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Microorganisms
Special Issues
Nontuberculous Mycobacteria: Recent Advancements in Infection, Diagnosis and Therapy
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Nontuberculous Mycobacteria: Recent Advancements in Infection, Diagnosis and Therapy

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

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 5225

Special Issue Editors

Dr. Masaki Fujita

E-Mail Website
Guest Editor
Department of Respiratory Medicine, Faculty of Medicine, Fukuoka University, Fukuoka 814-0180, Japan
Interests: development of novel treatment
Dr. Kozo Morimoto

E-Mail Website
Guest Editor
Division of Clinical Research, Fukujuji Hospital, Japan Anti-Tuberculosis Association, Tokyo 204-8522, Japan
Interests: nontuberculous mycobacteria; bronchiectasi; primary ciliary dyskinesia; environment; epidemiology; treatment
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mycobacterium spp. is a human pathogen which proliferates intracellularly in phagocytes and includes the Mycobaterium tuberculosis complex, M. leprae, and non-tuberculous mycobacteria. Tuberculosis is a well-known, highly contagious but treatable disease. By contrast, although non-tuberculous mycobacteriosis (NTM) is not contagious, it is particularly difficult to treat. M. avium-intracellulare complex (MAC) is often the culprit organism behind NTM, causing chronic progressive respiratory infection. M. abscessus infection is especially difficult to treat. The development of novel treatments for pulmonary NTM is therefore needed urgently.

The aim of this Special Issue is to provide a platform for researchers interested in pulmonary NTM to share their recent results. To achieve this, we are inviting you to submit research articles, short communications, and reviews related to the various aspects of epidemiology, genetic susceptibility, infection mechanism, and novel treatment. Information that will improve our understanding of the NTM and lead to novel treatment is especially welcome.

Dr. Masaki Fujita
Dr. Kozo Morimoto
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

  • Mycobacterium avium
  • Mycobacterium intracellulare
  • Mycobacterium abscessus
  • epidemiology
  • susceptibility
  • infection mechanism
  • novel treatment
  • liposomal amikacin
  • re-infection

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Published Papers (4 papers)

