Imene Ben Dhifallah; Afshin Borhani-Haghighi; Agnes Hamzaoui; Kamel Hamzaoui
Abstract
Background: Behçet's disease (BD) is a systemic inflammatory disease with a chronic, relapsing-remitting course of unknown etiology. Neuro-Behcet’s disease (NBD) induce serious CNS complications and are known to be the main cause of long-term morbidity and mortality. IL‐37 is a natural ...
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Background: Behçet's disease (BD) is a systemic inflammatory disease with a chronic, relapsing-remitting course of unknown etiology. Neuro-Behcet’s disease (NBD) induce serious CNS complications and are known to be the main cause of long-term morbidity and mortality. IL‐37 is a natural suppressor of innate inflammation which its role in NBD has not been fully understood. Objective: To determine the expression of IL-37 in cerebrospinal fluid (CSF) and its relationship with other inflammatory cytokines. Methods: Level of IL-37, IL-6, IL-17, IL-21, TSLP and TGF-β were measured in CSF of 22 patients with NBD and 12 non-inflammatory neurological disease (NIND) and 10 headache attributed to Behçet's disease (HaBD) by enzyme‐linked immunosorbent assay (ELISA). In addition, IL-37 mRNA relative expression was detected by quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR). Results: CSF level and mRNA expression of IL‐37 were elevated in NBD patients compared to those in NIND and HaBD patients. Levels of IL-6, IL-17, IL-21 and TSLP were found to be increased in NBD patients and were inversely associated with IL-37 level. Moreover, TGF-β level in CSF of NBD patients was positively correlated with IL-37 levels. IL-37 increased significantly after treatment and in remission group, but TGF-β was only increased in treatment group. Conclusion: IL‐37 expression increased in NBD patients, and correlated with disease activity. Our data conclude that IL-37 could be a disease marker in NBD, however it requires further studies.
Sadegh Izadi; Afshin Borhani-Haghighi; Kamal Bastani; Bahareh Kardeh; Golnaz Yadollahi-Khales; Mojtaba Neydavoodi
Abstract
Background: Cerebral sinovenous thrombosis (CSVT) is a neurovascular disorder that occurs when a blood clot develops in a vein near the brain. Evaluating the subsequent changes in inflammatory cytokines can better reveal the underlying pathogeneses. Objective: To assess the serum levels of interleukin-10 ...
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Background: Cerebral sinovenous thrombosis (CSVT) is a neurovascular disorder that occurs when a blood clot develops in a vein near the brain. Evaluating the subsequent changes in inflammatory cytokines can better reveal the underlying pathogeneses. Objective: To assess the serum levels of interleukin-10 (an anti-inflammatory cytokine) and IL-17 (a pro-inflammatory cytokine) in patients with aseptic non-vasculitic CSVT. Methods: In this prospective case-control study, 31 patients with aseptic non-vasculitic CSVT (admitted in Namazi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran) were enrolled. IL-10 and IL-17 serum levels were measured at diagnosis, before initiation of treatment (acute stage), 3 months later (subacute stage). These cytokines were also measured in samples obtained from 30 gender- and age-matched healthy subjects, which were considered as control values. Results: Patients’ IL-10 and IL-17 levels were higher in both acute and subacute stages as compared to controls. However, no significant differences existed between the acute stage and control groups for both cytokines. Moreover, subacute levels were significantly higher than their acute and control levels. Conclusion: This study demonstrated the alteration of IL-10 and IL-17 levels in aseptic non-vasculitic CSVT. The rise in subacute IL-10 can be explained by the assumption that IL-10 is released as an anti-inflammatory response to subside the effects of IL-17 mediated reactions. More importantly, the immediate sampling in the acute stage did not allow enough time for triggering the immune system to produce such mediators. However, a balance was established between IL-10 and IL-17 in the subacute stage to prevent further tissue damage.
