LFA-1. The expression of ICAM-1 and VCAM-1 were significantly higher in OLP. CONCLUSIONS: The immunological reaction begins with Langerhans cells activation, which presents an antigen to CD4+ lymphocytes. Those cells through ICAM-1 and LFA-1 promote epithelial destruction. Afterwards, cytokine production, ICAM-1 and VCAM-1 expression can activate CD8+ lymphocytes leading to the chronic form of the disease.     

Distribution of ICAM-1, LFA-3 and HLA-DR in healthy and diseased gingival tissues

Cell adhesion molecules are involved in recognition and effector aspects of the host response, including the control of migration of leukocytes into inflammatory sites. In this study we have demonstrated that the distribution of three cell-surface molecules involved in cell interactions, ICAM-1, LFA-3 and HLA-DR is distinct and different in healthy and diseased gingival tissue. ICAM-1 was consistently expressed by junctional epithelial cells in healthy gingiva and by pocket epithelium in diseased gingiva but was not detectable on the majority of keratinocytes in external gingival epithelium. ICAM-1 was also expressed by endothelial cells of gingival blood vessels and a subset of leukocytes in the infiltrated connective tissue in both healthy and diseased gingiva. HLA-DR and LFA-3 were also expressed by epithelial cells and endothelial cells but in patterns which were distinctly different from ICAM-1.     

Expression of the CD54 (ICAM-1) and CD11 a (LFA-1) adhesion molecules in oral mucosal inflammation

Previous studies of chronic dermatoses have suggested that expression of the CD54 cell surface antigen (intercellular adhesion molecule-1, ICAM-1) by keratinocytes is a feature of chronic inflammation. However, whether such expression is a prerequisite for intraepithelial migration of lymphocytes is unclear. The present study evaluated the expression of CD54 and its ligand, CD1 la (lymphocyte function-associated antigen, LFA-1) in oral lesions of lichen planus, recurrent aphthous stomatitis, secondary Sjögren's syndrome and traumatic ulceration using an immunoperoxidase technique. In 33 of 56 lesions examined, substantial numbers of CD1 la + cells were present within oral mucosal epithelium despite an absence of detectable keratinocyte CD54 antigen expression. Consequently, CD54/CD1 la adhesion interactions may not be critical in the initiation of oral mucosal inflammation.     

Induction and upregulation of adhesion receptors in oral and dermal lichen planus

The expression pattern of well-defined cell surface adhesion receptors called VLA-family, LFA-1 and ICAM-1 was determined semiquantitatively in biopsies of oral (n = 12) and dermal lichen planus (n = 5) and compared to normal uninvolved human oral mucosa (n = 12) and skin (n = 12) using an indirect immunoperoxidase technique. In both oral and dermal lichen planus, an induction of the beta 1-integrins VLA-1 and VLA-3 and an upregulation of VLA-6 was found in T cells infiltrating the basement membrane zone. These cell surface molecules function as receptors for collagen, fibronectin and laminin. A focal induction of ICAM-1 on basal keratinocytes could be detected at sites of intramucosal T cells. These results suggest that investigated adhesion receptors are crucially involved in the aggregation of T cells in both conditions. Further investigations have to be done to determine the functional role of these adhesion receptors in lichen planus.     

Expression of ICAM-1/LFA-1 in the pocket area of adult periodontitis]

OBJECTIVE: To study the expression of ICAM-1/LFA-1 in the pocket area of adult periodontitis. METHODS: Expressions of ICAM-1/LFA-1 in adult gingival of periodontitis and healthy subjects were studied by alkaline phosphorylase-antialkaline phosphorylase technique. RESULTS: Junctional epithelium and apical part of sulcus epithelium expressed ICAM-1 in both adult periodontitis and healthy gingiva, showing an ICAM-1 gradient change with maximal staining at tooth aspect and weaker staining in the basal layer of keratinocytes. Significantly more LFA-1 positive leukocytes were observed in connective tissues and within pocket epithelium in adult periodontitis than those in healthy gingiva. CONCLUSION: ICAM-1/LFA-1 may provide important adhesion pathway for leukocytes migration into gingiva sulcus in adult periodontitis lesions.     