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Research

13 pages, 3820 KiB  
Article
TNFR1 Mediated Apoptosis Is Protective against Mycobacterium avium in Mice
by Yuki Shundo, Rintaro On, Takemasa Matsumoto, Hiroshi Ouchi and Masaki Fujita
Microorganisms 2023, 11(3), 778; https://doi.org/10.3390/microorganisms11030778 - 17 Mar 2023
Cited by 2 | Viewed by 1839
Abstract
Mycobacterium avium is an intracellular proliferating pathogen that causes chronic refractory respiratory infection. Although apoptosis induced by M. avium has been reported in vitro, the role of apoptosis against M. avium infection in vivo remains unclear. Here, we investigated the role of apoptosis [...] Read more.
Mycobacterium avium is an intracellular proliferating pathogen that causes chronic refractory respiratory infection. Although apoptosis induced by M. avium has been reported in vitro, the role of apoptosis against M. avium infection in vivo remains unclear. Here, we investigated the role of apoptosis in mouse models of M. avium infection. Tumor necrosis factor receptor-1 knockout mice (TNFR1-KO) andTNFR2-KO micewere used. M. avium (1 × 107 cfu/body) was administered intratracheally to mice. Apoptosis in lungs was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling and lung histology as well as cell death detection kits using BAL fluids. TNFR1-KO mice were susceptible to M. avium infection compared with TNFR2-KO and wild type mice based on the bacterial number and lung histology. Higher numbers of apoptotic cells were detected in the lungs of TNFR2-KO and wild-type mice were compared with TNFR1-KO mice. The inhalation of Z-VAD-FMK deteriorated M. avium infection compared with vehicle-inhaled controls. Overexpression of Iκ-B alpha by adenovirus vector attenuated M. avium infection. Our study showed apoptosis had an important role in innate immunity against M. avium in mice. The induction of apoptosis in M. avium-infected cells might be a new strategy to control M. avium infection. Full article
(This article belongs to the Special Issue Nontuberculous Mycobacteria: Recent Advancements in Infection, Diagnosis and Therapy)
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19 pages, 11122 KiB  
Article
Methylprednisolone Promotes Mycobacterium smegmatis Survival in Macrophages through NF-κB/DUSP1 Pathway
by Anlong Li, Yonglin He, Chun Yang, Nan Lu, Jiajia Bao, Sijia Gao, Felycia Fernanda Hosyanto, Xintong He, Huichao Fu, Huajian Yan, Ningyu Ding and Lei Xu
Microorganisms 2023, 11(3), 768; https://doi.org/10.3390/microorganisms11030768 - 16 Mar 2023
Cited by 7 | Viewed by 2511
Abstract
Background: Mycobacterium tuberculosis (M. tuberculosis) is the causative agent of tuberculosis. As an important component of host immunity, macrophages are not only the first line of defense against M. tuberculosis but also the parasitic site of M. tuberculosis in the host. [...] Read more.
Background: Mycobacterium tuberculosis (M. tuberculosis) is the causative agent of tuberculosis. As an important component of host immunity, macrophages are not only the first line of defense against M. tuberculosis but also the parasitic site of M. tuberculosis in the host. Glucocorticoids can cause immunosuppression, which is considered to be one of the major risk factors for active tuberculosis, but the mechanism is unclear. Objective: To study the effect of methylprednisolone on the proliferation of mycobacteria in macrophages and try to find key molecules of this phenomenon. Methods: The macrophage line RAW264.7 infected by M. smegmatis was treated with methylprednisolone, and the intracellular bacterial CFU, Reactive Oxygen Species (ROS), cytokine secretion, autophagy, and apoptosis were measured. After the cells were treated with NF-κB inhibitor BAY 11-7082 and DUSP1 inhibitor BCI, respectively, the intracellular bacterial CFU, ROS, IL-6, and TNF-α secretion were detected. Results: After treatment with methylprednisolone, the CFU of intracellular bacteria increased, the level of ROS decreased, and the secretion of IL-6 and TNF-α decreased in infected macrophages. After BAY 11-7082 treatment, the CFU of M. smegmatis in macrophages increased, and the level of ROS production and the secretion of IL-6 by macrophages decreased. Transcriptome high-throughput sequencing and bioinformatics analysis suggested that DUSP1 was the key molecule in the above phenomenon. Western blot analysis confirmed that the expression level of DUSP1 was increased in the infected macrophages treated with methylprednisolone and BAY 11-7082, respectively. After BCI treatment, the level of ROS produced by infected macrophages increased, and the secretion of IL-6 increased. After the treatment of BCI combined with methylprednisolone or BAY 11-7082, the level of ROS produced and the secretion of IL-6 by macrophages were increased. Conclusion: methylprednisolone promotes the proliferation of mycobacteria in macrophages by suppressing cellular ROS production and IL-6 secretion through down-regulating NF-κB and up-regulating DUSP1 expression. BCI, an inhibitor of DUSP1, can reduce the level of DUSP1 in the infected macrophages and inhibit the proliferation of intracellular mycobacteria by promoting cellular ROS production and IL-6 secretion. Therefore, BCI may become a new molecule for host-directed therapy of tuberculosis, as well as a new strategy for the prevention of tuberculosis when treated with glucocorticoids. Full article
