And hello again!
One of this weeks articles discussed the role interleukin-17 (IL-17) plays in the effector phase of arthritis. Previous studies had shown that in the initial phase of arthritis, IL-17 may promote joint inflammation as well as tissue destruction. But does IL-17 continue to play a role in the symptoms of arthritis throughout the progression of the disease, or do other factors take over? The study used mice which were first immunized with collagen II and then after 21 days were given a booster injection of the collagen II to induce the arthritis. At the onset of arthritis the mice were treated with an injection of anti-IL-17 antibody treatment.
The treatment showed significant reduction in the progression and in the symptoms of the collagen induced arthritis (CIA). The study showed that treatment with anti-IL-17 antibody at the onset of CIA prevented chondrocyte death, cartilage surface erosion, bone erosion, and reduced synovitis. Treatment also suppressed serum IL6 levels, IL-1beta, and RANKL which all are pro-inflammatory mediators.
To assess the role IL-17 plays in prolonged CIA, mice were given the anti-IL-17 on day 28 instead of day 21. Even though the CIA had reached its effector phase, the anti-IL-17 still showed suppressed progression. This answered the initial question, and yes IL-17 still does play a role in prolonging CIA. If this was a factor that was not taken into considering prior to this study, then that could mean that there can be new approaches on how arthritis can be treated.
I personally liked this article because it was easy to follow. The objective was clear and the results were laid out very nicely. Is there anything that stood out for you in this article? Any additional comments, or side notes? What do you think this could mean in terms of future treatments for arthritis?
This method of anti-IL17 is definitely a step up in finding some resolution to arthritis. Attacking something that has inflammatory properties is something that we have seen before. The idea is sound and logical. However, there could be some side effects from blocking inflammation.
ReplyDeleteAs we have seen in previous articles dealing with reducing inflammation activity, there was an increased risk of developing infections. It makes sense that it will happen because we are altering the role of inflammation. I am not positively sure it will happen for the anti-IL17, but it seems to have the same concept as the other anti-inflammatory medications developed before.
The fact that there is evidence supporting the anti-IL-17 therapy is a remarkable breakthrough. Although the potential of anti-inflammatory treatments is not something that’s been newly thought of, these results seem promising. Because IL-17 is responsible for inducing and facilitating proinflammatory responses, it would make sense that blocking IL-17 would help reduce further inflammation, the root of arthritis.
ReplyDeleteHowever, what makes me skeptical is that there are so many different ways to reduce inflammation aside from blocking this particular cytokine. If there are so many anti-inflammatory alternatives, why haven’t they been proven to “cure” arthritis? Many drugs are designed to merely mask the symptoms, but not eliminate the problem. In addition, when dealing with the suppression of a cytokine that’s responsible for a proinflammatory response, one must consider the consequences such as a weakened immune system, which could have problems of its own.
In terms of the paper, I particularly liked the graphs as it made the paper even easier to understand. And like we mentioned in class, I do wish that the arthritis score had more partitions rather than being measured on such a small scale. This would have provided even more validity to the results.
But with that being said, this is a great step towards the future eradication of arthritis!