Behcet's disease is a chronic, multisystem, inflammatory disease of unknown etiology. Oral ulcers, genital ulcers, cutaneous lesions, and ocular and articular involvement are the prominent features of the disease. The aim of the study was to assess expression of microRNA-146a and its gene polymorphism in Egyptian Behcet's disease (BD) patients and to evaluate their possible relation with clinical manifestations and activity. This is a case-control study, included 47 BD Egyptian patients, recruited from the Rheumatology outpatient clinic, Kasr Alainy Hospital, Cairo University Hospitals, and 50 healthy controls. BD activity was assessed using the BD Current Activity Score. Quantitative expressions of serum microRNA-146a and microRNA-146a rs2910164 SNP genotyping were performed by real-time polymerase chain reaction (RT-PCR). P values < 0.05 were considered statistically significant. Serum microRNA-146a expression was significantly higher in BD patients than in controls (7. 27 ± 4.11, 1.13 ± .37) (P < 0.001). There was a significant association between microRNA-146a expression and eye activity (P = 0.033) and vascular activity (P = 0.041). miRNA-146a rs2910164 genotyping revealed that the frequency of CC genotype was higher in controls (12 vs 8.5%) and the frequency of GG genotype of rs2910164 was higher in the BD patients (59.6 vs 24%) (P = 0.138). MicroRNA-146a expression in Egyptian BD patients is significantly higher than that in controls; there is significant association between microRNA-146a expression and eye and vascular activity of BD. The frequency of CC genotype of rs2910164 was decreased; frequency of GG genotype of rs2910164 was increased in BD patients as compared to controls, suggesting that GG genotype of rs2910164 confers susceptibility to BD while CC genotype has a protective role against BD development.

Both hydrogen sulfide (H2S) and mesenchymal stem cells (MSCs) extracted microvesicles (MVs) are potent anti‐inflammatory molecules. They play an essential role in lowering the production of tumor necrosis factor‐alpha (TNF‐α). The latter could strongly stimulate MiR‐155 that contributes to neurodegeneration and Alzheimer's disease (AD). miR‐155 could repress the expression of inositol 5‐phosphatase‐1 (SHIP‐1) leading eventually to activation of Akt kinase and neurofibrillary development in AD. The current study was conducted to evaluate the role of miR‐155 in a rat model of lipopolysaccharide (LPS)‐induced AD and to investigate the effect of using MVs and H2S that were given either separately or combined in regulating pro‐inflammatory signaling. Thirty female Wistar albino rats aged 6 months to 1 year were equally divided into five groups; control group, LPS‐induced AD group, LPS + MVs group, LPS + NaHS group, and LPS + MVs and NaHS group. The increased miR‐155 level was associated with decreased SHIP‐1 level and positively correlated with TNF‐α. In addition, treatment with MVs and/or NaHS resulted in attenuation of inflammation, decreasing miR‐155, pAkt levels, and downregulation of apoptosis along with improvement of the hippocampal and cortical histopathological alterations. LPS enhanced production of malondialdehyde (MDA) and reduced glutathione (GSH) levels indicating oxidative stress‐induced neural damage, whereas MVs and NaHS could mitigate oxidative damage and accelerate antioxidant capacity via increasing catalase enzyme. In conclusion, downregulation of TNF‐α, miR‐155, and pAkt and increased SHIP‐1 could improve the neuro‐inflammatory state and cognitive function of LPS‐induced Alzheimer's disease.

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