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The endoplasmic reticulum stress response: A link with tuberculosis?
Yongyong Cui1, Deming Zhao1, Paul Andrew Barrow2
1The State Key Lab of Agrobiotechnology, Key Lab of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National TSE Lab, College of Veterinary Medicine, China Agricultural University, Beijing 100193, PR China.
Tuberculosis (Edinburgh, Scotland)
|March 17, 2016
Summary
Tuberculosis infection triggers endoplasmic-reticulum stress (ERS) to manage misfolded proteins. Uncontrolled ERS signaling pathways can lead to cell death, aiding mycobacterial spread.
Area of Science:
- Cellular Biology
- Immunology
- Microbiology
Background:
- Tuberculosis (TB) is a significant global health issue.
- Mycobacterial infection induces endoplasmic-reticulum stress (ERS), a cellular response to protein misfolding.
- The unfolded protein response (UPR) is activated to restore ER homeostasis.
Purpose of the Study:
- To summarize recent advancements in understanding ERS signaling pathways in TB.
- To explore the role of ERS in the host-pathogen interaction during TB.
Main Methods:
- Literature review of recent research on ERS and TB.
- Analysis of signaling pathways involved in the UPR (IRE1, PERK, ATF6).
Main Results:
- ERS is a critical cellular process in response to mycobacterial infection.
- Dysregulated ERS and UPR can lead to apoptosis, impacting TB pathogenesis.
- Specific signaling pathways (IRE1, PERK, ATF6) govern ERS outcomes.
Conclusions:
- Understanding ERS signaling diversity is crucial for TB research.
- Targeting ERS pathways may offer novel therapeutic strategies for TB.
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