Exploring and exploiting the host cell autophagy during Mycobacterium tuberculosis infection
Tuberculosis, caused by Mycobacterium tuberculosis , is a fatal infectious disease that prevails to be the second leading cause of death from a single infectious agent despite the availability of multiple drugs for treatment. The current treatment regimen involves the combination of several drugs fo...
Saved in:
Published in: | European journal of clinical microbiology & infectious diseases Vol. 42; no. 11; pp. 1297 - 1315 |
---|---|
Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Berlin/Heidelberg
Springer Berlin Heidelberg
01-11-2023
Springer Nature B.V |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Tuberculosis, caused by
Mycobacterium tuberculosis
, is a fatal infectious disease that prevails to be the second leading cause of death from a single infectious agent despite the availability of multiple drugs for treatment. The current treatment regimen involves the combination of several drugs for 6 months that remain ineffective in completely eradicating the infection because of several drawbacks, such as the long duration of treatment and the side effects of drugs causing non-adherence of patients to the treatment regimen. Autophagy is an intracellular degradative process that eliminates pathogens at the early stages of infection.
Mycobacterium tuberculosis’s
unique autophagy-blocking capability makes it challenging to eliminate compared to usual pathogens. The present review discusses recent advances in autophagy-inhibiting factors and mechanisms that could be exploited to identify autophagy-inducing chemotherapeutics that could be used as adjunctive therapy with the existing first-line anti-TB agent to shorten the duration of therapy and enhance cure rates from multidrug-resistant tuberculosis (MDR-TB) and extreme drug-resistant tuberculosis (XDR-TB). |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0934-9723 1435-4373 |
DOI: | 10.1007/s10096-023-04663-0 |