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Related Experiment Video

Updated: Apr 14, 2026

An Optimized Protocol to Analyze Glycolysis and Mitochondrial Respiration in Lymphocytes
08:40

An Optimized Protocol to Analyze Glycolysis and Mitochondrial Respiration in Lymphocytes

Published on: November 21, 2016

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Metabolic dysfunction in lymphocytes promotes postoperative morbidity.

Mark R Edwards1, Pervez Sultan1, Ana Gutierrez del Arroyo1

  • 1Clinical Physiology, Department of Medicine, University College London, London WC1E 6BT, U.K.

Clinical Science (London, England : 1979)
|April 21, 2015
PubMed
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Perioperative lymphopenia, characterized by low lymphocyte counts, increases infection risk due to impaired immune cell energy metabolism. This dysfunction, exacerbated by stress hormones, primes the inflammasome pathway, leading to immune suppression and complications.

Area of Science:

  • Immunology
  • Cellular Metabolism
  • Surgical Complications

Background:

  • Perioperative lymphopenia is linked to increased postoperative infectious complications, but underlying mechanisms are not fully understood.
  • Bioenergetic dysfunction is hypothesized to contribute to lymphopenia, impaired lymphocyte function, and subsequent infections.

Purpose of the Study:

  • To investigate the role of bioenergetic dysfunction in perioperative lymphopenia and its association with infectious complications.
  • To explore the impact of glucocorticoids on lymphocyte function and inflammasome activation.

Main Methods:

  • Prospective analysis of two patient cohorts undergoing joint replacement surgery (n=417 and 328).
  • Assessment of lymphocyte respirometry, mitochondrial bioenergetics, and function in patients (n=93).
Keywords:
apoptosisinflammasomelymphocytemetabolismmitochondriasepsis

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Last Updated: Apr 14, 2026

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Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells
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  • Evaluation of inflammasome activation (NLRP1, NLRP3) and lymphocyte apoptosis in response to glucocorticoids.

    • Main Results:

    • Preoperative lymphopenia was associated with higher rates of infectious complications and prolonged hospital stays.
    • Postoperative lymphocytes exhibited significantly reduced spare respiratory capacity and glycolytic capacity.
    • Lymphocytes from chronically lymphopenic patients showed a similar hypometabolic phenotype, linked to impaired T-cell proliferation, reduced cytokine production, and increased apoptosis.
    • Glucocorticoids induced mitochondrial reactive oxygen species, caspase-1 activation, and IL-1β release in lymphocytes, suggesting NLRP1 inflammasome activation.

    Conclusions:

    • A hypometabolic phenotype in lymphocytes, either pre-existing or acquired postoperatively, contributes to increased infection risk.
    • Glucocorticoid-induced activation of caspase-1 via the NLRP1 inflammasome pathway plays a critical role in lymphocyte dysfunction and apoptosis.
    • Targeting bioenergetic pathways and inflammasome activation may offer strategies to mitigate postoperative infectious complications.