Abstract
Diagnosis and therapy of chronic inflammatory lung disease is limited by the need for individualized biomarkers that provide insight into pathogenesis. Herein we show that mouse models of chronic obstructive lung disease exhibit an increase in lung chitinase production but cannot predict which chitinase family member may be equivalently increased in humans with corresponding lung disease. Moreover, we demonstrate that lung macrophage production of chitinase 1 is selectively increased in a subset of subjects with severe chronic obstructive pulmonary disease, and this increase is reflected in plasma levels. The findings provide a means to noninvasively track alternatively activated macrophages in chronic lung disease and thereby better differentiate molecular phenotypes in heterogeneous patient populations.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adipokines
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Aged
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Animals
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Biomarkers
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Chitinase-3-Like Protein 1
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Chitinases / biosynthesis*
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Chitinases / blood
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Chitinases / genetics
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Disease Models, Animal
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Gene Expression Profiling
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Glycoproteins / biosynthesis*
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Glycoproteins / blood
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Glycoproteins / genetics
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Humans
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Interleukin-13 / physiology
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Lectins
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Lung / enzymology
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Lung / pathology
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Macrophages, Alveolar / enzymology*
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Mice
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Mice, Inbred BALB C
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Middle Aged
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Ovalbumin / toxicity
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Phylogeny
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Pulmonary Disease, Chronic Obstructive / blood
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Pulmonary Disease, Chronic Obstructive / classification
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Pulmonary Disease, Chronic Obstructive / enzymology*
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Pulmonary Disease, Chronic Obstructive / pathology
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RNA, Messenger / biosynthesis
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Sequence Homology, Amino Acid
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Severity of Illness Index
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Smoking / blood
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Species Specificity
Substances
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Adipokines
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Biomarkers
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CHI3L1 protein, human
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Chil1 protein, mouse
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Chitinase-3-Like Protein 1
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Glycoproteins
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Interleukin-13
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Lectins
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RNA, Messenger
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Ovalbumin
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CHIA protein, human
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Chitinases