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Published ahead of print on January 4, 2007, doi:10.1165/rcmb.2006-0245OC

Am. J. Respir. Cell Mol. Biol., Volume 36, Number 5, May 2007, 562-572

A more recent version of this article appeared on May 1, 2007
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Submitted on July 7, 2006
Revised on January 4, 2007

Inhibitory Kappa B Kinase 2 Activates Airway Epithelial Cells to Stimulate Bone Marrow Macrophages

Biji Mathew1, Gye Young Park1, Hongmei Cao2, Anser C Azim1, Xuerong Wang1, Richard B Van Breemen2, Ruxana T Sadikot3, and John W Christman3*

1 Department of Medicine, Section of Pulmonary, Critical Care and Sleep Medicine, University of Illinois, IL, United States, 2 Department of Medicinal Chemistry and Pharmacognosy, University of Illinois, IL, USA, 3 Department of Medicine, Section of Pulmonary, Critical Care and Sleep Medicine, University of Illinois, IL, United States; Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA

* To whom correspondence should be addressed. E-mail: jwc{at}uic.edu.

It has not been resolved whether macrophages or airway epithelial cells primarily respond to infectious and inflammatory stimuli and initiate a cell-to-cell inflammatory interaction within the airways. We hypothesized that the airway epithelial cells are primary responders that activate macrophages in response to environmental stimuli. To investigate the unilateral contribution of airway epithelial cells in the activation of macrophages, we developed an in vitro system where the primary mouse tracheal epithelial cells (MTEC) and primary bone marrow derived macrophages (BMDM) were incubated together for a brief period of time in a transwell culture plate. MTEC were transfected with adenoviral vectors which express a constitutitively active form of IKK2 (Ad-cIKK2), Ad-{beta} Gal or PBS for 48 hours before incubating with the macrophages. Macrophage activation was determined by measuring surface expression of CD11b, activation of NF-{kappa}B, phagocytic activity and ROS production, and COX-2 gene expression and production of prostaglandins. Macrophage adherence to epithelial layer was confirmed by CD68 immunostaining and scanning electron microscopy. MTEC cells transfected with Ad-cIKK2 produced increased amounts of IL-6, KC, TNF-{alpha} and PGE2. Exposure of BMDM to MTEC, transfected with ad-cIKK2, led to an increase in the CD11b expression and increased adherence of macrophages to the epithelial cell layer. NF-{kappa}B activation, COX-2 gene expression and PGD2 synthesis were also increased in BMDM which were incubated with MTEC transfected with Ad-cIKK2. These data suggest that airway epithelial cells potentially play a primary role in generating inflammatory signals that result in activation of macrophage.




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