[A Case of Cytomegalovirus Reactivation after Chemoradiotherapy for Esophageal Cancer].

An 80-year-old man visited our hospital because of abdominal distension and epigastralgia. He was diagnosed esophageal cancer(Mt, SCC, T3N0M0, Stage Ⅱ). Because he was elderly, he received chemoradiotherapy(CRT)with S-1. At 54 Gy/27 Fr, he was admitted to the hospital because of cough exacerbation, fever, and food intake loss. A chest and abdominal CT showed a pneumonia pattern. First, antibiotics were started for suspected bacterial pneumonia. Nevertheless, elevation of inflammatory reactions and continuous fever were observed. As interstitial pneumonia was suspected, we started to administer an injection of prednisolone 60 mg. His respiratory symptoms were improved. However, we observed that disseminated erythema of the trunk spread throughout the body and liver enzymes further increased. As blood examination revealed elevated CMV-IgG antibody and C7-HRP positive, we diagnosed cytomegalovirus(CMV)reactivation. Administration of ganciclovir improved liver damage and disseminated erythema. He discharged our hospital while the steroid dose was reduced and valganciclovir continued administrating. The therapeutic effect of esophageal cancer was partial response(PR). We are following his symptoms and CT scan while adjusting the steroid dose. This is a rare case of CMV reactivation due to immunosuppression caused by steroids therapy during CRT against esophageal cancer. We should be aware of CMV infection during CRT and steroid therapy.

Suppressor of cytokine signaling-1 ameliorates dextran sulfate sodium-induced colitis in mice.

Inflammatory bowel disease (IBD) is a chronic disorder of the gastrointestinal tract. Although the etiology and pathogenesis of IBD remain unknown, pro-inflammatory cytokines including IFN-gamma play an important role in the development of IBD. Suppressor of cytokine signaling-1 (SOCS-1) is a crucial inhibitor of cytokine signaling, particularly of IFN-gamma. In this study, we investigated the role of SOCS-1 in the development of murine dextran sulfate sodium (DSS)-induced colitis, a model of colitis resembling human IBD. SOCS-1 heterozygous (SOCS-1(+/-)) and wild-type (WT) mice were given 3% DSS dissolved in drinking water for 5 days. Activation and expression of signal transducers and activators of transcription (STAT) in colonic tissues were assessed by western blot analysis. The expression of CD4, IFN-gamma, IL-4, IL-17 and Forkhead box P3 (Foxp3) in colonic lamina propria lymphocytes was analyzed by flow cytometry and cytokine concentrations in serum were measured. DSS-treated SOCS-1(+/-) mice developed more severe colitis than DSS-treated WT mice. Enhanced activation of STAT1, a higher ratio of CD4(+)IFN-gamma(+) T cells and a lower frequency of Foxp3(+) regulatory T (Treg) cells, were observed in the colon of DSS-treated SOCS-1(+/-) mice compared with DSS-treated WT mice. DSS-treated SOCS-1(+/-) mice showed higher levels of IFN-gamma in sera than did DSS-treated WT mice. Furthermore, T cell-specific SOCS-1-conditional knockout mice developed more severe colitis than control mice after DSS administration. Our findings suggest that SOCS-1, particularly in T cells, prevents the development of DSS-induced colitis in mice by inhibiting IFN-gamma/STAT1 signaling and by subsequently regulating Treg cell development.