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      Mycobacterium tuberculosis infection of host cells in space and time

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          ABSTRACT

          Tuberculosis (TB) caused by the bacterial pathogen Mycobacterium tuberculosis (Mtb) remains one of the deadliest infectious diseases with over a billion deaths in the past 200 years (Paulson 2013). TB causes more deaths worldwide than any other single infectious agent, with 10.4 million new cases and close to 1.7 million deaths in 2017. The obstacles that make TB hard to treat and eradicate are intrinsically linked to the intracellular lifestyle of Mtb. Mtb needs to replicate within human cells to disseminate to other individuals and cause disease. However, we still do not completely understand how Mtb manages to survive within eukaryotic cells and why some cells are able to eradicate this lethal pathogen. Here, we summarise the current knowledge of the complex host cell-pathogen interactions in TB and review the cellular mechanisms operating at the interface between Mtb and the human host cell, highlighting the technical and methodological challenges to investigating the cell biology of human host cell-Mtb interactions.

          Abstract

          The review describes the complex dynamics underlying the interactions between Mycobacterium tuberculosis and the human host cell with an emphasis on the cell biology approaches and potential challenges to study these processes.

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          Long‐term expanding human airway organoids for disease modeling

          Norman Sachs, Angelos Papaspyropoulos, Domenique D Zomer-van Ommen … (2019)
          Abstract Organoids are self‐organizing 3D structures grown from stem cells that recapitulate essential aspects of organ structure and function. Here, we describe a method to establish long‐term‐expanding human airway organoids from broncho‐alveolar resections or lavage material. The pseudostratified airway organoids consist of basal cells, functional multi‐ciliated cells, mucus‐producing secretory cells, and CC10‐secreting club cells. Airway organoids derived from cystic fibrosis (CF) patients allow assessment of CFTR function in an organoid swelling assay. Organoids established from lung cancer resections and metastasis biopsies retain tumor histopathology as well as cancer gene mutations and are amenable to drug screening. Respiratory syncytial virus (RSV) infection recapitulates central disease features, dramatically increases organoid cell motility via the non‐structural viral NS2 protein, and preferentially recruits neutrophils upon co‐culturing. We conclude that human airway organoids represent versatile models for the in vitro study of hereditary, malignant, and infectious pulmonary disease.
          Article 0 comments Cited 347 times – based on 0 reviews     Review now
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            Human Monocytes Engage an Alternative Inflammasome Pathway.

            Moritz M Gaidt, Thomas Ebert, Dhruv Chauhan … (2016)
            Interleukin-1β (IL-1β) is a cytokine whose bioactivity is controlled by activation of the inflammasome. However, in response to lipopolysaccharide, human monocytes secrete IL-1β independently of classical inflammasome stimuli. Here, we report that this constituted a species-specific response that is not observed in the murine system. Indeed, in human monocytes, lipopolysaccharide triggered an "alternative inflammasome" that relied on NLRP3-ASC-caspase-1 signaling, yet was devoid of any classical inflammasome characteristics including pyroptosome formation, pyroptosis induction, and K(+) efflux dependency. Genetic dissection of the underlying signaling pathway in a monocyte transdifferentiation system revealed that alternative inflammasome activation was propagated by TLR4-TRIF-RIPK1-FADD-CASP8 signaling upstream of NLRP3. Importantly, involvement of this signaling cascade was limited to alternative inflammasome activation and did not extend to classical NLRP3 activation. Because alternative inflammasome activation embraces both sensitivity and promiscuity of TLR4, we propose a pivotal role for this signaling cascade in TLR4-driven, IL-1β-mediated immune responses and immunopathology in humans.
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              Extracellular M. tuberculosis DNA targets bacteria for autophagy by activating the host DNA-sensing pathway.

              Robert O. Watson, Paolo S. Manzanillo, Jeffery S. Cox (2012)
              Eukaryotic cells sterilize the cytosol by using autophagy to route invading bacterial pathogens to the lysosome. During macrophage infection with Mycobacterium tuberculosis, a vacuolar pathogen, exogenous induction of autophagy can limit replication, but the mechanism of autophagy targeting and its role in natural infection remain unclear. Here we show that phagosomal permeabilization mediated by the bacterial ESX-1 secretion system allows cytosolic components of the ubiquitin-mediated autophagy pathway access to phagosomal M. tuberculosis. Recognition of extracelluar bacterial DNA by the STING-dependent cytosolic pathway is required for marking bacteria with ubiquitin, and delivery of bacilli to autophagosomes requires the ubiquitin-autophagy receptors p62 and NDP52 and the DNA-responsive kinase TBK1. Remarkably, mice with monocytes incapable of delivering bacilli to the autophagy pathway are extremely susceptible to infection. Our results reveal an unexpected link between DNA sensing, innate immunity, and autophagy and indicate a major role for this autophagy pathway in resistance to M. tuberculosis infection. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): FEMS Microbiol Rev
                Journal ID (iso-abbrev): FEMS Microbiol. Rev
                Journal ID (publisher-id): femsre
                Title: FEMS Microbiology Reviews
                Publisher: Oxford University Press
                ISSN (Print): 0168-6445
                ISSN (Electronic): 1574-6976
                Publication date (Electronic): 27 March 2019
                Publication date Collection: July 2019
                Publication date PMC-release: 27 March 2019
                Volume: 43
                Issue: 4
                Pages: 341-361
                Affiliations
                [1]Host-pathogen interactions in tuberculosis laboratory, The Francis Crick Institute, 1 Midland Road, London, NW1 1AT, United Kingdom
                Author notes
                Corresponding author: Host-pathogen interactions in tuberculosis laboratory, The Francis Crick Institute, 1 Midland Road, London, NW1 1AT, United Kingdom. Tel: +44(0)2037961460; E-mail: max.g@ 123456crick.ac.uk
                Author information
                http://orcid.org/0000-0003-3199-0337
                Article
                Publisher ID: fuz006
                DOI: 10.1093/femsre/fuz006
                PMC ID: 6606852
                PubMed ID: 30916769
                SO-VID: 128cc54f-89bc-4100-8224-f4378fe40c58
                Copyright © © FEMS 2019.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 16 December 2018
                Date accepted : 26 March 2019
                Page count
                Pages: 21
                Funding
                Funded by: Cancer Research UK 10.13039/501100000289
                Award ID: FC001092
                Funded by: Medical Research Council UK 10.13039/501100000265
                Award ID: FC001092
                Funded by: Wellcome Trust 10.13039/100004440
                Award ID: FC001092
                Funded by: European Research Council 10.13039/501100000781
                Award ID: 772022
                Categories
                Subject: Review Article
                Subject: Editor's Choice

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: mycobacterium tuberculosis,macrophage,phagosome,autophagy,tuberculosis
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: mycobacterium tuberculosis, macrophage, phagosome, autophagy, tuberculosis

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