Cell-wall-deficient bacteria： a major etiological factor for psoriasis？  

作　　者：WANG Guo-li LI Xiu-yun WANG Ming-yi XIAO De-gui ZHANG Yong-yu YUAN Xiao-yan WANG Qi-you SONG Jian-jing 

机构地区：[1]Department of Clinical Laboratory Weihai Municipal Hospital Affiliated to Dalian Medical University, Weihai, Shandong 264200, China [2]Department of Nuclear Medicine Weihai Municipal Hospital Affiliated to Dalian Medical University, Weihai, Shandong 264200, China [3]Department of Dermatology Weihai Municipal Hospital Affiliated to Dalian Medical University, Weihai, Shandong 264200, China [4]Department of Otolaryngology Weihai Municipal Hospital Affiliated to Dalian Medical University, Weihai, Shandong 264200, China

出　　处：《Chinese Medical Journal》2009年第24期3011-3016,共6页中华医学杂志（英文版）

摘　　要：Background Psoriasis is a common inflammatory skin disease, yet knowledge of the factors that may induce, trigger, or exacerbate psoriasis is not fully delineated. Recent advances have improved our understanding of the link between psoriasis and cell-wall-deficient bacteria （CWDB） infections. In the present study we assessed the prevalence of CWDB infection in patients with psoriasis. Methods The carriage rate of CWDB in the tonsil or pharynx of psoriasis patients, chronic tonsillitis patients and controls were investigated using hypertonic medium. Psoriasis patients with CWDB were randomly assigned to two groups and respectively treated with antibiotics or systemic therapy without antibiotic. Human peripheral blood mononuclear cells （PBMC） from psoriasis patients, chronic tonsillitis patients and control subjects were stimulated with bacteria antigens and extra-cellular levels of interferon-γ（IFN-γ） and interleukin （IL）-10 were measured in the supernatants using the ELISA technique, in vitro. Meanwhile, the proliferation ability of PBMC to respond to bacteria antigens was detected by MTT assay. Results CWDB were isolated from 74.2% of psoriasis patients, 23.5% of chronic tonsillitis patients and only 6.3% of controls. Antibiotic therapy was appropriate for approximately 80% of psoriasis patients with CWDB infection, and in only 8.9% psoriasis patients CWDB infection was detected after antibiotic therapy. Meanwhile, our study showed that CWDB and wide-type bacteria did remarkably enhance the production of IFN-γ, in vitro, and PBMC proliferation. Conclusion CWDB infection may be a virtual triggering factor in psoriasis by regulating T-cell activation.Background Psoriasis is a common inflammatory skin disease, yet knowledge of the factors that may induce, trigger, or exacerbate psoriasis is not fully delineated. Recent advances have improved our understanding of the link between psoriasis and cell-wall-deficient bacteria （CWDB） infections. In the present study we assessed the prevalence of CWDB infection in patients with psoriasis. Methods The carriage rate of CWDB in the tonsil or pharynx of psoriasis patients, chronic tonsillitis patients and controls were investigated using hypertonic medium. Psoriasis patients with CWDB were randomly assigned to two groups and respectively treated with antibiotics or systemic therapy without antibiotic. Human peripheral blood mononuclear cells （PBMC） from psoriasis patients, chronic tonsillitis patients and control subjects were stimulated with bacteria antigens and extra-cellular levels of interferon-γ（IFN-γ） and interleukin （IL）-10 were measured in the supernatants using the ELISA technique, in vitro. Meanwhile, the proliferation ability of PBMC to respond to bacteria antigens was detected by MTT assay. Results CWDB were isolated from 74.2% of psoriasis patients, 23.5% of chronic tonsillitis patients and only 6.3% of controls. Antibiotic therapy was appropriate for approximately 80% of psoriasis patients with CWDB infection, and in only 8.9% psoriasis patients CWDB infection was detected after antibiotic therapy. Meanwhile, our study showed that CWDB and wide-type bacteria did remarkably enhance the production of IFN-γ, in vitro, and PBMC proliferation. Conclusion CWDB infection may be a virtual triggering factor in psoriasis by regulating T-cell activation.

关 键 词：cell-wall-deficient bacteria PSORIASIS INTERFERON-Γ T lymphocytes proliferation antibiotic therapy 

分 类 号：R686[医药卫生—骨科学]