Neutrophil elastase and endogenous inhibitors in Behçet’s disease saliva

Aim. Cytokines and chemokines may be involved in the onset of oral ulcer in Behcet’s disease. The aim of our study is to assess the cytotoxic effects of proinflammatory cytokines and chemokines on reconstructed oral mucosal cell line (TR146) when treated with different concentrations of neutrophil elastase (NE). Objective. For this purpose, a culture of the oral mucosal model (OMM) prepared from a cell line derived from an oral squamous cell carcinoma of buccal mucosa (TR146) is treated with different concentrations of neutrophil elastase. The cultures were incubated for 4- and 24-hour intervals and designed as follows: culture + artificial saliva served as the negative control; culture + 0.01% SLS (sodium lauryl sulphate) served as the positive control; and culture + NE (10, 50, 100, and 200 nM) served as the treated group. Materials and Methods. We used sandwich ELISA technique to isolate IL-1β (interleukin 1β), IL-8, and TNF-α (tumor necrosis factor). Results. We found no significant level of IL-8 and TNF-α when treated with different concentrations of neutrophil elastase after 4- and 24-hour incubation. The IL-1β level was slightly higher when treated with 100 and 200 nM NE after 24 hours of incubation although a significantly high level was observed at 100 nM NE after 4 hours of incubation. Hence, we found an increase in the level of IL-1β when stimulating the reconstructed oral mucosal model (OMM) with different concentrations of NE. This is a preliminary in vitro study; however, further research is required to evaluate the cytotoxic effects of cytokines and chemokines released when treated with NE. Moreover, high concentrations of NE are recommended to stimulate the release of cytokines and chemokines against the OMM.

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HLA antigens associated with Behcet's disease

Archives of Dermatology ◽

10.1001/archderm.113.12.1720 ◽

1977 ◽

Vol 113 (12) ◽

pp. 1720-1721 ◽

Cited By ~ 4

Author(s):

F. Ersoy

Keyword(s):

Behçet’S Disease ◽

Behcet’S Disease ◽

Behçet's Disease ◽

Hla Antigens ◽

Behcet's Disease

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Coagulation and Fibrinolytic Activity in Behçet's Disease

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646409 ◽

1991 ◽

Vol 66 (03) ◽

pp. 292-294 ◽

Cited By ~ 57

Author(s):

K K Hampton ◽

M A Chamberlain ◽

D K Menon ◽

J A Davies

Keyword(s):

Plasminogen Activator ◽

Tissue Plasminogen Activator ◽

Behçet’S Disease ◽

Fibrinolytic Activity ◽

Behcet’S Disease ◽

Behçet's Disease ◽

Plasminogen Activator Inhibitor ◽

Behcet's Disease ◽

Tissue Plasminogen ◽

Von Willebrand

SummaryCoagulation and fibrinolytic activities were studied in 18 subjects with Behçet's disease and compared with results from 14 matched control patients suffering from sero-negative arthritis. Significantly higher plasma concentrations (median and range) were found in Behçet's patients for the following variables: fibrinogen 3.7 (1.7-6.9) vs 3.0 (2.0-5.1) g/1, p <0.05; von Willebrand factor antigen, 115 (72-344) vs 74 (60-119)%, p <0.002; plasminogen activator activity (106/ECLT2) 219 (94-329) vs 137 (78-197) units, p <0.002; tissue plasminogen activator inhibitor (t-PA-I) activity, 9.1 (5.5-19.3) vs 5.1 (1.8-12.0) IU/ml, p <0.002; and PAI-1 antigen, 13.9 (4.5-20.9) vs 6.4 (2.4-11.1) ng/ml, p <0.002. Protein C antigen was significantly lower: 97 (70-183) vs 126 (96-220)%, p <0.02. No differences were observed in antithrombin III activity or antigen, factor VIII coagulant activity, fibrinopeptides A and Bβ15-42, plasminogen, α-2-antiplasmin, functional and immunological tissue-plasminogen activator, thrombin-antithrombin complexes and D-dimer. Levels of tissue plasminogen activator inhibitor (activity and antigen) correlated with disease activity while fibrinogen and von Willebrand factor concentrations did not. Seven of the 18 subjects with Behçet's disease had suffered thrombotic events but it was not possible to distinguish these from the 11 patients without thrombosis using the assays performed. The results suggest the abnormal fibrinolytic activity in Behçet's disease is due to increased inhibition of tissue plasminogen activator. No abnormality of coagulation or fibrinolytic activity specific to Behçet's disease was detected.

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