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Microorganisms
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Immunometabolism in Mycobacterium tuberculosis (M.tb) Infection
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Immunometabolism in Mycobacterium tuberculosis (M.tb) Infection

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Molecular Microbiology and Immunology".

Deadline for manuscript submissions: closed (30 August 2024) | Viewed by 12913

Special Issue Editors

Dr. Pallavi Chandra

E-Mail Website
Guest Editor
Instructor in Medicine, Division of Infectious Diseases, Washington University School of Medicine, St louis, MO, USA
Interests: Mycobacterium tuberculosis pathogenesis; immunometabolism; autophagy
Dr. Selvakumar Subbian

E-Mail Website
Guest Editor
New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA
Interests: vaccines; innate immunity; macrophages; neutrophils; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tuberculosis (TB) is a leading infectious disease killer worldwide and is only second to COVID-19. Mycobacterium tuberculosis, the pathogen that causes TB, has the ability to persist in its host and evade multiple antimicrobial mechanisms. M. tuberculosis infection can result in diverse clinical outcomes such as latent asymptomatic infection, active pulmonary disease, and extrapulmonary manifestations. Global efforts to eradicate TB are marred by an alarming increase in multi-drug resistant infections. Thus, there is a pressing need for an advanced understanding of this disease for the development of novel therapies. Recent years have seen substantial research investigating the impact of cellular metabolism on immunity with respect to M. tuberculosis. How host and pathogen influence cellular metabolism and how these interactions shape infection outcomes are poorly understood.

As the Guest Editor of this Special Issue, I invite you to submit original research articles, short communications, and review articles related to immunometabolism in M. tuberculosis pathogenesis. Research articles and short communications may describe metabolic dysfunction underlying inadequate immune responses to M. tuberculosis infection alone or during comorbidities, and metabolic perturbations and metabolites that enhance immunity against TB. Reviews should present the latest advancements in our understanding of immunometabolic crosstalk during M. tuberculosis infections and address gaps in current knowledge. Future investigations into this evolving discipline will contribute to an improved understanding of M. tuberculosis pathogenesis and aid in the development of TB therapies and biomarkers.

This Special Issue is jointly organized with the Special Issue “Mycobacterial Pathogenesis, Drug Resistance and Intervention Strategies“ in journal Medicina. 

Dr. Pallavi Chandra
Dr. Selvakumar Subbian
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. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • metabolism
  • immunity
  • immunometabolism
  • tuberculosis, Mycobacterium tuberculosis

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Published Papers (5 papers)