(This article belongs to the Special Issue Nontuberculous Mycobacteria: Recent Advancements in Infection, Diagnosis and Therapy)
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14 pages, 3900 KiB  
Article
Activity of Drug Combinations against Mycobacterium abscessus Grown in Aerobic and Hypoxic Conditions
by Alessio Lanni, Emanuele Borroni, Angelo Iacobino, Cristina Russo, Leonarda Gentile, Lanfranco Fattorini and Federico Giannoni
Microorganisms 2022, 10(7), 1421; https://doi.org/10.3390/microorganisms10071421 - 14 Jul 2022
Cited by 11 | Viewed by 2648
Abstract
Infections caused by Mycobacterium abscessus (Mab), an environmental non-tuberculous mycobacterium, are difficult to eradicate from patients with pulmonary diseases such as cystic fibrosis and bronchiectasis even after years of antibiotic treatments. In these people, the low oxygen pressure in mucus and biofilm may [...] Read more.
Infections caused by Mycobacterium abscessus (Mab), an environmental non-tuberculous mycobacterium, are difficult to eradicate from patients with pulmonary diseases such as cystic fibrosis and bronchiectasis even after years of antibiotic treatments. In these people, the low oxygen pressure in mucus and biofilm may restrict Mab growth from actively replicating aerobic (A) to non-replicating hypoxic (H) stages, which are known to be extremely drug-tolerant. After the exposure of Mab A and H cells to drugs, killing was monitored by measuring colony-forming units (CFU) and regrowth in liquid medium (MGIT 960) of 1-day-old A cells (A1) and 5-day-old H cells (H5). Mab killing was defined as a lack of regrowth of drug-exposed cells in MGIT tubes after >50 days of incubation. Out of 18 drugs tested, 14-day treatments with bedaquiline-amikacin (BDQ-AMK)-containing three-drug combinations were very active against A1 + H5 cells. However, drug-tolerant cells (persisters) were not killed, as shown by CFU curves with typical bimodal trends. Instead, 56-day treatments with the nitrocompounds containing combinations BDQ-AMK-rifabutin-clarithromycin-nimorazole and BDQ-AMK-rifabutin-clarithromycin-metronidazole-colistin killed all A1 + H5 Mab cells in 42 and 56 days, respectively, as shown by lack of regrowth in agar and MGIT medium. Overall, these data indicated that Mab persisters may be killed by appropriate drug combinations. Full article
(This article belongs to the Special Issue Nontuberculous Mycobacteria: Recent Advancements in Infection, Diagnosis and Therapy)
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11 pages, 646 KiB  
Article
Mycobacterium chimaera Identification Using MALDI-TOF MS Technology: A Practical Approach for the Clinical Microbiology Laboratories
by Jessica Bagnarino, Daniela Barbarini, Giuseppe Russello, Mariangela Siciliano, Vincenzina Monzillo, Fausto Baldanti and Edoardo Carretto
Microorganisms 2022, 10(6), 1184; https://doi.org/10.3390/microorganisms10061184 - 9 Jun 2022
Cited by 7 | Viewed by 2400
Abstract
Mycobacterium chimaera (MC) is an environmental, slowly growing, non-tuberculous mycobacterium (NTM) belonging to Mycobacterium avium complex (MAC), which recently has been linked to severe cardiovascular infections following open heart and vascular surgery. The majority of the diagnostic laboratory tests used in routine are [...] Read more.
Mycobacterium chimaera (MC) is an environmental, slowly growing, non-tuberculous mycobacterium (NTM) belonging to Mycobacterium avium complex (MAC), which recently has been linked to severe cardiovascular infections following open heart and vascular surgery. The majority of the diagnostic laboratory tests used in routine are not able to distinguish MC from M. intracellulare (MI), because of the great genetic similarity existing between these two species. The Genotype Mycobacterium NTM-DR™ represents a valid method to differentiate between these species, but it is expensive, requiring also specialized personnel. Recently, MALDI-TOF MS has been proposed to identify relevant NTM. However, a software implementation is required to distinguish between MC and MI, presenting the two microorganisms’ overlapping spectra. The present study evaluates the feasibility of applying a MALDI-TOF logarithmic-based analysis in the routine of a clinical microbiology laboratory, and proposes an easy-to-use template spreadsheet to make the results quickly interpretable. The protocol was previously validated through the identification of 87 strains of MC/MI collected from clinical and environmental samples, and it was identified using the GenoType Mycobacterium NTM-DR™ and/or WGS. The proposed protocol provides accurate identification for the isolates tested; moreover, it is less expensive and more rapid than sequencing methods and can be implemented with minimum effort. Full article
(This article belongs to the Special Issue Nontuberculous Mycobacteria: Recent Advancements in Infection, Diagnosis and Therapy)
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