Am. J. Respir. Cell Mol. Biol., Vol 10, No. 2, Feb 1994, 142-147.
Increased expression of the monocyte chemoattractant protein-1 in bronchial tissue from asthmatic subjects
AR Sousa, SJ Lane, JA Nakhosteen, T Yoshimura, TH Lee and RN Poston
Department of Experimental Pathology, U.M.D.S., Guy's Hospital, London, United Kingdom.
The expression of the monocyte chemoattractant protein (MCP-1), a member of
the chemokine family of low molecular weight cytokines, was assessed by
immunohistochemistry in bronchial biopsies from 12 asthmatic and 12 normal
subjects. Both a monoclonal antibody (F9) and a polyclonal antibody were
employed to detect MCP-1, while the mouse myeloma protein (MOPC21) was used
as a negative control. Strong positive reactions for MCP-1 were seen in the
bronchial epithelium. Subepithelial macrophages, blood vessels, and
bronchial smooth muscle were also stained. Hue-saturation-intensity color
image analysis was used to quantify reactions of the monoclonal antibody in
the epithelial and subepithelial layers. With the monoclonal antibody,
asthmatic biopsies showed 51.8 +/- 3.7% (mean +/- SEM) of the epithelium
staining positively, whereas normal subjects reacted much less, with 6.4
+/- 1.9% of the epithelium staining (P < 0.0001); there was no overlap
between the two groups. Likewise, staining was increased in the
subepithelium of asthmatic airway biopsies, with 11.5 +/- 3.1% and 2.0 +/-
1.0% staining positively in asthmatic and normal subepithelium,
respectively, (P < 0.002). There was a significant correlation between
staining of the epithelium and subepithelium (r = 0.77, P < 0.001). The
polyclonal anti-MCP-1 antibody also gave strong reactions in the epithelium
and subepithelium, with 34.0 +/- 7.8% of the asthmatic and 1.6 +/- 1.0% of
the normal bronchial epithelium staining positively (P < 0.0001). These
increased levels of MCP-1 in the asthmatic airways suggest that they may
play a role in macrophage recruitment and activation and thereby contribute
to the inflammatory pathology of bronchial asthma.
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Copyright © 1994 American Thoracic Society.
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