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Related Concept Videos

Pulmonary Tuberculosis II01:28

Pulmonary Tuberculosis II

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Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
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Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
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Tuberculosis, more commonly referred to as TB, is an infectious disease stemming from Mycobacterium tuberculosis. While it primarily impacts the lungs, TB can also affect other body areas. Given its severity and global impact, timely and accurate diagnosis is crucial for controlling its spread and improving patient outcomes.
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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
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Tuberculosis (TB) is a contagious infection primarily affecting the lung parenchyma but which can also affect other body parts. TB can be classified based on disease development, presentation, and the affected anatomical site.
The first classification is based on the development of the disease, and it includes the following categories:
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Related Experiment Video

Updated: Jan 6, 2026

Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1
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Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1

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Inflammasome Activation Differences Underpin Different Mycobacterium tuberculosis Infection Outcomes.

Ranjeet Kumar1, Afsal Kolloli1, Gunapati Bhargavi1

  • 1The Public Health Research Institute at New Jersey Medical School Rutgers University Newark New Jersey USA.

Medcomm
|November 25, 2025
PubMed
Summary

Progressive tuberculosis involves increased guanylate-binding protein-1 (GBP1) and hypoxia-inducible factor-1 alpha (HIF-1α), leading to NLRP3 inflammasome activation. This cellular response dictates infection outcomes, differentiating latent from active disease.

Keywords:
host‐pathogen interactionsimmune response to infectiontuberculosis

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Area of Science:

  • Immunology
  • Microbiology
  • Cellular Biology

Background:

  • Tuberculosis (TB) outcomes vary from latent to active disease.
  • Cellular mechanisms driving these different TB outcomes are not fully understood.

Purpose of the Study:

  • Investigate cellular pathways differentiating progressive from nonprogressive Mycobacterium tuberculosis (Mtb) infection.
  • Identify key molecular players influencing TB disease progression.

Main Methods:

  • Infection of rabbit lungs and macrophages (rabbit, human, THP-1) with virulent and nonvirulent Mtb strains.
  • Analysis of guanylate-binding protein-1 (GBP1), hypoxia-inducible factor-1 alpha (HIF-1α), and NLRP3 inflammasome activation.
  • Assessment of mitochondrial stress, apoptosis, and necrosis.
  • Gene knockdown studies for HIF-1α and GBP1.

Main Results:

  • Progressive Mtb infection correlates with elevated GBP1, HIF-1α, and NLRP3 inflammasome activation.
  • HIF-1α and GBP1 drive NLRP3 inflammasome activation, causing mitochondrial stress, apoptosis, and necrosis in progressive infections.
  • These pathways are suppressed in nonprogressive TB and in cells with reduced HIF-1α or GBP1.

Conclusions:

  • Differential activation of HIF-1α- and GBP1-mediated NLRP3 inflammasome pathways influences Mtb infection outcomes.
  • These findings provide insight into the cellular basis of TB disease progression.
  • Targeting these pathways could offer new therapeutic strategies for TB.