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Department of Physiology and Biophysics, University of Alabama, Birmingham, AL 35294
Cytokines produced by activated macrophages and Th2 cells within
the lung play a key role in asthma-associated airway inflammation.
Additionally, recent studies suggest that the molecule CD40 modulates
lung immune responses. Because airway epithelial cells can act as
immune effector cells through the expression of inflammatory mediators,
the epithelium is now considered important in the generation of
asthma-associated inflammation. Therefore, the goal of the present
study was to examine the effects of proinflammatory and Th2-derived
cytokines on the function of CD40 in airway epithelia. The results show
that airway epithelial cells express CD40 and that engagement of
epithelial CD40 induces a significant increase in expression of the
chemokines RANTES, monocyte chemoattractant protein (MCP-1),
and IL-8 and the adhesion molecule ICAM-1. Cross-linking epithelial
CD40 had no effect on expression of the adhesion molecule VCAM-1. The
proinflammatory cytokines TNF-
and IL-1ß and the Th2-derived
cytokines IL-4 and IL-13 modulated the positive effects of CD40
engagement on inflammatory mediator expression in airway epithelial
cells. Importantly, CD40 ligation enhanced the sensitivity of airway
epithelial cells to the effects of TNF- and/or IL-1ß on expression
of RANTES, MCP-1, IL-8, and VCAM-1. In contrast, neither IL-4 nor IL-13
modified the effects of CD40 engagement on the expression of RANTES,
MCP-1, IL-8, or VCAM-1; however, both IL-4 and IL-13 attenuated the
effects of CD40 cross-linking on ICAM-1 expression. Together, these
findings suggest that interactions between CD40-responsive airway
epithelial cells and CD40 ligand+ leukocytes, such as
activated T cells, eosinophils, and mast cells, modulate
asthma-associated airway inflammation.
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