环孢素A对成纤维细胞表达细胞间粘附分子1的影响

目的　观察环孢素A (cyclosporinA ,CSA)对体外培养的人类口腔粘膜成纤维细胞(fibroblasts ,FB)表达细胞间粘附分子 1 (intercellularadhesionmolecule 1 ,ICAM 1 )的影响 ,了解CSA治疗口腔粘膜疾病的可能机制。方法　从健康的人类口腔粘膜中培养出FB ,向培养基中加入不同浓度的CSA ,培养 48h后用细胞酶联免疫法检测FB的ICAM 1表达水平。结果　表示ICAM 1表达水平高低的A值在健康人口腔粘膜FB中为 0 32 4± 0 0 30 ,CSA在 0 0 75～ 0 30 0ng/L的范围内以浓度 效应依赖关系下调FB的ICAM 1表达水平。结论　CSA对FB表达ICAM 1的水平具有下调作用 ,提示CSA可能是通过下调ICAM 1的表达来减缓口腔粘膜的炎症反应 ,从而达到治疗口腔粘膜疾病的效果     

Expression of adhesion and activation molecules in human buccal epithelial cell lines and normal human buccal epithelium in situ

An in vitro culture system may be used to analyse interactions between T cells and epithelium. We have analysed two human buccal squamous epithelial cell lines: SqCC/Y1, derived from a buccal carcinoma, and SVpgC2a, an SV-transformed healthy buccal squamous epithelium. Under serum-free culture conditions, the cell lines resemble normal buccal squamous epithelium in situ in their expression of MHC class I, CD29 (beta1 integrin), CD40, CD44, CD54 (ICAM-1), CD58 (LFA-3), CD95 (Fas), and E-cadherin. Furthermore, when the SVpgC2a cell line was treated with T-cell derived cytokines, upregulation of CD40 expression was observed when the cells were treated with IL-4, whereas IFN-gamma caused upregulation in expression of CD40, CD54 and MHC class II. These buccal squamous epithelial cell lines, therefore, provide a good tool for analysing interactions between epithelium and T cells in vitro.     

Localized adhesion molecule expression and circulating LFA-3 levels in adult and early onset forms of periodontitis

Because of their importance in mediating cellular interactions in chronic inflammatory diseases, this study has examined the expression of a number of adhesion molecules in adult (n=11), generalized early onset (n=5) and localized early onset (n=2) forms of periodontitis. In comparison with immunostaining profiles of cryostat sections of healthy gingival tissue (n=7), the beta 1 integrins VLA-1, VLA-2 and VLA-4 were found to be up-regulated in periodontitis, with VLA-6 being markedly elevated. Although only small differences were observed in ICAM-1 and LFA-3 expression in the gingival epithelium, there was particularly notable up-regulation of these adhesion molecules within the inflammatory infiltrates of the diseased tissues. However, there were no statistically significant differences between the serum levels of a soluble form of LFA-3 in periodontitis patients (n=47) compared with healthy control subjects (n=40), although the generalized early onset and adult periodontitis groups exhibited wider ranges of circulating LFA-3. These findings show that there is localized modulation of adhesion molecule expression in the chronic inflammatory periodontal diseases studied, but that the levels of LFA-3 in the circulation nevertheless remain unaffected.     

