Inflammation Research

, Volume 61, Issue 9, pp 1013–1020

Prevention of lung injury by Muc1 mucin in a mouse model of repetitive Pseudomonas aeruginosa infection

Authors

  • Tsuyoshi Umehara
    • Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine
    • Department of Otorhinolaryngology, Faculty of MedicineShimane University
  • Kosuke Kato
    • Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine
  • Yong Sung Park
    • Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine
  • Erik P. Lillehoj
    • Department of PediatricsUniversity of Maryland School of Medicine
  • Hideyuki Kawauchi
    • Department of Otorhinolaryngology, Faculty of MedicineShimane University
    • Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine
    • Department of PhysiologyTemple University School of Medicine
Original Research Paper

DOI: 10.1007/s00011-012-0494-y

Cite this article as:
Umehara, T., Kato, K., Park, Y.S. et al. Inflamm. Res. (2012) 61: 1013. doi:10.1007/s00011-012-0494-y

Abstract

Objective and design

To determine whether repetitive airway Pseudomonas aeruginosa (Pa) infection results in lung inflammation and injury and, if so, whether these responses are affected by Muc1 mucin. Muc1 wild type (WT) and knockout (KO) mice were compared for body weights, lung inflammatory responses, and airspace enlargement using a chronic lung infection model system.

Materials

Mice were treated intranasally with Pa (107 CFU) on days 0, 4, 7 and 10. On day 14, body weights, inflammatory cell numbers in bronchoalveolar lavage fluid (BALF), and airspace enlargement were measured. Differences in inflammatory responses between groups were statistically analyzed by the Student’s t test and ANOVA.

Results

Muc1 WT mice exhibited mild degrees of both inflammation and airspace enlargement following repetitive airway Pa infection. However, Muc1 KO mice exhibited significantly decreased body weights, greater macrophage numbers in the BALF, and increased airspace enlargement compared with Muc1 WT mice.

Conclusions

This is the first report demonstrating that Muc1 deficiency can lead to lung injury during chronic Pa infection in mice. These results suggest that MUC1 may play a crucial role in the resolution of inflammation during chronic respiratory infections and that MUC1 dysfunction likely contributes to the pathogenesis of chronic inflammatory respiratory disease.

Keywords

RespiratoryMUC1 mucinPseudomonas aeruginosaInflammationAirspace enlargement

Copyright information

© Springer Basel AG 2012