Combination therapy of infliximab and thalidomide for refractory entero-Behcet's disease: a case report.

BACKGROUND: Behcet's disease (BD) is a systemic inflammatory disease with the histopathological features of leukocytoclastic vasculitis that affects nearly all organs and systems. When it involves the intestine, it is called entero-Behcet's disease (entero-BD). CASE PRESENTATION: Here we described a 23-year-old man with entero-BD refractory to conventional therapies who responded well to the combination therapy of infliximab, an anti-tumor-necrosis-factor (TNF)-alpha antibody, and thalidomide. After combination treatment, the patient's symptoms improved greatly and his Crohn's Disease Activity Index (CDAI) score decreased from 344 to 52 points, accompanied by a body weight increase from 53 kg to 64 kg. A follow-up endoscopy performed 10 weeks after the treatment showed significant improvement and the patient's multiple ulcers had healed well. CONCLUSION: The combination therapy of infliximab and thalidomide appears to be clinically effective in a patient with refractory entero-BD. However, further studies need to be performed to evaluate the efficacy of this combination therapy.

miR-224 suppresses HBV replication posttranscriptionally through inhibiting SIRT1-mediated autophagy.

Hepatitis B virus (HBV) enters the host and successfully completes replication by using several mechanisms, including autophagy. However, previous studies revealed that microRNAs (miRNAs) widely participate in regulation of various cellular processes, such as autophagy and viral replication. Hence, the purpose of this study was to investigate the role of miR-224 in HBV infection and to determine whether its role depended on the miR-224/SIRT1/autophagy axis. Our results show that secretions of HBeAg and HBsAg, and HBV replication significantly declined in Huh7-1.3 cells, established by transfecting recombinant pcDNA 3.0-1.3 mer containing the 1.3 mer fragment of HBV genomic DNA,with miR-224 mimic transfection as compared to the Huh7-1.3 group. Moreover, it was discovered that HBV could induce autophagy, while miR-224 inhibited autophagy caused by HBV. Additionally, miR-224 could suppress SIRT1, LC3 expression, and facilitate p62 expression. SIRT1 was identified as the target gene of miR-224 and down-regulation of SIRT1 via miR-224 or si-SIRT1 transfected treatment in Huh7-1.3 cells repressed LC3 expression and enhanced p62 expression. In conclusion, these results suggest that miR-224 might hinder HBV replication through attenuating SIRT1-mediated autophagy, thereby these findings open a new avenue for the treatment of HBV infection.