Abstract
171* The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease
Highlights
Chronic lung disease determines the morbidity and mortality of cystic fibrosis (CF) patients [1]
YKL-40 levels in CF sputa and CF sera showed a broad range of detection from levels similar to healthy control levels up to 30-fold higher levels in CF patients compared to healthy controls (Figure 1A right graph).YKL-40 serum levels correlated positively with YKL-40 sputum levels in both CF patients (r = 0.69, p,0.01) and, to a lesser extent, healthy control individuals (r = 0.42, p,0.05)
Consistent with human CF lung disease, protein levels of the murine YKL-40 homologue breast regression protein of 39 kDa (BRP-39) were highly increased in bronchoalveolar lavage fluid (BALF) from bENaC-Tg mice compared to BALF from WT mice (Figure 1B)
Summary
Chronic lung disease determines the morbidity and mortality of cystic fibrosis (CF) patients [1]. CF lung disease is characterized by a nonresolving neutrophilic inflammation with impaired antibacterial killing and proteolytic destruction of pulmonary tissue [2]. But they express chitinases and chitinaselike proteins (CLP). Both chitinases and CLP belong to the 18glycosyl-hydrolase family, including acidic mammalian chitinase (AMCase), chitotriosidase, oviductin, YKL-40 in humans, while YM-1, YM-2, AMCase, oviductin, and breast regression protein (BRP-39) have been described in mice. CLPs bind chitin, but do not have enzymatic chitinase activity due to mutations in their highly conserved putative enzyme sites [3]. The prototypical CLP YKL-40 (YKL for the first three N-terminal residues of a 40 kDa protein, termed human cartilage glycoprotein (HcGP)-39)
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