Search

Behcet’s disease (BD) is an auto-immune vasculitis, characterized by episodic inflammation of multiple organs. The neutrophil to lymphocyte ratio (NLR) is used as a marker of inflammation in several diseases nowadays. While nitric oxide (NO) seem to be involved in BD pathogenicity. Our study aims to investigate the NLR as an inflammatory marker of BD activity as well as to evaluate the relationship between the NO production and NLR in Algerian BD patients with different clinical manifestations before and under colchicine + corticosteroid treatment. For this purpose, we evaluated the NLR as the ratio of neutrophil count to lymphocyte count in naive and treated active BD patients with different clinical manifestations and in inactive ones. Furthermore, we assessed NO production by the Griess’ method in the same patients. Additionally, we evaluated in vivo interferon-γ (IFN-γ) and interleukin-4 (IL-4) levels using ELISA. Our results indicate that the NLR and nitrite levels were higher in naive active BD patients. Interestingly, this high ratio and NO production differed according to the clinical manifestations and was associated with an increased risk of mucocutaneous and vascular involvement. Importantly, in treated BD patients NLR was higher in active patients especially in those with mucocutaneous involvement while increased nitrites levels were regardless of the clinical manifestations studied. Both NLR and NO production decreased in these treated active patients. In addition, IL-4 production differed according to the clinical manifestations studied contrary to the IFN-γ production. Collectively our results suggest that the NLR is a potential marker of BD activity in Algerian patients, predicting the disease severity. Moreover, the positive relationship between the NLR and NO production is related to an increased risk of mucocutaneous lesions and vascular involvement. Thus, the application of these two accessible tools could be benefit for the clinical prognosis and treatment of BD.

Behcet disease (BD) is a chronic multisystem disease. It stands at the crossroads between the auto-immunity and auto-inflammatory disorders. Our study aims to evaluate corticosteroids therapy effects on serum immunoglobulin isotypes and anti-phospholipid auto-anti-body production in Algerian BD patients with different clinical manifestations. We evaluated serum immunoglobulin isotypes and anti-phospholipid (anti-cardiolipin, anti-β2glycoprotein I, anti-prothrombin) auto-anti-body production using Turbidimetric or Luminex platform assays. Our study was conducted in naive active BD patients and in corticosteroid-treated patients with different clinical manifestations. Our results indicate that IgM, IgG, and IgA levels were higher in naive active patients. The increase in sera isotypes did not differ according to the clinical manifestation, except for IgA production, which was associated with an increased risk of mucocutaneous and ocular involvement. Interestingly, in corticosteroid-treated active patients, no difference was reported between each clinical subgroup. Furthermore,anti-cardiolipin, anti-β2glycoprotein I and anti-prothrombin auto-anti-body levels were elevated in naive active patients. Contrary to anti-prothrombin, high anti-cardiolipin and anti-β2glycoprotein I, production differed according to the clinical manifestations and was associated with an increased risk of mucocutaneous and ocular involvement. Importantly, corticosteroid therapy significantly reduced these immune markers regardless of the clinical manifestations. Our results suggest that high IgA production could be a risk marker of uveitis in naive active patients. Moreover, concomitant high anti-cardiolipin, anti-β2glycoprotein I and anti-prothrombin production is related to an increased risk of mucocutaneous lesions, ocular and vascular involvement. Collectively, our data indicate the importance of evaluating the corticosteroid effect on immune responses associated with BD to ensure an adequate investigation of each related clinical manifestation.

Behcet’s disease (BD) is a chronic multisystemic inflammatory disease with complex etiopathogenesis. Th1-proinflammatory cytokines seem to be involved in its pathogenesis. Our current study aims to evaluate interleukin-18 (IL-18) and nitric oxide (NO) involvement in the development of different clinical manifestations of BD as well as to investigate the corticosteroid therapy effect on this production in Algerian patients. For this purpose, we evaluated in vivo and ex vivo IL-18, interferon-γ (IFN-γ) levels using ELISA and NO production by the Griess’ method in naive-active and corticosteroid-treated BD patients with different clinical manifestations. Additionally, we assessed CD40/CD40L expression by flow cytometrics assay in these groups of patients. Our results indicate that IL-18 and nitrite levels were higher in naive-active BD patients. Interestingly, this high production differed according to the clinical manifestations and was associated with an increased risk of mucocutaneous and vascular involvement. Concerning corticosteroid treated-active BD patients, no difference was observed in this production between each clinical subgroup. However, IFN-γ levels increased in all categories of active patients. Interestingly, corticosteroid therapy reduced significantly these inflammatory mediators regardless of the clinical manifestations studied. In addition, the CD40/CD40L expression differed according to the clinical presentations. Collectively, our results suggest that concomitant high production of IL-18 and NO in naive-active BD patients is related to an increased risk of mucocutaneous lesions and vascular involvement. Moreover, the relationship between these two inflammatory markers could constitute a predictable tool of BD clinical presentations and an early factor of therapy efficiency.

Behcet's disease (BD) is an inflammatory multisystemic disorder associated with orogenital ulcers, uveitis and skin lesions with unpredictable episodes of exacerbations and remissions. Even though several immunological and environmental factors contribute to BD progression, its ethiopathogenesis remains uncertain and elusive. Considered as one of the potent environmental factors that can increase prevalence of some autoimmune and inflammatory disorders, vitamin D deficiency has been linked to several diseases as BD. The aim of this study is to assess vitamin D status in Algerian BD patients and its relationship with disease activity. Immunomodulatory effect of this vitamin on nitric oxide (NO), inflammatory mediator, was also undertaken. Serum 25(OH) vitamin D levels were measured in healthy controls (HC), active and inactive BD patients with an electrochemiluminescence method. After treatment of HCs' and patients' peripheral blood mononuclear cells with different concentrations of vitamin D3, NO production was evaluated with Griess method, while inducible nitric oxide synthase (iNOS) and NF-κB expression with immunofluorescence test. A high decrease of vitamin D levels was noted in active BD patients compared to those of inactive stage and HC. However, a higher NO production was observed during active stage of BD compared to inactive one. In inactive BD, vitamin D levels correlates negatively with NO. Interestingly, vitamin D3 inhibits ex vivo NO production, iNOS and NF-κB expression in BD patients. In conclusion, vitamin D deficiency was associated with active BD. This vitamin down-modulates NO production in BD patients, suggesting that it may be considered as promising therapy modulating inflammation during BD.

The aim of the current study is to situate CDs expression (CD3+, CD4+, CD8+) and their relationship with IFNγ and NO production in Algerian patients with Behçet disease (n = 34 ). Our results revealed an elevated expression of T cells markers tested in patients in active stage of the disease in relation to IFNγ and NO increase levels. Most interestingly, we noted that CD4+/CD8+ expression correlated with IFNγ and NO production in active stage. In contrast, we observed a decrease of these mediators in inactive stage. Collectively, our results indicate a dependent relation between these parameters and inflammatory response associated with the evolutionary stage of the disease.