What question did this study set out to answer?

To determine whether inducible overexpression of the asthma-associated cytokine interleukin-13 in adult lungs drives emphysema and to identify the proteolytic pathways responsible.

November 1, 2000Journal of Clinical InvestigationOpen Access

Inducible targeting of IL-13 to the adult lung causes matrix metalloproteinase– and cathepsin-dependent emphysema

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Authors

TZTao ZhengHunan University of Traditional Chinese Medicine ZZZhou ZhuChinese Academy of Medical Sciences & Peking Union Medical College ZWZhongde WangUtah State University

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Implication

Experimental mouse study demonstrates that interleukin-13 induces metalloproteinase- and cathepsin-dependent emphysema, highlighting shared pathogenic mechanisms between asthma and chronic...

Key Points

To determine whether inducible overexpression of the asthma-associated cytokine interleukin-13 in adult lungs drives emphysema and to identify the proteolytic pathways responsible.
Inducibly overexpressed interleukin-13 (IL-13) in the lungs of adult mice.
Assessed changes in lung volume, compliance, inflammation, mucus metaplasia, and expression profiles of matrix metalloproteinases (MMPs) and cathepsins.
Administered pharmacological antagonists of MMPs or cysteine proteinases to evaluate their effects on lung damage and inflammation.
Inducible IL-13 overexpression significantly increased lung volumes, compliance, inflammation, and mucus metaplasia in adult mice.
IL-13 stimulated marked upregulation of MMP-2, -9, -12, -13, and -14 as well as cathepsins B, S, L, H, and K in lung tissue.
Treatment with MMP or cysteine proteinase antagonists significantly attenuated emphysema and inflammatory responses without altering mucus metaplasia.

Cite This Study

Zheng et al. (2000) studied this question.

synapsesocial.com/papers/6a70d75ffebe604dd7099d37 https://doi.org/10.1172/jci10458

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November 1, 2000Journal of Clinical InvestigationOpen Access

Inducible targeting of IL-13 to the adult lung causes matrix metalloproteinase– and cathepsin-dependent emphysema

View Full Paper

Ask AI

Bookmark

Authors

TZTao ZhengHunan University of Traditional Chinese Medicine ZZZhou ZhuChinese Academy of Medical Sciences & Peking Union Medical College ZWZhongde WangUtah State University

Discussion

Member takes

Implication

Experimental mouse study demonstrates that interleukin-13 induces metalloproteinase- and cathepsin-dependent emphysema, highlighting shared pathogenic mechanisms between asthma and chronic...

Key Points

To determine whether inducible overexpression of the asthma-associated cytokine interleukin-13 in adult lungs drives emphysema and to identify the proteolytic pathways responsible.
Inducibly overexpressed interleukin-13 (IL-13) in the lungs of adult mice.
Assessed changes in lung volume, compliance, inflammation, mucus metaplasia, and expression profiles of matrix metalloproteinases (MMPs) and cathepsins.
Administered pharmacological antagonists of MMPs or cysteine proteinases to evaluate their effects on lung damage and inflammation.
Inducible IL-13 overexpression significantly increased lung volumes, compliance, inflammation, and mucus metaplasia in adult mice.
IL-13 stimulated marked upregulation of MMP-2, -9, -12, -13, and -14 as well as cathepsins B, S, L, H, and K in lung tissue.
Treatment with MMP or cysteine proteinase antagonists significantly attenuated emphysema and inflammatory responses without altering mucus metaplasia.

Cite This Study

Zheng et al. (2000) studied this question.

synapsesocial.com/papers/6a70d75ffebe604dd7099d37 https://doi.org/10.1172/jci10458

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