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Related Concept Videos

Pulmonary Tuberculosis I01:29

Pulmonary Tuberculosis I

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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 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 (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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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 IV01:26

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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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Leukocyte disorders can lead to either leukopenia, characterized by an abnormally low leukocyte count, or leukocytosis, marked by a very high leukocyte number.
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Profiling leucocyte subsets in tuberculosis-diabetes co-morbidity.

Nathella Pavan Kumar1,2, Kadar Moideen1, Sharmila D Dhakshinraj1

  • 1National Institutes of Health-NIRT-International Centre for Excellence in Research, Chennai, India.

Immunology
|June 23, 2015
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Summary

Diabetes significantly alters immune cell profiles in individuals with tuberculosis (TB). The study reveals changes in T cells, B cells, monocytes, and dendritic cells, impacting the pathogenesis of this TB-diabetes comorbidity.

Keywords:
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Area of Science:

  • Immunology
  • Infectious Diseases
  • Endocrinology

Background:

  • The interplay between tuberculosis (TB) and type 2 diabetes mellitus (DM) significantly impacts disease pathogenesis.
  • Understanding the immune cell subset distribution in individuals with co-occurring TB and DM is crucial for managing this comorbidity.
  • Current knowledge gaps exist regarding leukocyte phenotypes at homeostasis in active or latent TB patients with diabetes.

Purpose of the Study:

  • To characterize the influence of diabetes on leukocyte phenotypes in individuals with active pulmonary tuberculosis (PTB) or latent tuberculosis infection (LTB).
  • To examine the frequency of leukocyte subsets in individuals across four groups: PTB with/without DM, LTB with/without DM, and non-TB infected (NTB) with/without DM.

Main Methods:

  • Flow cytometry was used to analyze the frequency of various leukocyte subsets.
  • Participants were categorized into groups based on TB status (active, latent, or none) and diabetes status (DM or no DM).
  • Leukocyte subset frequencies were compared across these distinct participant groups.

Main Results:

  • Diabetes was associated with lower effector memory CD4+ T cells in latent TB patients.
  • In active TB patients, diabetes correlated with lower effector memory CD8+ T cells and higher central memory CD8+ T cells.
  • Diabetes altered B cell populations (higher classical memory in PTB; higher activated/atypical in LTB) and reduced classical/intermediate monocytes and myeloid/plasmacytoid dendritic cells across all TB statuses.

Conclusions:

  • Coincident diabetes mellitus significantly alters the distribution of T cell, B cell, monocyte, and dendritic cell subsets in individuals with both active and latent tuberculosis.
  • These diabetes-induced immune cell alterations may play a critical role in the pathogenesis of the TB-DM comorbidity.
  • The findings highlight the complex immune dysregulation occurring in individuals with co-existing TB and diabetes.