The adhesion molecules NCAM, HCAM, PECAM-1 and ICAM-1 in normal salivary gland tissues and salivary gland malignancies

BACKGROUND: Some malignant salivary gland tumors are known for their propensity to exhibit perineural invasion and vascular metastases. It was hypothesized that alterations in the expression of cell adhesion molecules are involved in these processes. METHODS: The expression and distribution of neural cell adhesion molecule (NCAM), HCAM (CD44), platelet-endothelial cell adhesion molecule-1 (PECAM-1), and intercellular cell adhesion molecule-1 (ICAM-1) in normal salivary gland tissues and selected salivary gland malignancies, especially adenoid cystic carcinoma (AdCyCa) and polymorphous low-grade adenocarcinoma (PMLG), were determined immunohistochemically, and their influence on histologically demonstrated perineural invasion, vascular invasion, and tumor recurrence/patient death were investigated. RESULTS: NCAM, HCAM, and ICAM-1 were often found to be expressed by neoplastic cells, but no correlation to perineural invasion, tumor behavior, or patient prognosis was found. PECAM-1 was rarely and only focally expressed in three tumors, all of which were related to tumor metastases and patient death. CONCLUSIONS: Immunohistochemical demonstration of NCAM, HCAM, and ICAM-1 is not related to perineural invasion or tumor behavior. PECAM-1 expression was related to vascular invasion and poor patient prognosis in three cases.     

Immunoregulatory roles of adhesive interactions between lymphocytes and gingival fibroblasts

Chronic adult periodontitis is usually characterized by inflammatory cell accumulation in the extravascular periodontal connective tissue. In order to reveal how the lymphocyte migration and retention in periodontal lesions is regulated, we have focused on the molecular basis for the adhesive interactions between lymphocytes and human gingival fibroblasts (HGF). In this study, we investigated the involvement of cell adhesion molecules in adhesive interactions between lymphocytes and HGF. We found that activated lymphocytes bound strongly to HGF and VLA integrins, extracellular matrix receptors, play crucial roles in the binding. Interestingly, we first revealed that CD44 molecules (hyaluronate receptor) on lymphocytes also participated in lymphocyte-HGF interactions and that hyaluronate anchored on the surface of HGF functioned as the ligand for CD44. In addition. when HGF were stimulated with inflammatory cytokines such as IL-1. TNFα and IFNγ, the binding avidity between lymphocytes and HGF was significantly increased and the adhesion was mainly mediated by LFA-l/ICAM-1 pathway. We then examined the possibility whether lymphocyte-HGF interaction may cause activation of HGF. When HGF directly interacted with lymphocytes for 3 h, IL-lβ mRNA expression was clearly increased in HGF. These findings suggested that the adhesive interactions between lymphocytes and HGF was mediated at least by VLA integrins, LFA-l/ICAM-1 and CD44/hyaluronate and that the heterotypic cell-cell interactions could mutually cause intracellular signal transduction.     

Immune-activation in recurrent oral ulcers (ROU)

Tissue specimens from eight patients with recurrent oral ulcers (ROU) were analyzed for possible signs of active lymphocyte involvement. A total of 13 specimens were analyzed, eight (8) taken at the ulcer site and five (5) from clinically unaffected mucosa at a site opposite the ulcer. Monoclonal antibodies or heterologous antisera were applied using the avidin-biotin-peroxidase complex (ABC) or peroxidase-antiperoxidase complex (PAP) methods to visualize cell-activation-associated marker proteins. In specimens from the ulcer area, approximately 43 ± 18% of all inflammatory cells were positive for the MHC locus II coded Ia antigen. Furthermore, markers for cycling cells, interleukin-2 (CD25, 13 ± 6%) and transferrin (CD71, 23 ± 14%) receptors, were frequent in the specimens studied. Staining for CDI (5 ± 2%) disclosed dendritic intraepithelial cells in diseased and in clinically unaffected mucosa. Mobilization of such cells is suggested by their presence in submucosa in ROU specimens, but not in clinically unaffected mucosa. The presence of CD1 cells, presumably denoting their identity as potent antigen-presenting Lagerhans' cells, and the rich presence of Ia suggest that local conditions are favorable for induction of T-cell-mediated responses. The simultaneous presence in such infiltrates of activation marker positive T-cells suggests activation de facto. This together with the rarity of activated B-cells, i.e. plasmablasts/cells containing cytoplasmic immunoglobulin, suggests active involvement of the local cells of the T-lymphocyte lineage in the pathogenesis of ROU.     

