Interleukin-26 activates macrophages and facilitates killing of Mycobacterium tuberculosis

Heike C. Hawerkamp, Lasse van Geelen, Jan Korte, Jeremy Di Domizio, Marc Swidergall, Afaque Ahmad Imtiyaz Momin, Francisco J. Guzmán-Vega, Stefan T. Arold, Joachim Ernst, Michel Gilliet, Rainer Kalscheuer, Bernhard Homey, Stephan Meller

Research output: Contribution to journalArticlepeer-review

Abstract

Abstract Tuberculosis-causing Mycobacterium tuberculosis (Mtb) is transmitted via airborne droplets followed by a primary infection of macrophages and dendritic cells. During the activation of host defence mechanisms also neutrophils and T helper 1 (TH1) and TH17 cells are recruited to the site of infection. The TH17 cell-derived interleukin (IL)-17 in turn induces the cathelicidin LL37 which shows direct antimycobacterial effects. Here, we investigated the role of IL-26, a TH1- and TH17-associated cytokine that exhibits antimicrobial activity. We found that both IL-26 mRNA and protein are strongly increased in tuberculous lymph nodes. Furthermore, IL-26 is able to directly kill Mtb and decrease the infection rate in macrophages. Binding of IL-26 to lipoarabinomannan might be one important mechanism in extracellular killing of Mtb. Macrophages and dendritic cells respond to IL-26 with secretion of tumor necrosis factor (TNF)-α and chemokines such as CCL20, CXCL2 and CXCL8. In dendritic cells but not in macrophages cytokine induction by IL-26 is partly mediated via Toll like receptor (TLR) 2. Taken together, IL-26 strengthens the defense against Mtb in two ways: firstly, directly due to its antimycobacterial properties and secondly indirectly by activating innate immune mechanisms.
Original languageEnglish (US)
JournalScientific Reports
Volume10
Issue number1
DOIs
StatePublished - Oct 14 2020

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