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Expression and function of the purinergic receptor P2X7 in patients with pulmonary tuberculosis

S Franco-Martínez1, P Niño-Moreno, S Bernal-Silva

  • 1Department of Immunology, Facultad de Medicina, UASLP, San Luis Potosí, SLP, Mexico.

Clinical and Experimental Immunology
|October 13, 2006
PubMed

Insights

Tuberculosis patients show altered gene expression in response to adenosine triphosphate (ATP), suggesting a defective P2X(7) channel receptor function crucial for fighting Mycobacterium tuberculosis.

Area of Science:

  • Immunology
  • Molecular Biology
  • Infectious Diseases

Background:

  • P2X(7) receptor is an ATP-gated ion channel involved in host defense against intracellular pathogens.
  • Mycobacterium tuberculosis infection, causing tuberculosis (TB), poses a significant global health challenge.
  • Understanding immune cell function in TB is critical for developing effective treatments.

Purpose of the Study:

  • To investigate the role of the P2X(7) receptor in immune responses during pulmonary tuberculosis.
  • To compare P2X(7) expression and function in patients with TB and healthy controls.

Main Methods:

  • Flow cytometry to assess P2X(7) expression on peripheral blood mononuclear cells (PBMC).
  • Analysis of P2X(7) mRNA levels.
  • Functional assays including ATP-induced apoptosis, Lucifer yellow uptake, and ERK phosphorylation.
  • mRNA macroarray analysis of gene expression changes upon ATP stimulation.

Main Results:

  • P2X(7) expression levels were similar, but mRNA levels were higher in TB patients.
  • No significant differences in P2X(7) functional assays (apoptosis, dye uptake, ERK phosphorylation) between groups.
  • ATP stimulation induced a higher number of cytokine genes and fewer apoptosis genes in TB patients' PBMC compared to controls.

Conclusions:

  • TB patients exhibit distinct ATP-induced gene expression patterns in PBMC, despite normal P2X(7) expression and basic function.
  • These findings suggest a potential P2X(7) functional defect in TB patients' immune cells.
  • This defect may impair the ability to control Mycobacterium tuberculosis infection.

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