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Cellular and Molecular Mechanisms in Mycobacterial Infection 3.0
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Cellular and Molecular Mechanisms in Mycobacterial Infection 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 2450

Special Issue Editors

Dr. Natalie Nieuwenhuizen

E-Mail Website
Guest Editor
Institute for Hygiene and Microbiology, Julius-Maximilians-Universität Würzburg, Josef-Schneider-Str. 2, 97080 Würzburg, Germany
Interests: infectious disease; immunology; host-pathogen interactions; tuberculosis; vaccines; fungal infection; leishmaniasis; helminth infection; IL-4 receptor alpha; TGF-beta; activin A
Special Issues, Collections and Topics in MDPI journals
Dr. Joanna Evans

E-Mail Website
Guest Editor
The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK
Interests: infectious diseases; microbiology; tuberculosis; nontuberculous mycobacteria; drug discovery; molecular biology; bacterial physiology and metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mycobacterium tuberculosis (M.tb) caused over 10 million cases of tuberculosis (TB) and 1.3 million deaths in 2022. The current TB vaccine, a live attenuated form of M. bovis named M. bovis Calmette–Guerin (BCG), provides insufficient protection. In addition, the emergence of multiple and extremely drug-resistant strains of M.tb is a growing problem. Novel vaccines and drug therapies are urgently required. The primary host cell of M.tb, the macrophage, serves as the first line of defense. Multiple pattern-recognition receptors sense mycobacterial molecular patterns, triggering intracellular signaling cascades and induction of proinflammatory cytokines, chemokines, and antimicrobial molecules. Macrophage-derived cytokines such as tumor necrosis factor, interleukin-12, IL-1β and IL-18 are critical for host defense against tuberculosis. Adaptive responses, including antigen-specific T cells, are critical in controlling the growth of M. tb by producing interferon-gamma, activating macrophages, and orchestrating granuloma formation. 

This Special Issue aims to cover a selection of original research articles, short communications, and current review articles exploring mycobacterial research, including immunity against mycobacteria, signaling transduction in TB, host–pathogen interactions, mycobacterial metabolism, drug resistance mechanisms, biomarkers of disease, and novel drugs and vaccines within the scope of molecular biology.

Dr. Natalie Nieuwenhuizen
Dr. Joanna Evans
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tuberculosis
  • mycobacteria
  • bacterial metabolism
  • bacterial infection
  • antibiotic resistance
  • vaccines
  • biomarkers
  • signaling pathways
  • immune system
  • host-directed therapy
  • host–pathogen interaction
  • drug discovery

Published Papers (2 papers)

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Research

18 pages, 1733 KiB  
Article
Negative Regulation of Autophagy during Macrophage Infection by Mycobacterium bovis BCG via Protein Kinase C Activation
by Rafael Maldonado-Bravo, Tomás Villaseñor, Martha Pedraza-Escalona, Leonor Pérez-Martínez, Rogelio Hernández-Pando and Gustavo Pedraza-Alva
Int. J. Mol. Sci. 2024, 25(6), 3145; https://doi.org/10.3390/ijms25063145 - 9 Mar 2024
Viewed by 745
Abstract
Mycobacterium tuberculosis (Mtb) employs various strategies to manipulate the host’s cellular machinery, overriding critical molecular mechanisms such as phagosome-lysosome fusion, which are crucial for its destruction. The Protein Kinase C (PKC) signaling pathways play a key role in regulating phagocytosis. Recent [...] Read more.
Mycobacterium tuberculosis (Mtb) employs various strategies to manipulate the host’s cellular machinery, overriding critical molecular mechanisms such as phagosome-lysosome fusion, which are crucial for its destruction. The Protein Kinase C (PKC) signaling pathways play a key role in regulating phagocytosis. Recent research in Interferon-activated macrophages has unveiled that PKC phosphorylates Coronin-1, leading to a shift from phagocytosis to micropinocytosis, ultimately resulting in Mtb destruction. Therefore, this study aims to identify additional PKC targets that may facilitate Mycobacterium bovis (M. bovis) infection in macrophages. Protein extracts were obtained from THP-1 cells, both unstimulated and mycobacterial-stimulated, in the presence or absence of a general PKC inhibitor. We conducted an enrichment of phosphorylated peptides, followed by their identification through mass spectrometry (LC-MS/MS). Our analysis revealed 736 phosphorylated proteins, among which 153 exhibited alterations in their phosphorylation profiles in response to infection in a PKC-dependent manner. Among these 153 proteins, 55 are involved in various cellular processes, including endocytosis, vesicular traffic, autophagy, and programmed cell death. Importantly, our findings suggest that PKC may negatively regulate autophagy by phosphorylating proteins within the mTORC1 pathway (mTOR2/PKC/Raf-1/Tsc2/Raptor/Sequestosome-1) in response to M. bovis BCG infection, thereby promoting macrophage infection. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Mycobacterial Infection 3.0)
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29 pages, 2349 KiB  
Article
Drug-Tolerant Mycobacterium tuberculosis Adopt Different Survival Strategies in Alveolar Macrophages of Patients with Pulmonary Tuberculosis
by Elena G. Ufimtseva and Natalya I. Eremeeva
Int. J. Mol. Sci. 2023, 24(19), 14942; https://doi.org/10.3390/ijms241914942 - 6 Oct 2023
Viewed by 1193
Abstract
The rapid spread of drug-resistant M. tuberculosis (Mtb) strains and the phenomenon of phenotypic tolerance to drugs present challenges toward achieving the goal of tuberculosis (TB) elimination worldwide. By using the ex vivo cultures of alveolar macrophages obtained from lung tissues [...] Read more.
The rapid spread of drug-resistant M. tuberculosis (Mtb) strains and the phenomenon of phenotypic tolerance to drugs present challenges toward achieving the goal of tuberculosis (TB) elimination worldwide. By using the ex vivo cultures of alveolar macrophages obtained from lung tissues of TB patients after intensive antimicrobial chemotherapy before surgery, different subpopulations of multidrug-tolerant Mtb with a spectrum of phenotypic and growth features were identified in the same TB lesions. Our results are indicative of not only passive mechanisms generating nonheritable resistance of Mtb to antibiotics, which are associated mainly with a lack of Mtb growth, but also some active mechanisms of Mtb persistence, such as cell wall and metabolic pathway remodeling. In one of the subpopulations, non-acid-fast Mtb have undergone significant reprogramming with the restoration of acid-fastness, lipoarabinomannan expression and replication in host cells of some patients after withdrawal of anti-TB drugs. Our data indicate the universal stress protein Rv2623 as a clinically relevant biomarker of Mtb that has lost acid-fastness in human lungs. The studies of Mtb survival, persistence, dormancy, and resumption and the identification of biomarkers characterizing these phenomena are very important concerning the development of vaccines and drug regimens with individualized management of patients for overcoming the resistance/tolerance crisis in anti-TB therapy. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Mycobacterial Infection 3.0)
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