A study has found a link between a gene variant and some environmental factors such as cigarette smoking and rheumatoid arthritis.
Researchers from Michigan Medicine suggest that smokers who carry human leukocyte antigen (HLA) are at a higher risk of developing rheumatoid arthritis and the effects of the disease are more severe. This could lead to swelling, greater pain, and severe bone destruction.
“We found a particular enzyme that acts as a channel, or pathway, in the cell for a conversation between two culprits, so they work together to greater damage. Individually they are bad, but together, they’re worse,” said Joseph Holoshitz, the associate chief for research in the division of Rheumatology at the University Of Michigan School Of Medicine.
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According to the team, smoking remains the major environmental factor leading to the development of rheumatoid arthritis. Living in the proximity of environmental pollutants is another factor causing the disease such as, living near highways and in urban areas, regardless of cigarette use.
“One scenario is that air pollution from vehicles on highways produces dioxin or other pollutants. Dioxin is just one of many chemicals that similarly activate this pathway,” Holoshitz added.
Dioxin also has shown to increase severity in an experimental model of another autoimmune disease, multiple sclerosis.
“We’ve shown in the study that the interaction between dioxin and the HLA gene variant activates events known to be associated with rheumatoid arthritis. And we’ve demonstrated quite convincingly that this facilitates bone destruction,” said Holoshitz.
Hyperactivity of certain bone cells called osteoclasts, which absorb bone tissue cause the bone degeneration in rheumatoid arthritis.
Holoshitz stated, “In our research with the combination of dioxin and the HLA gene variant, we saw that osteoclasts are overactive and overabundant, and that bone is destroyed because of it.”
According to Holoshitz, the treatments available for rheumatoid arthritis focus primarily on inflammation but do not target bone destruction.
“Once we have drugs that directly and specifically address bone destruction in the disease, we’ll have better treatment,” asserted Holoshitz.
“As a separate project, we have a couple of early-stage drug candidates that block the HLA gene-activated pathway and are effective in preventing bone damage. These drugs almost completely inhibit experimental rheumatoid arthritis and bone damage in mice.”
The findings were published in the Proceeding of the National Academy of Sciences.