Investigating the Role of Everolimus in mTOR Inhibition and Autophagy Promotion as a Potential Host-Directed Therapeutic Target in Mycobacterium tuberculosis Infection
Tuberculosis (TB) is a serious infectious disease caused by the pathogen ( ). The current therapy consists of a combination of antibiotics over the course of four months. Current treatment protocols run into problems due to the growing antibiotic resistance of and poor compliance to the multi-drug-r...
Saved in:
Published in: | Journal of clinical medicine Vol. 8; no. 2; p. 232 |
---|---|
Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
Switzerland
MDPI
11-02-2019
|
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Tuberculosis (TB) is a serious infectious disease caused by the pathogen
(
). The current therapy consists of a combination of antibiotics over the course of four months. Current treatment protocols run into problems due to the growing antibiotic resistance of
and poor compliance to the multi-drug-resistant TB treatment protocol. New treatments are being investigated that target host intracellular processes that could be effective in fighting
infections. Autophagy is an intracellular process that is involved in eliminating cellular debris, as well as intracellular pathogens. Mammalian target of rapamycin (mTOR) is an enzyme involved in inhibiting this pathway. Modulation of mTOR and the autophagy cellular machinery are being investigated as potential therapeutic targets for novel
treatments. In this review, we discuss the background of
pathogenesis, including its interaction with the innate and adaptive immune systems, the mTOR and autophagy pathways, the interaction of
with these pathways, and finally, the drug everolimus, which targets these pathways and is a potential novel therapy for TB treatment. |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 These authors contributed equally to this work. |
ISSN: | 2077-0383 2077-0383 |
DOI: | 10.3390/jcm8020232 |