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Am J Physiol Cell Physiol (July 5, 2006). doi:10.1152/ajpcell.00451.2005
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Submitted on September 6, 2005
Accepted on June 22, 2006

Interleukin-8: Novel roles in human airway smooth muscle cell contraction and migration

Vasanthi Govindaraju1, Marie-Claire Michoud1, Mustafa Al-Chalabi1, Pasquale Ferraro1, William S Powell1, and James G. Martin1*

1 Meakins-Christie Laboratories, McGill University, Montreal, Canada; Dpt. of Surgery, University of Montreal Hospital Center, Montreal, Canada

* To whom correspondence should be addressed. E-mail: james.martin{at}mcgill.ca.

In cystic fibrosis (CF) and asthma elevated levels of interleukin-8 (IL-8) are found in the airways. IL-8 is a CXC chemokine which is a chemoattractant for neutrophils through CXCR1 and CXCR2, G-protein coupled receptors. We hypothesized that IL-8 acts directly on airway smooth muscle cells (ASMC) in a way that may contribute to the enhanced airway responsiveness and airway remodeling observed in CF and asthma. The aim of this study was to determine if human ASMC (HASMC) express functional IL-8 receptors (CXCR1 and CXCR2) linked to cell contraction and migration. Experiments were conducted on cells harvested from human lung specimens. Real time PCR and FACS analysis showed that HASMC expressed mRNA and protein for both CXCR1 and CXCR2. Intracellular Ca2+ concentration ([Ca2+]i) increased from 115 nM to 170 nM in response to IL-8 (100 nM) and this response decreased following inhibition of phospholipase C (PLC) with U-73122. On blocking the receptors with specific neutralizing antibodies, changes in [Ca2+]i were abrogated. IL-8 also contracted the HASMC, decreasing the length of cells by 15% and induced a 2.5 fold increase in migration. These results indicate that HASMC constitutively express functional CXCR1 and CXCR2 that mediate IL-8 triggered Ca2+ release, contraction and migration. These data suggest a potential role for IL-8 in causing abnormal airway structure and function in asthma and CF.




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