© 1997 American Heart Association, Inc.
Articles |
Emigrated Rat Neutrophils Adhere to Cardiac Myocytes via 
4 Integrin
From the Immunology (P.H.R., P.K.) and Cardiovascular (C.A.W., W.R.G.) Research Groups, University of Calgary (Canada).
Correspondence to Dr Paul Kubes, Immunology Research Group, Department of Medical Physiology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1.
Abstract Previous work has shown that neutrophils isolated
from whole blood adhere to cardiac myocytes via CD18 (ß2
integrin) to cause injury to the heart cells. In vitro, we have found
that upon endothelial transmigration, neutrophils can
also express 4ß1; however, whether this
contributes to neutrophil adhesion to parenchymal cells remains
entirely unknown. Unstimulated and tumor necrosis
factor-–stimulated rat cardiac myocytes adherent to gelatin-coated
coverslips supported N-formyl-Met-Leu-Phe (fMLP)–induced
neutrophil (isolated from whole blood) adhesion entirely via CD18
(blocked with monoclonal antibody [mAb] WT-3). Emigrated neutrophils
spontaneously adhered to cardiac myocytes also entirely via CD18.
However, if fMLP was used to restimulate emigrated neutrophils, the
adhesion to cardiac myocytes was entirely independent of CD18. Although
an anti–4 integrin antibody (mAb TA-2) alone did not
reduce the emigrated neutrophil-myocyte interaction, dual
administration of TA-2 and WT-3 reduced adhesion by 81%.
4 integrin was expressed in small amounts on the surface
of circulating neutrophils, increased following transmigration, and
then increased >5-fold after restimulation of these emigrated
neutrophils. In the presence of the anti-CD18 antibody, a fibronectin
fragment (FN-40) but not a vascular cell adhesion molecule-1 antibody
(mAb 5F10) inhibited neutrophil-myocyte interactions by 80%. Similar
results were seen when the rat chemokine CINC-gro was used instead of
fMLP, suggesting that the 4-dependent adhesion was not
specific to fMLP. These data demonstrate that 4 integrin
can be physiologically induced to increase in
number and avidity after neutrophil emigration and that this adhesion
molecule can cause firm adhesion to fibronectin on parenchymal cells,
including rat cardiac myocytes.
Key Words: cardiac myocyte • neutrophil • adhesion • inflammation • 4 integrin
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