Etiological and biological aspects of cigarette smoking in rheumatoid arthritis.
Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by the chronic inflammation of the synovium, which develops to joint destruction. Quite interestingly RA has not been present in the old world until 17 century. Tobacco has come from the new world, and epidemiological studies revealed cigarette smoking as a major risk factor for the disease. However, the mechanism how cigarette smoking contributes to RA has been largely unknown. It has been demonstrated that polycyclic aromatic hydrocarbons, constituents of cigarette smoke, and cigarette smoke extracts are able to induce proinflammatory cytokines from RA patient-derived fibroblast-like synoviocytes. Recent studies also suggest an important role of Th17 in RA and contribution of aryl hydrocarbon receptor to the induction and development of Th17 and RA. These new findings lead to uncovering the basis for the etiological role of cigarette smoking in the disease.
Onozaki
Kikuo
K
Department of Molecular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, Mizuho, Nagoya 467-8603, Japan. konozaki@phar.nagoya-cu.ac.jp
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000209:etiology* / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D020381:Interleukin-17 / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon / Q000378:metabolism*; D012907:Smoking / Q000009:adverse effects*; D013583:Synovial Membrane / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D014026:Nicotiana
D016207:Cytokines; D018836:Inflammation Mediators; D020381:Interleukin-17; D018336:Receptors, Aryl Hydrocarbon