BALF N-acetylglucosaminidase and β-galactosidase activities in idiopathic pulmonary fibrosis

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Item Type:	Article
Title:	BALF N-acetylglucosaminidase and β-galactosidase activities in idiopathic pulmonary fibrosis
Creators Name:	Gessner, C., Wirtz, H., Sack, U., Winkler, J., Stiehl, P., Schauer, J. and Wolff, G.
Abstract:	The lysosomal enzymes N-acetylglucosaminidase (N-ACGA) and {beta}-galactosidase ({beta}-gal) are involved in cellular collagen metabolism and may, therefore, be markers of fibrosis in idiopathic interstitial pneumonias, such as idiopathic pulmonary fibrosis (IPF). N-ACGA and {beta}-gal were analyzed in the bronchoalveolar lavage fluid (BALF) of patients with the histologic pattern of usual interstitial pneumonia (UIP, n=10) and controls (n=9). Cellular distribution in BALF as well as the concentration of TGF-{beta} a well-known mediator of fibroblast matrix deposition were correlated to the enzyme activities in both groups of patients. We found that both, N-ACGA (UIP: 25.2 nmol/ls ± 3.4; controls: 7.3 nmol/ls ± 1.3) and {beta}-gal (UIP: 4.7 nmol/ls ±0.5; controls: 2.4 nmol/ls ± 0.3) were elevated significantly in BALF of patients with IPF compared to that of control patients (P<0.003). This increase was paralleled by an increase in neutrophils (IPF: 17.9% ± 21.8; controls: 5.4% ± 6.3; P=0.03) and eosinophils (IPF: 2.0% ± 1.5; controls: 0.2% ± 0.45; P=0.002) in BALF fluid. In addition, N-ACGA activity correlated closely with lung function (FVC, TLC, and DLCO), transforming growth factor-beta (TGF-{beta}) in BALF (r=0.77, P=0.008) and activated lymphocytes (r=0.66, P=0.0021). Our findings suggest that measurement of lysosomal enzymes such as N-ACGA may represent a useful indicator of fibrotic activity in IPF.
Keywords:	{beta}-Galactosidase, N-Acetylglucosaminidase, IPF, BAL, Collagen Metabolism
Source:	Respiratory Medicine
ISSN:	0954-6111
Publisher:	Saunders
Volume:	96
Number:	9
Page Range:	751-756
Date:	September 2002
Official Publication:	https://doi.org/10.1053/rmed.2002.1344
PubMed:	View item in PubMed

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