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Related Concept Videos

Pulmonary Tuberculosis I01:29

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Tuberculosis, often called TB, is a contagious illness primarily caused by Mycobacterium tuberculosis. It mainly affects the lung parenchyma but can also impact other body parts.
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
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Pulmonary Tuberculosis V01:28

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Medical management of tuberculosis (TB) patients involves a comprehensive approach that includes diagnosis, treatment, and monitoring. The specific strategies can vary depending on the type of tuberculosis (latent or active), the patient's overall health status, and other considerations.
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Pulmonary Tuberculosis II01:28

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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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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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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.
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Related Experiment Video

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An Automated Culture System for Use in Preclinical Testing of Host-Directed Therapies for Tuberculosis
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Vitamin D, cell death pathways, and tuberculosis.

Manik Retno Wahyunitisari1, Ni Made Mertaniasih1, Muhammad Amin2

  • 1Department of Medical Microbiology, Faculty of Medicine, Airlangga University, Surabaya, East Java, Indonesia.

International Journal of Mycobacteriology
|November 25, 2017
PubMed
Summary

Vitamin D3 supplementation enhances second-line tuberculosis drug therapy by increasing autophagy and apoptosis, thereby reducing Mycobacterium tuberculosis-induced necrosis and bacterial load. This combination therapy is crucial for improving treatment outcomes in tuberculosis.

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A 3D Human Lung Tissue Model for Functional Studies on Mycobacterium tuberculosis Infection
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Area of Science:

  • Immunology
  • Microbiology
  • Pharmacology

Background:

  • Tuberculosis (TB) infection caused by Mycobacterium tuberculosis can lead to cellular necrosis, potentially promoting disease spread.
  • Investigating strategies to enhance the effectiveness of second-line anti-TB drug therapy is critical for managing multidrug-resistant strains.

Purpose of the Study:

  • To analyze the effects of Vitamin D3 supplementation on the efficacy of second-line anti-TB drug therapy.
  • To investigate the impact of Vitamin D3 on cell death pathways, including apoptosis and autophagy, in the context of TB infection.

Main Methods:

  • A mouse model of multidrug-resistant TB was used, with groups receiving either second-line therapy alone or in combination with Vitamin D3.
  • Immunohistochemistry was employed to assess markers of Vitamin D receptor, apoptosis (caspase-3), autophagy (LC3B), necrosis (RIPK3), and matrix metalloproteinase-1 (MMP1).
  • Bacterial load was quantified using colony-forming units, and data were analyzed using partial least square structural equation modeling.

Main Results:

  • Vitamin D3 supplementation alongside second-line anti-TB therapy significantly increased Vitamin D receptor, CRAMP, LC3B, and caspase-3 expression.
  • This combined therapy suppressed MMP1 expression and reduced the bacterial load in the lungs.
  • Structural equation modeling indicated that increased autophagy pathways reduce necrosis by lowering MMP1, while apoptosis reduces necrosis by decreasing bacterial numbers.

Conclusions:

  • Decreasing necrosis in tuberculosis requires the enhancement of both autophagy and apoptosis pathways.
  • Vitamin D3 supplementation shows promise as an adjunct therapy to improve the effectiveness of second-line anti-TB drugs by modulating cell death mechanisms.