Polymorphisms and Haplotypes of Acid Mammalian Chitinase Are Associated with Bronchial Asthma

Bierbaum, Sibylle; Nickel, Renate; Koch, Anja; Lau, Susanne; Deichmann, Klaus A.; Wahn, Ulrich; Superti‐Furga, Andrea; Heinzmann, Andrea

doi:10.1164/rccm.200506-890oc

Cited by 125 publications

(125 citation statements)

References 28 publications

Supporting

Mentioning

118

Contrasting

Order By: Relevance

“…This hypothesis is in agreement with recent studies suggesting that genetic polymorphisms in AMCase, but not ChTRase, are associated with bronchial asthma in Caucasian pediatric populations. 25,26 We have recently shown that, similarly to ChTRase, the chitinase-like protein YKL-40 is up-regulated in BAL and alveolar macrophages from COPD patients, but not asthmatics.…”

Section: Discussionmentioning

confidence: 99%

Lung Chitinolytic Activity and Chitotriosidase Are Elevated in Chronic Obstructive Pulmonary Disease and Contribute to Lung Inflammation

Létuvé

Kozhich²,

Humbles³

et al. 2010

The American Journal of Pathology

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation and emphysematous alveolar destruction. In this study, we have investigated whether chitotriosidase (ChTRase) and acidic mammalian chitinase, two chitinases with chitinolytic activity, are selectively augmented in COPD and contribute to its pathogenesis. We found that smokers with COPD, but not asthmatics, had higher chitinolytic activity and increased levels of ChTRase in bronchoalveolar lavage, more ChTRasepositive cells in bronchial biopsies, and an elevated proportion of alveolar macrophages expressing ChTRase than smokers without COPD or never-smokers. ChTRase accounted for approximately 80% of bronchoalveolar lavage chitinolytic activity, while acidic mammalian chitinase was undetectable. Bronchoalveolar lavage chitinolytic activity and ChTRase were associated with airflow obstruction and emphysema and with the levels of interleukin (IL)؊1␤, IL-8, tumor-necrosis factor (TNF)-␣, and its type II soluble receptor. Tumor necrosis factor-␣ stimulated ChTRase release only from alveolar macrophages from smokers with COPD, and exposure of these cells to ChTRase promoted the release of IL-8, monocyte-chemoattractant protein-1, and metalloproteinase-9. Finally, ChTRase overexpression in the lung of normal mice promoted macrophage recruitment and the synthesis of the murine homologue of IL-8, keratinocyte-derived cytokine, and of monocyte-chemoattractant protein-1. We conclude that pulmonary ChTRase overexpression may represent a novel important mechanism involved in COPD onset and progression. (Am J

show abstract

Section: Discussionmentioning

confidence: 99%

Lung Chitinolytic Activity and Chitotriosidase Are Elevated in Chronic Obstructive Pulmonary Disease and Contribute to Lung Inflammation

Létuvé

Kozhich²,

Humbles³

et al. 2010

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…Zhu et al (2004) reported that acid mammalian chitinase may be an important mediator of IL13-induced responses in Th2-dominated disorders such as asthma. An association between acid mammalian chitinase polymorphisms and asthma further supports the involvement of acid mammalian chitinase in asthma development (Bierbaum et al, 2005).…”

Section: Introductionmentioning

confidence: 62%

Ym1 and Ym2 expression in a mouse model exposed to diesel exhaust particles

Song

Jang

Ahn

et al. 2008

Environmental Toxicology

View full text Add to dashboard Cite

Background: Chitinase may play a role in regulating allergic diseases. Objective: We studied the role of chitinase in a mouse model exposed to diesel exhaust particles (DEP). Mice were exposed to intranasal DEP (0.6 mg/mL) for 5 days and challenged with aerosolized DEP (6 mg/m 3 ) on days 6-8. Enhanced pause (Penh), as an airway obstruction marker, was measured on day 9, and bronchoalveolar lavage (BAL) fluid and lung tissues were collected on day 10. The expression of Ym1 and Ym2 mRNA was assessed in lung tissue extracts by reverse transcription-polymerase chain reaction. Results: DEP induced significant increases in methacholine-induced Penh and IL-4 levels in BAL fluid relative to the control group. Peribronchial and perivascular inflammatory cell infiltrates were prominent in the DEP group. DEP induced Ym1 and Ym2 mRNA expression in lung tissue extracts relative to the control group.-Conclusion: These results demonstrate that DEP induced airway hyperresponsiveness and Ym mRNA expression via a Th2 cell-biased response, suggesting that chitinase may play an important role in airway inflammation and responsiveness upon exposure to DEP in a mouse model, and may therefore be involved in regulating allergic diseases. #

show abstract

“…Acid mammalian chitinase may also be an important mediator of IL13-induced responses in Th2 disorders, such as asthma (Zhu et al, 2004). Indeed, polymorphisms in acid mammalian chitinase are associated with asthma, further supporting the involvement of acid mammalian chitinase in asthma development (Bierbaum et al, 2005). DEP induces airway hyper-responsiveness as well as Ym mRNA expression, a Th2 cell-biased response by activated macrophages.…”

Section: Innate Immunitymentioning

confidence: 95%

Particulate Air Pollutants and Respiratory Diseases

Jang¹

2012

Air Pollution - A Comprehensive Perspective

View full text Add to dashboard Cite

Polymorphisms and Haplotypes of Acid Mammalian Chitinase Are Associated with Bronchial Asthma

Abstract: This newly described association between AMCase polymorphisms and asthma adds further evidence supporting the involvement of AMCase in the development of asthma.

Cited by 125 publications

References 28 publications

Lung Chitinolytic Activity and Chitotriosidase Are Elevated in Chronic Obstructive Pulmonary Disease and Contribute to Lung Inflammation

Lung Chitinolytic Activity and Chitotriosidase Are Elevated in Chronic Obstructive Pulmonary Disease and Contribute to Lung Inflammation

Ym1 and Ym2 expression in a mouse model exposed to diesel exhaust particles

Particulate Air Pollutants and Respiratory Diseases

Contact Info

Product

Resources

About