Upregulation of IL-5 receptor expression on bone marrow-derived CD34+ cells from patients with asthma.

C. L. Chou*, C. H. Wang, Han-Ping Kuo

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

11 Scopus citations


BACKGROUND: Interleukin-5 (IL-5) is a potent eosinophilopoietic factor implicated in the chronic inflammatory cell accumulation accompanying bronchial asthma. We studied the expression of the IL-5 receptor alpha-subunit (IL-5R alpha) on bone marrow-derived cluster of differentiation molecule 34 positive (CD34+) progenitor cells in asthmatics to prove the ability of progenitor cells to respond to IL-5 more readily. METHODS: Non-adherent non-T cells (NANT) were separated from heparinized bone marrow blood from 6 asthmatics and 3 normal subjects, loaded with CD34+ and IL-5R alpha monoclonal antibodies conjugated with immunofluorescence and then analyzed by flow cytometry. Colonies grown from progenitor cells cultured in methylcellulose were determined for 14 days in the presence or absence of growth factors, including granulocyte-monocyte colony stimulating factor, stem cell factor, and interleukin-3. RESULTS: The proportion of IL-5R alpha expression on the CD34+ cell surface was significantly increased in asthmatics (12.9 +/- 3.3%, n = 6, p = 0.0163) compared to normal subjects (1.8 +/- 0.6%, n = 3). A significantly greater number of colonies committed to eosinophilic differentiation were found in the asthmatic subjects. CONCLUSION: We demonstrated an increased expression of IL-5R alpha on bone marrow-derived progenitor cells in asthmatics. This supports the concept that bone marrow-derived progenitor cells are ready for eosinophilopoiesis.

Original languageEnglish
Pages (from-to)416-422
Number of pages7
JournalChang Gung Medical Journal
Issue number3
StatePublished - 1999


Dive into the research topics of 'Upregulation of IL-5 receptor expression on bone marrow-derived CD34+ cells from patients with asthma.'. Together they form a unique fingerprint.

Cite this