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Published in: Respiratory Research 1/2008

Open Access 01-12-2008 | Research

Endotoxin receptor CD14 in PiZ α-1-antitrypsin deficiency individuals

Authors: Caroline S Sandström, Natalia Novoradovskaya, Corrado M Cilio, Eeva Piitulainen, Tomas Sveger, Sabina Janciauskiene

Published in: Respiratory Research | Issue 1/2008

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Abstract

Background

CD14, a receptor for lipopolysaccharides (LPS), is found in both a membrane-bound form (mCD14) and a soluble form (sCD14). It is suggested that sCD14 is mainly released from blood monocytes by serine protease-mediated shedding. Because α1-antitrypsin (AAT), an inhibitor of serine proteases, has been shown to regulate CD14 expression in human monocytes in vitro, we sought to investigate plasma levels of sCD14 and monocyte expression of mCD14 in subjects at age 30 years with normal MM and deficient PiZZ and PiSZ genotypes of AAT.

Methods

Plasma levels of AAT and sCD14 were measured in 75 PiZZ and 34 PiSZ individuals with normal lung function identified from the Swedish neonatal AAT deficiency screening, and in 95 age matched PiMM controls. The mCD14 expression in monocytes from 9 PiZZ, 6 PiSZ and 11 PiMM subjects was analysed by FACS and Quantitative Real Time Reverse Transcription PCA.

Results

As expected, plasma AAT concentrations were PiMM>PiSZ>PiZZ (p < 0.001). Plasma sCD14 levels were higher in PiZZ than in PiMM subjects (p < 0.01). The expression level of mCD14 was higher (1.89-fold) in monocytes isolated from PiZZ subjects compared to PiMM controls (p = 0.00189).

Conclusion

This study is the first to show higher levels of plasma sCD14 and monocyte mCD14 expression in young, clinically healthy PiZZ AAT subjects.
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Metadata
Title
Endotoxin receptor CD14 in PiZ α-1-antitrypsin deficiency individuals
Authors
Caroline S Sandström
Natalia Novoradovskaya
Corrado M Cilio
Eeva Piitulainen
Tomas Sveger
Sabina Janciauskiene
Publication date
01-12-2008
Publisher
BioMed Central
Published in
Respiratory Research / Issue 1/2008
Electronic ISSN: 1465-993X
DOI
https://doi.org/10.1186/1465-9921-9-34

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