Immune-inflammatory cells in recurrent oral ulcers (ROU)

Abstract— Tissue lesions from eight patients with recurrent oral ulcers (ROU) were subjected to detailed immunohistopathologic studies. In five patients, a specimen of an unaffected area from the opposite site was obtained. The main inflammatory cells in situ were CD3 positive T lymphocytes, with CD4 cells forming approximately half (range 30-60%) and CD8 cells 20% (range 10-30%) of all cells. CD19 positive B lymphocytes formed 5-12% of all cells. Furthermore, 45% (range 15-65%) of all lymphoid cells had signs of previous antigenous contact and had helper/inducer CDw29 type. Suppressor/inducer CD45R cells formed only about 20% (range 7-50%) of all cells. Although this observation suggests involvement of antigen as a causative and/or triggering stimulus, elements of a non-specific inflammatory response were observed as well. Endogenous peroxidase-positive neutrophils were present at the ulcer site, and were occasionally observed intravascularly and in th extracellular matrix in areas characterized by inflammatory mononuclear cell infiltrates. Although the proportion of endogenous peroxidase-positive, recently recruited monocytes was low, CD11b and nonspecific esterase-positive mature tissue macrophages formed about 14% (range 5-35%) of all inflammatory cells in situ, particularly at the periphery of the lymphoid cell infiltrates. Mast cells were also observed in all samples studied, forming 2-5% of inflammatory cells in the richly vascularized connective tissue beneath the basement membrane. In the specimens from clinically unaffected areas, inflammatory cells were rare. Our observations stress the multifaceted nature and participation of multiple effector systems in the local tissue pathogenesis of ROU.     

Immune-inflammatory cells in recurrent oral ulcers (ROU).

Tissue lesions from eight patients with recurrent oral ulcers (ROU) were subjected to detailed immunohistopathologic studies. In five patients, a specimen of an unaffected area from the opposite site was obtained. The main inflammatory cells in situ were CD3 positive T lymphocytes, with CD4 cells forming approximately half (range 30-60%) and CD8 cells 20% (range 10-30%) of all cells. CD19 positive B lymphocytes formed 5-12% of all cells. Furthermore, 45% (range 15-65%) of all lymphoid cells had signs of previous antigenous contact and had helper/inducer CDw29 type. Suppressor/inducer CD45R cells formed only about 20% (range 7-50%) of all cells. Although this observation suggests involvement of antigen as a causative and/or triggering stimulus, elements of a non-specific inflammatory response were observed as well. Endogenous peroxidase-positive neutrophils were present at the ulcer site, and were occasionally observed intravascularly and in the extracellular matrix in areas characterized by inflammatory mononuclear cell infiltrates. Although the proportion of endogenous peroxidase-positive, recently recruited monocytes was low, CD11b and nonspecific esterase-positive mature tissue macrophages formed about 14% (range 5-35%) of all inflammatory cells in situ, particularly at the periphery of the lymphoid cell infiltrates. Mast cells were also observed in all samples studied, forming 2-5% of inflammatory cells in the richly vascularized connective tissue beneath the basement membrane. In the specimens from clinically unaffected areas, inflammatory cells were rare. Our observations stress the multifaceted nature and participation of multiple effector systems in the local tissue pathogenesis of ROU.     

