Role of vascular cell adhesion molecules and leukocyte apoptosis in the lymphopenia and thrombocytopenia of patients with severe acute respiratory syndrome (SARS)

Rong Fu Chen, Jen Chieh Chang, Wen Tien Yeh, Chen Hsiang Lee, Jien Wei Liu, Hock Liew Eng, Kuender D. Yang*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

51 Scopus citations

Abstract

The immunopathogenesis of leukopenia and thrombocytopenia in patients with severe acute respiratory syndrome (SARS) is unclear. In order to explore the leukopenia mechanism, we studied 15 SARS patients who were previously healthy, and 15 age-matched normal controls in a paired design. Soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble Fas ligand (sFasL) in plasma were measured by ELISA, and intracellular activated caspase-3 fragment in different leukocytes was determined by flow cytometry. Patients with SARS had significantly lower lymphocyte and platelet counts and significantly higher sVCAM-1 and sFasL levels compared to healthy controls. sVCAM-1 levels correlated negatively with total leukocytes and platelet counts, but positively with plasma sFasL levels. Intracellular cleaved caspase-3 expression was also significantly higher in lymphocytes from SARS patients in acute phase than in convalescent stage. Lymphopenia and thrombocytopenia in SARS patients may be caused, in part, by enhanced vascular sequestration associated with increased sVCAM-1 levels. However, lymphopenia may be due to enhanced cell death. Inhibition of cell adhesion and caspase-3 activation could, therefore, have prevented SARS patients from developing thrombocytopenia and lymphopenia.

Original languageEnglish
Pages (from-to)122-127
Number of pages6
JournalMicrobes and Infection
Volume8
Issue number1
DOIs
StatePublished - 01 2006
Externally publishedYes

Keywords

  • Apoptosis
  • Caspase
  • Lymphopenia
  • SARS
  • sFasL
  • sVCAM-1

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