Stress Response in Tuberculosis

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Bacterial Pathogens".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1699

Special Issue Editor

Seattle Children’s Research Institute, Seattle, WA 98109, USA
Interests: tuberculosis; drug response; host–pathogen interactions; systems biology

Special Issue Information

Dear Colleagues,

Tuberculosis (TB) is a serious global health concern, and its impact has been worsened by the increased burden on global healthcare systems imposed by COVID-19. The disease is so successful in part due to the capacity of the pathogen Mycobacterium tuberculosis to adapt and respond to a broad range of stresses from a diverse array of environmental and drug conditions.  Understanding the mechanisms by which Mycobacterium tuberculosis (Mtb) can tolerate, persist, and adapt to these stresses could help improve TB intervention strategies.

The aim of this Special Issue is to publish original research papers, meta-analyses, reviews, or perspective pieces that explore the effects of different environmental or drug-associated stresses on modulating disease or treatment outcomes in TB. Clinical research focused on epidemiological trends or patient outcomes associated with exposure to these stresses, as well as basic research that studies the phenotypic and molecular mechanisms of stress response and adaptation, are most welcome.

Dr. Shuyi Ma
Guest Editor

Manuscript Submission Information

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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

  • tuberculosis
  • stress response
  • stress adaptation
  • host–pathogen interactions
  • host stress
  • host adaptation
  • microenvironment adaptation
  • adaptive niche
  • drug response
  • drug adaptation
  • drug resistance

Published Papers (1 paper)

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Review

16 pages, 328 KiB  
Review
Cigarette Smoking as a Risk Factor for Tuberculosis in Adults: Epidemiology and Aspects of Disease Pathogenesis
by Charles Feldman, Annette J. Theron, Moloko C. Cholo and Ronald Anderson
Pathogens 2024, 13(2), 151; https://doi.org/10.3390/pathogens13020151 - 07 Feb 2024
Viewed by 1165
Abstract
It has been noted by the World Health Organisation that cases of tuberculosis in 2022 globally numbered 10.6 million, resulting in 1.3 million deaths, such that TB is one of the infectious diseases causing the greatest morbidity and mortality worldwide. Since as early [...] Read more.
It has been noted by the World Health Organisation that cases of tuberculosis in 2022 globally numbered 10.6 million, resulting in 1.3 million deaths, such that TB is one of the infectious diseases causing the greatest morbidity and mortality worldwide. Since as early as 1918, there has been an ongoing debate as to the relationship between cigarette smoking and TB. However, numerous epidemiological studies, as well as meta-analyses, have indicated that both active and passive smoking are independent risk factors for TB infection, development of reactivation TB, progression of primary TB, increased severity of cavitary disease, and death from TB, among several other considerations. With this considerable body of evidence confirming the association between smoking and TB, it is not surprising that TB control programmes represent a key potential preventative intervention. In addition to coverage of the epidemiology of TB and its compelling causative link with smoking, the current review is also focused on evidence derived from clinical- and laboratory-based studies of disease pathogenesis, most prominently the protective anti-mycobacterial mechanisms of the alveolar macrophage, the primary intracellular refuge of M. tuberculosis. This section of the review is followed by an overview of the major strategies utilised by the pathogen to subvert these antimicrobial mechanisms in the airway, which are intensified by the suppressive effects of smoke inhalation on alveolar macrophage function. Finally, consideration is given to a somewhat under-explored, pro-infective activity of cigarette smoking, namely augmentation of antibiotic resistance due to direct effects of smoke per se on the pathogen. These include biofilm formation, induction of cellular efflux pumps, which eliminate both smoke-derived toxicants and antibiotics, as well as gene modifications that underpin antibiotic resistance. Full article
(This article belongs to the Special Issue Stress Response in Tuberculosis)
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