Abstract
Human neutrophils have been known to release neutrophil extracellular traps (NETs), antimicrobial DNA structures capable of capturing and killing microbes. Recently, a similar phenomenon has been reported in macrophages infected with various pathogens. However, a role for macrophages extracellular traps (METs) in host defense responses against Mycobacterium massiliense (M. mass) has yet to be described. In this study, we show that M. mass, a rapid growing mycobacterium (RGM), also induces the release of METs from PMA-differentiated THP-1 cells. Intriguingly, this process is not dependent on NADPH oxidase activity, which regulates NET formation. Instead, M. mass-induced MET formation partially depends on calcium influx and requires phagocytosis of high bacterial load. The METs consist of a DNA backbone embedded with microbicidal proteins such as histone, MPO and elastase. Released METs entrap M. mass and prevent their dissemination, but do not have bactericidal activity. Instead, they result in enhanced bacterial growth. In this regard, METs were considered to provide interaction of M. mass with cells and an environment for bacterial aggregation, which may facilitate mycobacterial survival and growth. In conclusion, our results demonstrate METs as an innate defense response against M. mass infection, and suggest that extracellular traps play a multifaceted role in the interplay between host and bacteria.
Highlights
The Mycobacterium abscessus (M. abscessus) complex is a group of rapidly growing nontuberculous mycobacteria (NTM) that cause inflammatory disease ranging from localized abscess to disseminated infection in patients with immune deficiency such as cystic fibrosis or immunocompromised patients [1, 2, 3]
We show that M. mass, a rapid growing mycobacteria (RGM), induces the release of extracellular traps from phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 macrophages
When PMAdifferentiated THP-1 macrophages were infected by M. mass cells released extracellular fiber structures that merged together (Fig 1A)
Summary
The Mycobacterium abscessus (M. abscessus) complex is a group of rapidly growing nontuberculous mycobacteria (NTM) that cause inflammatory disease ranging from localized abscess to disseminated infection in patients with immune deficiency such as cystic fibrosis or immunocompromised patients [1, 2, 3]. The M. abscessus complex comprises of three genetically related species: M. abscessus (sensu stricto), M. massiliense, and M. bolletii [4]. M. abscessus and M. massiliense (M. mass) are often isolated from patients with respiratory disease, and are known to be hard to treat and take longer to cure because they often acquire resistance to multiple antibiotics [5].
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