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Research

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14 pages, 11615 KiB  
Article
miR-4687-5p Affects Intracellular Survival of Mycobacterium tuberculosis through Its Regulation of NRAMP1 Expression in A549 Cells
by Chaoqun Meng, Guangxin Chen, Yue Liu, Da Wen, Jia Cui, Li Dong, Zhiqiang Yang, Hangting Meng, Yuanting Gao, Jiao Feng, Xiaogang Cui and Changxin Wu
Microorganisms 2024, 12(1), 227; https://doi.org/10.3390/microorganisms12010227 - 22 Jan 2024
Viewed by 1599
Abstract
Tuberculosis (TB), as one of the leading causes of death, poses a serious predicament to the world. MicroRNAs (miRNAs) play a role in the post-transcriptional regulation of gene expression. It has been reported that the expression of miRNAs changes upon mycobacterial infection; the [...] Read more.
Tuberculosis (TB), as one of the leading causes of death, poses a serious predicament to the world. MicroRNAs (miRNAs) play a role in the post-transcriptional regulation of gene expression. It has been reported that the expression of miRNAs changes upon mycobacterial infection; the screening and identification of miRNAs regulating the expression of genes could benefit our understanding of TB pathogenesis and generate effective strategies for its control and prevention. In this study, luciferase assays showed that miR-4687-5p is bound to the 3′-untranslated region of natural resistance-associated macrophage protein 1 (NRAMP1). Additionally, we found a significant increase in miR-4687-5p expression in Mycobacterium tuberculosis (Mtb)-infected A549 cells. Concomitantly, we detected a reduced level of NRAMP1 expression, suggesting that NRAMP1 is one of the targets of miR-4687-5p. Infection experiments evidenced that the transfection of miR-4687-5p induced a decrease in NRAMP1 expression and increased intracellular Mtb loads post-infection, indicating that miR-4687-5p promotes the intracellular survival of Mtb through its downregulation of the NRAMP1 protein level. We also found that the transfection of miR-4687-5p induced increased apoptosis and decreased cell proliferation post-infection with Mtb. The results presented in our study suggest that miR-4687-5p may be indicative of the susceptibility of Mtb infection to humans and could act as a potential therapeutic target for tuberculosis treatment. Full article
(This article belongs to the Special Issue Immunometabolism in Mycobacterium tuberculosis (M.tb) Infection)
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19 pages, 14382 KiB  
Article
Temporal Profiling of Host Proteome against Different M. tuberculosis Strains Reveals Delayed Epigenetic Orchestration
by Prabhakar Babele, Mukul K. Midha, Kanury V. S. Rao and Ajay Kumar
Microorganisms 2023, 11(12), 2998; https://doi.org/10.3390/microorganisms11122998 - 16 Dec 2023
Viewed by 1443
Abstract
Apart from being preventable and treatable, tuberculosis is the deadliest bacterial disease afflicting humankind owing to its ability to evade host defence responses, many of which are controlled by epigenetic mechanisms. Here, we report the temporal dynamics of the proteome of macrophage-like host [...] Read more.
Apart from being preventable and treatable, tuberculosis is the deadliest bacterial disease afflicting humankind owing to its ability to evade host defence responses, many of which are controlled by epigenetic mechanisms. Here, we report the temporal dynamics of the proteome of macrophage-like host cells after infecting them for 6, 18, 30, and 42 h with two laboratory strains (H37Ra and H37Rv) and two clinical strains (BND433 and JAL2287) of Mycobacterium tuberculosis (MTB). Using SWATH-MS, the proteins characterized at the onset of infection broadly represented oxidative stress and cell cytoskeleton processes. Intermediary and later stages of infection are accompanied by a reshaping of the combination of proteins implicated in histone stability, gene expression, and protein trafficking. This study provides strain-specific and time-specific variations in the proteome of the host, which might further the development of host-directed therapeutics and diagnostic tools against the pathogen. Also, our findings accentuate the importance of proteomic tools in delineating the complex recalibration of the host defence enabled as an effect of MTB infection. To the best of our knowledge, this is the first comprehensive proteomic account of the host response to avirulent and virulent strains of MTB at different time periods of the life span of macrophage-like cells. The mass spectrometry proteomics data have been deposited in the ProteomeXchange Consortium via the PRIDE repository with the dataset identifier PXD022352. Full article
(This article belongs to the Special Issue Immunometabolism in Mycobacterium tuberculosis (M.tb) Infection)
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12 pages, 2854 KiB  
Article
Evaluation of the Toxic Activity of the Graphene Oxide in the Ex Vivo Model of Human PBMC Infection with Mycobacterium tuberculosis
by Alessandro Salustri, Flavio De Maio, Valentina Palmieri, Giulia Santarelli, Ivana Palucci, Delia Mercedes Bianco, Federica Marchionni, Silvia Bellesi, Gabriele Ciasca, Giordano Perini, Maurizio Sanguinetti, Michela Sali, Massimiliano Papi, Marco De Spirito and Giovanni Delogu
Microorganisms 2023, 11(3), 554; https://doi.org/10.3390/microorganisms11030554 - 22 Feb 2023
Cited by 3 | Viewed by 1955
Abstract
Graphene Oxide has been proposed as a potential adjuvant to develop improved anti-TB treatment, thanks to its activity in entrapping mycobacteria in the extracellular compartment limiting their entry in macrophages. Indeed, when administered together with linezolid, Graphene Oxide significantly enhanced bacterial killing due [...] Read more.
Graphene Oxide has been proposed as a potential adjuvant to develop improved anti-TB treatment, thanks to its activity in entrapping mycobacteria in the extracellular compartment limiting their entry in macrophages. Indeed, when administered together with linezolid, Graphene Oxide significantly enhanced bacterial killing due to the increased production of Reactive Oxygen Species. In this work, we evaluated Graphene Oxide toxicity and its anti-mycobacterial activity on human peripheral blood mononuclear cells. Our data show that Graphene Oxide, different to what is observed in macrophages, does not support the clearance of Mycobacterium tuberculosis in human immune primary cells, probably due to the toxic effects of the nano-material on monocytes and CD4+ lymphocytes, which we measured by cytometry. These findings highlight the need to test GO and other carbon-based nanomaterials in relevant in vitro models to assess the cytotoxic activity while measuring antimicrobial potential. Full article
(This article belongs to the Special Issue Immunometabolism in Mycobacterium tuberculosis (M.tb) Infection)
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Review

