Lactobacillus casei cell wall extract directly stimulates the expression of COX2 independent of Toll-like receptor 2 in rat glial cells

Kawasaki disease is an acute illness of early childhood that is characterized by prolonged fever and vasculitis of unknown pathogenesis. Lactobacillus casei cell wall extract (LCWE)-induced vasculitis in mice is a well-validated model of Kawasaki disease. In the nervous system, glial cells play an important role in fever development. This study investigated whether LCWE directly stimulates glial cells, resulting in the induction of cyclooxygenase-2 (COX2), which is required for prostaglandin synthesis and fever development. We found that LCWE induced COX2 expression and activated the nuclear factor-κB signaling pathway in rat B92 glial cells, but Toll-like receptor-2, which is one of the receptors for LCWE, could not be detected in the cells. These results suggest that LCWE activates the nuclear factor-κB signaling pathway and induces COX2 in rat B92 glial cells through another LCWE receptor other than Toll-like receptor-2. © 2012

衝突型を呈した重複癌(膀胱腫瘍・S状結腸癌)により形成された膀胱結腸痩の1例

50歳男, S状結腸癌摘除と膀胱の部分切除を行ったA patient with vesicosigmoid fistula due to "collision" tumor between adenocarcinoma of the sigmoid colon and transitional cell carcinoma of the urinary bladder is presented. Resection of the sigmoid colon and partial cystectomy were performed. The clinical symptoms, diagnostic procedures and treatments are discussed

A case of systemic lupus erythematosus with Evans syndrome occurring after the remission of minimal change nephrotic syndrome

Evans syndrome is defined as the concomitant or sequential association of autoimmune hemolytic anemia with immune thrombocytopenia, and less frequently autoimmune neutropenia. Here, we encountered a female patient who developed Evans syndrome associated with systemic lupus erythematosus (SLE) during follow-up for minimal change nephrotic syndrome (MCNS). The patient was diagnosed with MCNS at 14 years old. At 17 years old, she came to our hospital with fever, headache, and conjunctival icterus. Blood tests revealed hemolytic anemia, thrombocytopenia, and acute kidney injury. The direct Coombs test was positive, meeting six criteria for the diagnosis of SLE by the American College of Rheumatology. The patient was diagnosed with Evans syndrome secondary to SLE. The renal dysfunction and hematological abnormalities rapidly improved with the administration of prednisolone. Renal biopsy showed more than half of the glomeruli with endocapillary proliferation and wire-loop lesions. Some glomeruli showed segmental sclerosis. Immunofluorescence disclosed granular deposits of IgG, IgM, IgA, C3, and C1q in the glomerular basement membrane and mesangial region. Electron microscopy revealed dense electron deposits in the glomerular vascular endothelium. The patient was further diagnosed with Class IV-S (A/C)-type lupus nephritis and was treated with tacrolimus, with no relapse. Autoimmune disorders of the patient may be involved in the development of nephrotic syndrome. An interesting aspect of this case was the common pathogenesis of SLE and Evans syndrome, which are autoimmune diseases. In addition to the immunological disorders of the host, the influence of external factors may have contributed to the pathogenesis.departmental bulletin pape