Interleukin-11 drives early lung inflammation during mycobacterium tuberculosis infection in genetically susceptible mice

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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. © 2011 Kapina et al.

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Kapina, M. A., Shepelkova, G. S., Avdeenko, V. G., Guseva, A. N., Kondratieva, T. K., Evstifeev, V. V., & Apt, A. S. (2011). Interleukin-11 drives early lung inflammation during mycobacterium tuberculosis infection in genetically susceptible mice. PLoS ONE, 6(7). https://doi.org/10.1371/journal.pone.0021878

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