Chest · 2005
Expression of CXC chemokine receptors 1 and 2 in human bronchial epithelial cells.
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Farkas Laszlo, Hahn Marie-Christine, Schmoczer Marc, Jentsch Nico, Krätzel Kirsten, Pfeifer Michael, Schulz Christian
Аннотация
INTRODUCTION: CXC chemokine receptor 1 (CXCR1) and CXC chemokine receptor 2 (CXCR2) have been shown to play an important role in transepithelial migration of neutrophil granulocytes during inflammation in various tissues. This study investigated the regulation of gene expression and surface expression of CXCR1 and CXCR2 in a human bronchial epithelial cell line (BEAS-2B), as well as in primary bronchial epithelial cells (PBECs) from 10 COPD patients and 10 control subjects.
METHODS AND RESULTS: The transcription expression of CXCR1 and CXCR2 was quantitatively assessed by means of real-time polymerase chain reaction (PCR) under various inflammatory conditions. Flow cytometry was used to measure CXCR1 and CXCR2 surface expression. There was a low baseline expression of CXCR1 and CXCR2 in real-time PCR in PBECs from COPD patients and control subjects as well as in BEAS-2B cells, and no significant regulation occurred under various inflammatory conditions in PBECs and BEAS-2B cells. Furthermore, unstimulated surface expression of CXCR1 and CXCR2 on BEAS-2B cells was very low, and no significant regulation was detectable under time-dependent inflammatory stimulation up to 24 h.
CONCLUSION: Various inflammatory responses that are of potential relevance in COPD pathophysiology do not affect transcription regulation and surface expression of the interleukin-8 receptors CXCR1 and CXCR2 on human bronchial epithelial cells.
METHODS AND RESULTS: The transcription expression of CXCR1 and CXCR2 was quantitatively assessed by means of real-time polymerase chain reaction (PCR) under various inflammatory conditions. Flow cytometry was used to measure CXCR1 and CXCR2 surface expression. There was a low baseline expression of CXCR1 and CXCR2 in real-time PCR in PBECs from COPD patients and control subjects as well as in BEAS-2B cells, and no significant regulation occurred under various inflammatory conditions in PBECs and BEAS-2B cells. Furthermore, unstimulated surface expression of CXCR1 and CXCR2 on BEAS-2B cells was very low, and no significant regulation was detectable under time-dependent inflammatory stimulation up to 24 h.
CONCLUSION: Various inflammatory responses that are of potential relevance in COPD pathophysiology do not affect transcription regulation and surface expression of the interleukin-8 receptors CXCR1 and CXCR2 on human bronchial epithelial cells.