A Novel Function of MUC18
Bacterial infection plays a critical role in exacerbations of various lung diseases, including chronic pulmonary obstructive disease (COPD) and asthma. Excessive lung inflammation is a prominent feature in disease exacerbations, but the underlying mechanisms remain poorly understood. Cell surface gl...
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| Published in | The American journal of pathology Vol. 182; no. 3; pp. 819 - 827 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Elsevier Inc
01.03.2013
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| Subjects | |
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| Abstract | Bacterial infection plays a critical role in exacerbations of various lung diseases, including chronic pulmonary obstructive disease (COPD) and asthma. Excessive lung inflammation is a prominent feature in disease exacerbations, but the underlying mechanisms remain poorly understood. Cell surface glycoprotein MUC18 (alias CD146 or melanoma cell adhesion molecule) has been shown to promote metastasis in several tumors, including melanoma. We explored the function of MUC18 in lung inflammatory responses to bacteria (eg, Mycoplasma pneumoniae) involved in lung disease exacerbations. MUC18 expression was increased in alveolar macrophages from lungs of COPD and asthma patients, compared with normal healthy human subjects. Mouse alveolar macrophages also express MUC18. After M. pneumoniae lung infection, Muc18−/− mice exhibited lower levels of the lung proinflammatory cytokines KC and TNF-α and less neutrophil recruitment than Muc18+/+ mice. Alveolar macrophages from Muc18−/− mice produced less KC than those from Muc18+/+ mice. In Muc18−/− mouse alveolar macrophages, adenovirus-mediated MUC18 gene transfer increased KC production. MUC18 amplified proinflammatory responses in alveolar macrophages, in part through enhancing the activation of nuclear factor-κB (NF-κB). Our results demonstrate, for the first time, that MUC18 exerts a proinflammatory function during lung bacterial infection. Up-regulated MUC18 expression in lungs (eg, in alveolar macrophages) of COPD and asthma patients may contribute to excessive inflammation during disease exacerbations. |
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| AbstractList | Bacterial infection plays a critical role in exacerbations of various lung diseases, including chronic pulmonary obstructive disease (COPD) and asthma. Excessive lung inflammation is a prominent feature in disease exacerbations, but the underlying mechanisms remain poorly understood. Cell surface glycoprotein MUC18 (alias CD146 or melanoma cell adhesion molecule) has been shown to promote metastasis in several tumors, including melanoma. We explored the function of MUC18 in lung inflammatory responses to bacteria (eg, Mycoplasma pneumoniae ) involved in lung disease exacerbations. MUC18 expression was increased in alveolar macrophages from lungs of COPD and asthma patients, compared with normal healthy human subjects. Mouse alveolar macrophages also express MUC18. After M. pneumoniae lung infection, Muc18 −/− mice exhibited lower levels of the lung proinflammatory cytokines KC and TNF-α and less neutrophil recruitment than Muc18 +/+ mice. Alveolar macrophages from Muc18 −/− mice produced less KC than those from Muc18 +/+ mice. In Muc18 −/− mouse alveolar macrophages, adenovirus-mediated MUC18 gene transfer increased KC production. MUC18 amplified proinflammatory responses in alveolar macrophages, in part through enhancing the activation of nuclear factor-κB (NF-κB). Our results demonstrate, for the first time, that MUC18 exerts a proinflammatory function during lung bacterial infection. Up-regulated MUC18 expression in lungs (eg, in alveolar macrophages) of COPD and asthma patients may contribute to excessive inflammation during disease exacerbations. Bacterial infection plays a critical role in exacerbations of various lung diseases, including chronic pulmonary obstructive disease (COPD) and asthma. Excessive lung inflammation is a prominent feature in disease exacerbations, but the underlying mechanisms remain poorly understood. Cell surface glycoprotein MUC18 (alias CD146 or melanoma cell adhesion molecule) has been shown to promote metastasis in several tumors, including melanoma. We explored the function of MUC18 in lung inflammatory responses to bacteria (eg, Mycoplasma pneumoniae) involved in lung disease exacerbations. MUC18 expression was increased in alveolar macrophages from lungs of COPD and asthma patients, compared with normal healthy human subjects. Mouse alveolar macrophages also express MUC18. After M. pneumoniae lung infection, Muc18−/− mice exhibited lower levels of the lung proinflammatory cytokines KC and TNF-α and less neutrophil recruitment than Muc18+/+ mice. Alveolar macrophages from Muc18−/− mice produced less KC than those from Muc18+/+ mice. In Muc18−/− mouse alveolar macrophages, adenovirus-mediated MUC18 gene transfer increased KC production. MUC18 amplified proinflammatory responses in alveolar macrophages, in part through enhancing the activation of nuclear factor-κB (NF-κB). Our results demonstrate, for the first time, that MUC18 exerts a proinflammatory function during lung bacterial infection. Up-regulated MUC18 expression in lungs (eg, in alveolar macrophages) of COPD and asthma patients may contribute to excessive inflammation during disease exacerbations. |
| Author | Jiang, Di Hartney, John Bowler, Russell P. Wu, Qun Karimpour-Fard, Anis Case, Stephanie R. Minor, Maisha N. Wang, Jieru Martin, Richard J. Chu, Hong Wei |
| Author_xml | – sequence: 1 givenname: Qun surname: Wu fullname: Wu, Qun organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado – sequence: 2 givenname: Stephanie R. surname: Case fullname: Case, Stephanie R. organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado – sequence: 3 givenname: Maisha N. surname: Minor fullname: Minor, Maisha N. organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado – sequence: 4 givenname: Di surname: Jiang fullname: Jiang, Di organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado – sequence: 5 givenname: Richard J. surname: Martin fullname: Martin, Richard J. organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado – sequence: 6 givenname: Russell P. surname: Bowler fullname: Bowler, Russell P. organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado – sequence: 7 givenname: Jieru surname: Wang fullname: Wang, Jieru organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado – sequence: 8 givenname: John surname: Hartney fullname: Hartney, John organization: Department of Immunology, National Jewish Health, Denver, Colorado – sequence: 9 givenname: Anis surname: Karimpour-Fard fullname: Karimpour-Fard, Anis organization: Department of Pharmacology, School of Medicine, University of Colorado Denver, Aurora, Colorado – sequence: 10 givenname: Hong Wei surname: Chu fullname: Chu, Hong Wei email: chuhw@njhealth.org organization: Pulmonary Division, Department of Medicine, National Jewish Health, Denver, Colorado |
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