Interleukin-Blocking RA Drugs Leave Patients More Exposed to Flesh-Eating Strep Infections

Interleukin-1β (IL-1beta), a cytokine that plays in important role in the body’s immune response, turns out to be part of the body’s early defense system for bacterial infections. Anti-inflammation treatments for autoimmune conditions like rheumatoid arthritis (RA) often times inhibit IL-1beta to mitigate the inflammation that it initiates when infection is detected.

Unfortunately, by disabling this response, the body is dramatically exposed to infections, as much as 300 times more vulnerable to Group A Streptococcal infections.

IL-1beta is originally produced by the body in a long, inactive form that does not become active until it is “cleaved” into smaller portions. Challenging previous belief, which held that only the body itself could initiate this cleaving process and thus activate the inflammation response, a new study has found that some strep infections can do so as well. Many strep infections actually release an enzyme called SpeB that can cleave the Interleukin and cause an immune response, perhaps as a means of wiping out other competing bacteria.

More invasive forms of Strep, including the flesh-eating varieties, have a mutation blocking their SpeB production in order to establish themselves undetected. Combined with drugs, such as anakinra, that inhibit IL-1beta production, this can cause a huge vulnerability to invasive strep infections among those simply trying to reduce their RA inflammation.

“Inhibiting the body’s bacterial sensor can put a person at risk for invasive infection,” said Victor Nizet, MD at UC San Diego, in an accompanying press release, “but just the fact that we now know that this patient population is at higher risk and why means we can take simple steps-such as close monitoring and prophylactic antibiotics-to prevent it from happening. ”