Smoking and the Microbiome in the Pathogenesis of Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic, destructive, inflammatory, polyarticular joint disease, characterized by infiltration of inflammatory cells, followed by the destruction of cartilage and bone [1]. Inflammatory cytokines such as tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and interleukin-1 (IL-1) as well as chemokines such as pulmonary and activation-regulated chemokine /CCL18 and monocyte chemoattractant protein-4 /CCL13 play important roles in the pathogenesis of RA. These cytokines have emerged as important pro-inflammatory mediators and dominant molecular targets for the therapeutic strategies [2]. The nuclear factor κB (NF-κB) family of transcriptional activators regulates the expression of a variety of cytokines involved in the pathology of RA, including TNFα, IL-6 and IL-1 [3]. Thus, NF-κB is also an important target of RA treatment [4].