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Monocyte chemotactic protein-1 in the migration of differentiated leukaemic cells toward alveolar epithelial cells

¹ Dept of Physiology, School of Medicine, National Yang-Ming University, ² Division of Hematology and Oncology, Dept of Medicine, ⁴ Medical Research and Education, Taipei-Veterans General Hospital, ³ Dept of Respiratory Therapy, Taipei Medical University, ⁶ Dept of Medicine, Taipei City Hospital-Yang-Ming Branch, Taipei, Taiwan, Republic of China. ⁵ Division of Neurology, The Children's Hospital of Philadelphia, Philadelphia, PA, USA. ⁷ Both authors contributed equally to this manuscript.

CORRESPONDENCE: H-C. Hsu, Division of Hematology and Oncology, Dept of Medicine, Taipei City Hospital-Yang-Ming Branch, 105 Yusheng St, Shilin District, Taipei, Taiwan, 11146, Republic of China. , Fax: 886 228347528 E-mail: hchsu{at}vghtpe.gov.tw

Keywords: Acute respiratory distress syndrome, all-trans retinoic acid, chemokine, leukocyte infiltration, monocyte chemotactic protein-1, retinoid acid syndrome

Received: October 15, 2007
Accepted December 27, 2007

All-trans retinoic acid (ATRA) can induce acute respiratory distress syndrome in patients with acute promyelocytic leukaemia (APL). The current study investigated the role of monocyte chemotactic protein (MCP)-1 in the chemotactic transmigration of ATRA-treated NB4 (ATRA-NB4) APL cells toward A549 alveolar epithelial cells.

NB4 and A549 cells were separately cultured with ATRA and/or dexamethasone (DEX). ATRA-NB4 cells were then placed in an upper insert and co-incubated with A549 cells or their conditioned medium (CM) located in a lower plate to test their transmigration activity.

ATRA stimulated NB4 cells to transmigrate toward the A549 cells. The secretion of MCP-1 was enhanced by ATRA treatment in both A549 and NB4 cells. The binding assay demonstrated that ATRA-NB4 cells bound MCP-1. Pre-treatment of both CM-A549 cells with antibodies against MCP-1 and of ATRA-NB4 cells with antibodies against MCP-1 receptors reduced ATRA-NB4 cell transmigration. DEX did not suppress MCP-1 secretion and transmigration in ATRA-NB4 cells, although when applied to A549 cells, MCP-1 secretion was suppressed and ATRA-NB4 cell transmigration was attenuated.

Monocyte chemotactic protein-1 secreted from alveolar epithelial cells plays an important role in the cell–cell interaction involved in the chemotactic transmigration of all-trans retinoic acid-treated acute promyelocytic leukaemia cells toward alveolar epithelial cells.