AI Article Synopsis
- IL-11 is a cytokine whose role in pulmonary tuberculosis (TB) is not well understood, but blocking it can reduce lung damage and inflammation in susceptible mice.
- Administering specific antibodies against IL-11 lowers its levels and other inflammatory cytokines, suggesting that IL-11 may amplify inflammation through a feedback mechanism.
- These results indicate that IL-11 might play a harmful role in the early stages of TB infection in genetically vulnerable individuals.
Article Abstract
IL-11 is multifunctional cytokine whose physiological role in the lungs during pulmonary tuberculosis (TB) is poorly understood. Here, using in vivo administration of specific antibodies against IL-11, we demonstrate for the first time that blocking IL-11 diminishes histopathology and neutrophilic infiltration of the lung tissue in TB-infected genetically susceptible mice. Antibody treatment decreased the pulmonary levels of IL-11 and other key inflammatory cytokines not belonging to the Th1 axis, and down-regulated IL-11 mRNA expression. This suggests the existence of a positive feedback loop at the transcriptional level, which is further supported by up-regulation of IL-11 mRNA expression in the presence of rIL-11 in in vitro cultures of lung cells. These findings imply a pathogenic role for IL-11 during the early phase of Mycobacterium tuberculosis-triggered disease in a genetically susceptible host.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3137601 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0021878 | PLOS |
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