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13 pages, 1493 KiB  
Review
Differential Regulation of TFEB-Induced Autophagy during Mtb Infection and Starvation
by Richa Dwivedi and Piyush Baindara
Microorganisms 2023, 11(12), 2944; https://doi.org/10.3390/microorganisms11122944 - 8 Dec 2023
Cited by 2 | Viewed by 1670
Abstract
Through the promotion of phagolysosome formation, autophagy has emerged as a crucial mechanism to eradicate intracellular Mycobacterium tuberculosis (Mtb). A cell-autonomous host defense mechanism called lysosome biogenesis and autophagy transports cytoplasmic cargos and bacterial phagosomes to lysosomes for destruction during infection. Similar occurrences [...] Read more.
Through the promotion of phagolysosome formation, autophagy has emerged as a crucial mechanism to eradicate intracellular Mycobacterium tuberculosis (Mtb). A cell-autonomous host defense mechanism called lysosome biogenesis and autophagy transports cytoplasmic cargos and bacterial phagosomes to lysosomes for destruction during infection. Similar occurrences occurred in stressful or starvation circumstances and led to autophagy, which is harmful to the cell. It is interesting to note that under both hunger and infection states, the transcription factor EB (TFEB) acts as a master regulator of lysosomal activities and autophagy. This review highlighted recent research on the multitier regulation of TFEB-induced autophagy by a variety of host effectors and Mtb sulfolipid during Mtb infection and starvation. In general, the research presented here sheds light on how lysosome biogenesis and autophagy are differentially regulated by the TFEB during Mtb infection and starvation. Full article
(This article belongs to the Special Issue Immunometabolism in Mycobacterium tuberculosis (M.tb) Infection)
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14 pages, 1018 KiB  
Review
Possible Mechanisms of Lymphopenia in Severe Tuberculosis
by Fei Li, Dandan Chen, Qingqing Zeng and Yunjie Du
Microorganisms 2023, 11(11), 2640; https://doi.org/10.3390/microorganisms11112640 - 27 Oct 2023
Cited by 4 | Viewed by 4221
Abstract
Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis (M. tuberculosis). In lymphopenia, T cells are typically characterized by progressive loss and a decrease in their count results. Lymphopenia can hinder immune responses and lead to systemic immunosuppression, which [...] Read more.
Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis (M. tuberculosis). In lymphopenia, T cells are typically characterized by progressive loss and a decrease in their count results. Lymphopenia can hinder immune responses and lead to systemic immunosuppression, which is strongly associated with mortality. Lymphopenia is a significant immunological abnormality in the majority of patients with severe and advanced TB, and its severity is linked to disease outcomes. However, the underlying mechanism remains unclear. Currently, the research on the pathogenesis of lymphopenia during M. tuberculosis infection mainly focuses on how it affects lymphocyte production, survival, or tissue redistribution. This includes impairing hematopoiesis, inhibiting T-cell proliferation, and inducing lymphocyte apoptosis. In this study, we have compiled the latest research on the possible mechanisms that may cause lymphopenia during M. tuberculosis infection. Lymphopenia may have serious consequences in severe TB patients. Additionally, we discuss in detail potential intervention strategies to prevent lymphopenia, which could help understand TB immunopathogenesis and achieve the goal of preventing and treating severe TB. Full article
(This article belongs to the Special Issue Immunometabolism in Mycobacterium tuberculosis (M.tb) Infection)
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