Adhesion molecule expression in chronic inflammatory periodontal disease tissue

Differences in lymphocyte populations have been demonstrated in gingivitis and periodontitis lesions. A differential expression of adhesion molecules may play a role in lymphocyte trafficking in these tissues. An indirect avidin biotin immunoperoxidase technique was used to stain a range of adhesion molecules in tissue sections of 21 gingival biopsies from both gingivitis and periodontitis subjects. These specimens were placed into three groups according to the size of the infiltrate. ICAM-1, PECAM-1 and LECAM-1 expression on mononuclear cells in the inflammatory infiltrates increased significantly with increasing size of infiltrate. Approximately 50% of these mononuclear cells were LFA-1 + and CD29+. When specimens were grouped according to their putative disease status there were no significant differences between mononuclear cell adhesion molecule expression in small infiltrates from either gingivitis or adult periodontitis subjects. This was also the case with larger lesions from both clinical groups. Therefore there does not appear to be a differential expression of adhesion molecules on lymphocytes in gingivitis and periodontitis tissue. Endothelial cells were positive for ICAM-1, PECAM-1, CD29, GMP-140 but negative for ELAM-1. Keratinocyte expression of ICAM-1 increased with increasing size of infiltrate although in heavy infiltrates, cells in the region of the junctional epithelium which were positive in small lesions, became ICAM-1 negative. The upper layers of the oral epithelium were positive for LECAM-1 in small infiltrates and with increasing size of infiltrate, the lower layers and many of the sulcular and junctional epithelium keratinocytes were positive. The basal epithelium and keratinocytes in the lower layers were CD29+ and in larger infiltrates, the upper layers were also positive. This study suggests that if specific homing of different lymphocyte clones occurs in gingivitis compared with periodontitis, this is not reflected in the pattern of adhesion molecule expression observed in this investigation. The present study may help to elucidate the roles played by endothelial cells and keratinocytes in lymphocyte trafficking in inflamed tissues.     

CD99 ligation induces intercellular cell adhesion molecule-1 expression and secretion in human gingival fibroblasts

ObjectiveTo examine CD99 expression and its functional role in ICAM-1 induction in human gingival fibroblasts (HGFs) and human gingival epithelial cells (HGECs) by activating cells with anti-CD99 monoclonal antibody, MT99/3.BackgroundEngagement of CD99 with agonistic antibodies has been shown to regulate immune responses, cell adhesion and migration, and cell death in several studies. Particularly, this engagement results in transendothelial migration of leukocytes mediated by intercellular adhesion molecule-1 (ICAM-1) induction in endothelial cells.MethodsTotal mRNA and protein were isolated from HGFs and HGECs for analyses of CD99 and ICAM-1 expression. Surface expression of CD99 and ICAM-1 was analysed by flow cytometry, and the detection of soluble ICAM-1 was assayed by immunoprecipitation and ELISA.ResultsCD99 surface expression was constitutive on HGFs to a greater extent than that on HGECs. CD99 ligation with MT99/3 induced ICAM-1 mRNA expression in HGFs, but not in HGECs. Interestingly, CD99 ligation led to an increased level of soluble ICAM-1 detected in culture supernatant, whereas interleukin-1β (IL-1β) treatment induced expression of membrane-bound ICAM-1. Furthermore, ICAM-1 induction by CD99 engagement was demonstrated to involve the activation of the p50 subunit of nuclear factor-kappaB (NF-κB), extracellular signal-regulated kinase, and p46 c-Jun N-terminal kinase that differed from that by IL-1β treatment.ConclusionOur study has shown the involvement of CD99 ligation in the up-regulation of ICAM-1 expression and its secretion in gingival fibroblasts, which may be essential for better understanding of the pathogenesis of periodontal disease.     

粘附分子在复发性口腔溃疡的发病机制中作用的探讨

目的：探讨可溶性血管内皮细胞粘附分子(sVCAM-1)、可溶性细胞间粘附分子(sICAM-1)在复发性口腔溃疡(recurrent oral ulceration，ROU)发病机制中的作用。方法：采用双抗体夹心酶联免疫吸附实验法检测血清中的sVCAM-1、sICAM-1浓度。结果：ROU患者的sVCAM-1浓度高于健康对照组，差异有显著性。ROU患者的sICAM-1浓度与健康对照组相比无显著性差异。sVCAM-1、sICAM-1两者浓度在活动期与静止期差异无显著性。结论：sVCAM-1在复发性口腔溃疡发病机制中可能有重要意义。