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  A keratan sulfate disaccharide prevents inflammation and the progression of emphysema in murine models

Gao, C., Fujinawa, R., Yoshida, T., Ueno, M., Ota, F., Kizuka, Y., et al. (2017). A keratan sulfate disaccharide prevents inflammation and the progression of emphysema in murine models. American Journal of Physiology - Lung Cellular and Molecular Physiology, 312(2), L268-L276. doi:10.1152/ajplung.00151.2016.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002C-32EB-5 Version Permalink: http://hdl.handle.net/21.11116/0000-0006-596E-C
Genre: Journal Article

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 Creators:
Gao, Congxiao, Author
Fujinawa, Reiko, Author
Yoshida, Takayuki, Author
Ueno, Manabu, Author
Ota, Fumi, Author
Kizuka, Yasuhiko, Author
Hirayama, Tetsuya, Author
Korekane, Hiroaki, Author
Kitazume, Shinobu, Author
Maeno, Toshitaka, Author
Ohtsubo, Kazuaki, Author
Yoshida, Keiichi, Author
Yamaguchi, Yoshiki, Author
Lepenies, Bernd, Author
Aretz, Jonas1, Author              
Rademacher, Christoph1, Author              
Kabata, Hiroki, Author
Hegab, Ahmed E., Author
Seeberger, Peter H.2, Author              
Betsuyaku, Tomoko, Author
Kida, Kozui, AuthorTaniguchi, Naoyuki, Author more..
Affiliations:
1Christoph Rademacher, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society, ou_1863300              
2Peter H. Seeberger - Vaccine Development, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society, ou_1863308              

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 Abstract: Emphysema is a typical component of chronic obstructive pulmonary disease (COPD), a progressive and inflammatory airway disease. However, no effective treatment currently exists. Here we show that keratan sulfate (KS), one of the major glycosaminoglycans (GAGs) produced in the small airway, decreased in lungs of cigarette-smoke-exposed mice. In order to confirm the protective effect of KS in the small airway, a disaccharide repeating unit of KS designated L4 ([SO3--6]Galβ1-4[SO3--6]GlcNAc) was administered to two murine models: elastase-induced-emphysema and LPS-induced exacerbation of a cigarette smoke-induced emphysema. Histological and micro-computed tomography (micro-CT) analyses revealed that, in the elastase-induced emphysema model mice, administration of L4 attenuated alveolar destruction. Treatment with L4 significantly reduced neutrophil influx and the levels of inflammatory cytokines, tissue-degrading enzymes (MMPs), and myeloperoxidase (MPO) in bronchoalveolar lavage (BAL) fluid, suggesting that L4 suppressed inflammation in the lung. L4 consistently blocked the chemotactic migration of neutrophils in vitro. Moreover, in the case of the exacerbation model, L4 inhibited inflammatory cell accumulation to the same extent as that of dexamethasone. Taken together, L4 represents one of the potential glycan-based drugs for the treatment of COPD through its inhibitory action against inflammation.

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 Dates: 2016-12-232017
 Publication Status: Published in print
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 Identifiers: DOI: 10.1152/ajplung.00151.2016
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Title: American Journal of Physiology - Lung Cellular and Molecular Physiology
  Other : Am. J. Physiol.-Lung Cell. Mol. Physiol.
Source Genre: Journal
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Publ. Info: Bethesda, MD : American Physiological Society
Pages: - Volume / Issue: 312 (2) Sequence Number: - Start / End Page: L268 - L276 Identifier: ISSN: 1040-0605