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Zinc: An Emerging Axis of Host-Pathogen Interaction in Tuberculosis
Jordan Holl1,2, Jamie Corro1,2, Bibhuti B Mishra3
1Division of Genetics, Wadsworth Center, New York State Department of Health, Albany, NY 12208, USA.
Vaccines
|July 27, 2026
Summary
Zinc limitation is a key host defense against tuberculosis. Mycobacterium tuberculosis (Mtb) adapts to low zinc environments, contributing to its long-term persistence within the host during infection.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Tuberculosis (TB) is caused by Mycobacterium tuberculosis (Mtb), a pathogen requiring essential micronutrients like zinc.
- The host employs nutritional immunity, including zinc sequestration, to restrict pathogen growth.
- Calprotectin, a neutrophil protein, is crucial in limiting microbial access to zinc.
Purpose of the Study:
- To review recent findings on zinc-responsive adaptations in Mtb.
- To explore the role of host zinc limitation in Mtb persistence and pathogenesis.
Main Methods:
- Literature review of studies on zinc homeostasis and Mtb.
- Analysis of Mtb's adaptive strategies to nutrient-scarce environments.
- Synthesis of current understanding of host-pathogen interactions regarding zinc.
Main Results:
- Mtb possesses sophisticated mechanisms to sense and respond to zinc scarcity.
- Host-induced zinc limitation is a significant factor influencing Mtb's ability to persist.
- Understanding these adaptations is crucial for developing novel therapeutic strategies.
Conclusions:
- Host zinc limitation is a critical, yet often underestimated, factor in Mtb pathogenesis.
- Mtb's adaptive responses to zinc deficiency facilitate its long-term survival and persistence.
- Targeting zinc metabolism in Mtb or modulating host immunity could offer new avenues for TB treatment.
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