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Effect of protein synthesis inhibition by cycloheximide on lymphocyte circulation

J L Wiebke1, W M Quinlan, L Graham

  • 1Department of Pediatrics, Indiana University, Indianapolis.

Laboratory Investigation; a Journal of Technical Methods and Pathology
|March 1, 1994
PubMed

Insights

Inhibiting protein synthesis increases circulating lymphocytes by reducing their homing to specific lymphoid tissues like the spleen and lymph nodes, but not the lungs. This rapid regulation affects all lymphocyte types.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Lymphocyte recirculation is crucial for immune surveillance and is mediated by specific adhesion molecules.
  • The homing of lymphocytes to various lymphoid tissues depends on the expression of these glycoprotein adhesion molecules.

Purpose of the Study:

  • To investigate the impact of inhibiting new protein synthesis on lymphocyte circulation and tissue homing.
  • To determine if protein synthesis inhibition affects lymphocyte distribution in different lymphoid organs.

Main Methods:

  • Administration of cycloheximide (protein synthesis inhibitor) or buffer to rabbits and rats.
  • Measurement of total circulating lymphocyte counts and lymphocyte subsets.
  • Tracking of autologous, radiolabeled lymphocytes to assess organ distribution post-treatment.

Main Results:

  • Cycloheximide treatment led to a significant increase in circulating lymphocytes, including T cells, B cells, and L-selectin-positive cells.
  • Radiolabeled lymphocytes showed decreased homing to Peyer's patches, mesenteric lymph nodes, and spleen in treated animals.
  • Lymphocyte homing to the lungs remained unaffected by cycloheximide administration.

Conclusions:

  • Protein synthesis inhibition induces lymphocytosis by impairing lymphocyte homing to specific lymphoid tissues.
  • The observed effect is not specific to particular lymphocyte subsets, indicating a general mechanism.
  • Rapidly turning-over molecules regulate lymphocyte homing, suggesting protein translation is key in inflammatory responses.
Abstract

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