What Is The Connection Between Smoking and RA Autoimmunity?

Specialists, for quite some time now, have considered that one can find genetic and environmental factors working in tandem to cause rheumatoid arthritis. Exactly how this occurs continues to be mysterious. Research is pointing to the reality that there may be a variety of pathways to getting RA.

One of those dangerous factors is cigarette smoking. In depth investigation convincingly demonstrates that cigarette use can play a role in the development of RA if the genetic conditions are right. Consequently, the question now being investigated is, "precisely how will smoking trigger an aggressive form of RA in some people?

Genetic and Environment Interactions in RA

Of all the environmental factors suspected or identified, smoking is undoubtedly most convincingly connected with RA. Study after study has implicated smoking as being a contributor to the disease in certain people.

A major aspect in the connection betwee
RA and smoking might lie in the SE gene. The combination of smoking and the SE gene is, show that cigarette smokers who have got a copy of the SE gene from both parents (2 total), possess a risk of getting the extremely aggressive ACPA-associated RA , that is 21 times that of nonsmokers who have no copies whatsoever of the SE gene. Cigarette smokers having two copies of the SE gene (one from each parent) have 21 times the potential risk of ACPA-associated RA as nonsmokers without any copies of the SE gene.

Smoking As a Cause

Unfortunately, research workers don't truly know or know the method in which genetics and smoking interact with each other to trigger RA. At this time there is some speculation that smoking could possibly trigger some misguided output of autoantibodies and faulty immune functioning in an individual who carries a hereditary predisposition. One prominent theory involves smoking, the SE gene, and "citrullinated" proteins.

Experts in Sweden have come up with a theory precisely how this might occur in a person who has an immunity mechanism which is genetically altered. The crux of this idea focuses around the hypothesis that long term exposure to tobacco smoke ends up creating a substantial variety of what are called citrulinated proteins, which in conjunction with the modified immunity, leads to an autoimmune reaction (development of antibodies) which will eventually zero in on the joints as well as other tissues.

This in turn has spurred various other researchers into presenting other hypotheses as well. One being that RA could develop in our lungs and that cigarette smoking is exactly what triggers the RA condition. Today, a team of experts at the University of Colorado are specifically looking into this possibility.

These researchers are researching individuals who have yet to show any kind of RA symptoms, but because they have family members who do have the disease and have a positive test for ACPSs, are considered to be at a extremely high risk of acquiring RA. Dr. Kristen Demoruelle, MD, a part of this research team says, "We know that autoantibodies are present in most people who develop autoantibody-positive RA months or even years before they develop any sign of joint disease. Something had to happen prior to this." She explains that, "Some event which could be an environmental exposure like smoking or an infection, in a person with appropriate genetic factors may lead to the development of autoimmunity and eventually, the symptoms of RA."

They discovered that people who don't have RA but do have the high risk antibodies show a higher amount of lung inflammation compared to people who don't have RA and who don't have the high risk autoantibodies. Thereby leading them to believe that there is something taking place within the lungs in the course of what would be referred to as a preclinical period. Their goal, not surprisingly, will be to nail down precisely what that is.The team found that individuals not having RA, who may have the high-risk autoantibodies, are more likely to have evidence of inflammation in their lungs as compared to individuals without RA who don't possess the high-risk autoantibodies. These studies suggest that there is something taking place within the lungs in the preclinical period, and the group is trying to figure out what it is and precisely what it means.

Doctors admit that they still have many unanswered questions regarding the mechanistic link between cigarette smoke and the onset of RA.

The bigger question for people is not surprisingly, "Will not smoking stop RA from developing in some men and women?"

The Swedish research gives a definite 'Yes" to this particular question. Smoking is a big, preventable risk factor for rheumatoid arthritis. Their research suggests that no less than 20% of RA cases and over 35% of ACPA RA cases are brought on and are directly connected to smoking. Once the researchers looked at just the ACPA-associated RA, they determined that 55 % of cases that involves two copies of the SE gene are due directly to smoking.