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Macrophage Epithelial Reprogramming Underlies Mycobacterial Granuloma Formation and Promotes Infection.

Abstract：

:Mycobacterium tuberculosis infection in humans triggers formation of granulomas, which are tightly organized immune cell aggregates that are the central structure of tuberculosis. Infected and uninfected macrophages interdigitate, assuming an altered, flattened appearance. Although pathologists have described these changes for over a century, the molecular and cellular programs underlying this transition are unclear. Here, using the zebrafish-Mycobacterium marinum model, we found that mycobacterial granuloma formation is accompanied by macrophage induction of canonical epithelial molecules and structures. We identified fundamental macrophage reprogramming events that parallel E-cadherin-dependent mesenchymal-epithelial transitions. Macrophage-specific disruption of E-cadherin function resulted in disordered granuloma formation, enhanced immune cell access, decreased bacterial burden, and increased host survival, suggesting that the granuloma can also serve a bacteria-protective role. Granuloma macrophages in humans with tuberculosis were similarly transformed. Thus, during mycobacterial infection, granuloma macrophages are broadly reprogrammed by epithelial modules, and this reprogramming alters the trajectory of infection and the associated immune response.

journal_name

Immunity

journal_title

Immunity

authors

Cronan MR,Beerman RW,Rosenberg AF,Saelens JW,Johnson MG,Oehlers SH,Sisk DM,Jurcic Smith KL,Medvitz NA,Miller SE,Trinh LA,Fraser SE,Madden JF,Turner J,Stout JE,Lee S,Tobin DM

doi

10.1016/j.immuni.2016.09.014

subject

Has Abstract

pub_date

2016-10-18 00:00:00

pages

861-876

issue

4

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(16)30383-1

journal_volume

45

pub_type

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