Activation of type 3 innate lymphoid cells and interleukin 22 secretion in the lungs during streptococcus pneumoniae infection
(2014) The Journal of Infectious Diseases — Vol. 210, n° 3, p. 493-503 (2014)
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- Abstract
- Mucosal sites are continuously exposed to pathogenic microorganisms and are therefore equipped to control respiratory infections. Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. The present study aimed at analyzing the distribution and function of ILC3 in the respiratory tract. We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. In conclusion, boosting lung ILC3 might represent an interesting strategy to fight respiratory bacterial infections. © The Author 2014.
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Van Maele, L., Sirard, J.-C., Faveeuw, C., Trottein, F., Benecke, A. G., Eberl, G., Renauld, J.-C., Chabalgoity, J. A., Deruy, E., Porte, R., Ivanov, S., Cayet, D., & Carnoy, C. (2014). Activation of type 3 innate lymphoid cells and interleukin 22 secretion in the lungs during streptococcus pneumoniae infection. The Journal of Infectious Diseases, 210(3), 493-503. https://doi.org/10.1093/infdis/jiu106 (Original work published 2014)