Active pulmonary tuberculosis (APTB) has been around for centuries and is now a treatable condition. However, within the developing world the statistics of people catching, and dying, from the immune infection are still high. A person infected with APTB may be latent for months, if not years before presenting any symptoms. This means they are unknowingly infecting those around them, with some estimations reported that each year someone with APTB infects another 15 people per year. This, coupled with the 2012 statistic that 1.3 million people died of their infection, (1) has resulted in numerous studies trying to identify the best treatments.
New research published in Molecular Immunology (2) aimed to assess the role of serum inflammatory cytokines in active pulmonary APTB patients after the administration of anti-tuberculosis drug therapy.
Blood samples were collected from both APTB patients and compared to that of healthy subjects (total n =204) at study baseline, and then 2, 4 and 6 months post therapy. Serum samples were tested for the pro-inflammatory cytokines of IL-12p40, IFNy, TNFa, IL-1b and IL-6 as well as anti-inflammatory cytokines IL-10, TGFb1 and IL-4.
When APTB serum samples were compared to that of healthy subjects it was found that baseline levels of IL-12p40 (P < 0.001), IFNy (P < 0.001), TNFa (P < 0.01), IL-1b (P < 0.001) and IL-6 (P < 0.001) pro-inflammatory cytokines were elevated.
Baseline samples also indicated that anti-inflammatory cytokine levels were also elevated, IL-10 (P < 0.001) and TGF-β1 (P < 0.001). However, IL-4 showed no change between the two groups.
Interestingly results showed that IFNy, TNFa, IL-6 and TGF-b1 directly related to the bacterial load whilst TNFa, IL-1b, IL-6 and TGF-b1 related to radiological severity within the APTB group of patients.
Significantly baseline levels of IL-6 in the healthy subjects and APTB patients differed most, however by month 4 of treatment IL-6 levels within APTB samples rapidly decreased and stabilised. This subtle reduction of IL-6 indicates that it plays a key role in immune-protection upon host infection of APTB, and can be noted as a useful marker to determine the effectiveness of therapy within patients.