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An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung
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| Zeitschriftentitel: | American Journal of Physiology-Lung Cellular and Molecular Physiology |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , |
| In: | American Journal of Physiology-Lung Cellular and Molecular Physiology, 314, 2018, 1, S. L150-L156 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Hvorecny, Kelli L. Dolben, Emily Moreau-Marquis, Sophie Hampton, Thomas H. Shabaneh, Tamer B. Flitter, Becca A. Bahl, Christopher D. Bomberger, Jennifer M. Levy, Bruce D. Stanton, Bruce A. Hogan, Deborah A. Madden, Dean R. Hvorecny, Kelli L. Dolben, Emily Moreau-Marquis, Sophie Hampton, Thomas H. Shabaneh, Tamer B. Flitter, Becca A. Bahl, Christopher D. Bomberger, Jennifer M. Levy, Bruce D. Stanton, Bruce A. Hogan, Deborah A. Madden, Dean R. |
|---|---|
| author |
Hvorecny, Kelli L. Dolben, Emily Moreau-Marquis, Sophie Hampton, Thomas H. Shabaneh, Tamer B. Flitter, Becca A. Bahl, Christopher D. Bomberger, Jennifer M. Levy, Bruce D. Stanton, Bruce A. Hogan, Deborah A. Madden, Dean R. |
| spellingShingle |
Hvorecny, Kelli L. Dolben, Emily Moreau-Marquis, Sophie Hampton, Thomas H. Shabaneh, Tamer B. Flitter, Becca A. Bahl, Christopher D. Bomberger, Jennifer M. Levy, Bruce D. Stanton, Bruce A. Hogan, Deborah A. Madden, Dean R. American Journal of Physiology-Lung Cellular and Molecular Physiology An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology |
| author_sort |
hvorecny, kelli l. |
| spelling |
Hvorecny, Kelli L. Dolben, Emily Moreau-Marquis, Sophie Hampton, Thomas H. Shabaneh, Tamer B. Flitter, Becca A. Bahl, Christopher D. Bomberger, Jennifer M. Levy, Bruce D. Stanton, Bruce A. Hogan, Deborah A. Madden, Dean R. 1040-0605 1522-1504 American Physiological Society Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology http://dx.doi.org/10.1152/ajplung.00383.2017 <jats:p> The opportunistic pathogen Pseudomonas aeruginosa colonizes the lungs of susceptible individuals by deploying virulence factors targeting host defenses. The secreted factor Cif (cystic fibrosis transmembrane conductance regulator inhibitory factor) dysregulates the endocytic recycling of CFTR and thus reduces CFTR abundance in host epithelial membranes. We have postulated that the decrease in ion secretion mediated by Cif would slow mucociliary transport and decrease bacterial clearance from the lungs. To test this hypothesis, we explored the effects of Cif in cultured epithelia and in the lungs of mice. We developed a strategy to interpret the “hurricane-like” motions observed in reconstituted cultures and identified a Cif-mediated decrease in the velocity of mucus transport in vitro. Presence of Cif also increased the number of bacteria recovered at two time points in an acute mouse model of pneumonia caused by P. aeruginosa. Furthermore, recent work has demonstrated an inverse correlation between the airway concentrations of Cif and 15-epi-lipoxin A<jats:sub>4,</jats:sub> a proresolving lipid mediator important in host defense and the resolution of pathogen-initiated inflammation. Here, we observe elevated levels of 15-epi-lipoxin A<jats:sub>4</jats:sub> in the lungs of mice infected with a strain of P. aeruginosa that expresses only an inactive form of cif compared with those mice infected with wild-type P. aeruginosa. Together these data support the inclusion of Cif on the list of virulence factors that assist P. aeruginosa in colonizing and damaging the airways of compromised patients. Furthermore, this study establishes techniques that enable our groups to explore the underlying mechanisms of Cif effects during respiratory infection. </jats:p> An epoxide hydrolase secreted by <i>Pseudomonas aeruginosa</i> decreases mucociliary transport and hinders bacterial clearance from the lung American Journal of Physiology-Lung Cellular and Molecular Physiology |
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| title |
An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_unstemmed |
An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_full |
An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_fullStr |
An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_full_unstemmed |
An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_short |
An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_sort |
an epoxide hydrolase secreted by <i>pseudomonas aeruginosa</i> decreases mucociliary transport and hinders bacterial clearance from the lung |
| topic |
Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology |
| url |
http://dx.doi.org/10.1152/ajplung.00383.2017 |
| publishDate |
2018 |
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L150-L156 |
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<jats:p> The opportunistic pathogen Pseudomonas aeruginosa colonizes the lungs of susceptible individuals by deploying virulence factors targeting host defenses. The secreted factor Cif (cystic fibrosis transmembrane conductance regulator inhibitory factor) dysregulates the endocytic recycling of CFTR and thus reduces CFTR abundance in host epithelial membranes. We have postulated that the decrease in ion secretion mediated by Cif would slow mucociliary transport and decrease bacterial clearance from the lungs. To test this hypothesis, we explored the effects of Cif in cultured epithelia and in the lungs of mice. We developed a strategy to interpret the “hurricane-like” motions observed in reconstituted cultures and identified a Cif-mediated decrease in the velocity of mucus transport in vitro. Presence of Cif also increased the number of bacteria recovered at two time points in an acute mouse model of pneumonia caused by P. aeruginosa. Furthermore, recent work has demonstrated an inverse correlation between the airway concentrations of Cif and 15-epi-lipoxin A<jats:sub>4,</jats:sub> a proresolving lipid mediator important in host defense and the resolution of pathogen-initiated inflammation. Here, we observe elevated levels of 15-epi-lipoxin A<jats:sub>4</jats:sub> in the lungs of mice infected with a strain of P. aeruginosa that expresses only an inactive form of cif compared with those mice infected with wild-type P. aeruginosa. Together these data support the inclusion of Cif on the list of virulence factors that assist P. aeruginosa in colonizing and damaging the airways of compromised patients. Furthermore, this study establishes techniques that enable our groups to explore the underlying mechanisms of Cif effects during respiratory infection. </jats:p> |
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| author | Hvorecny, Kelli L., Dolben, Emily, Moreau-Marquis, Sophie, Hampton, Thomas H., Shabaneh, Tamer B., Flitter, Becca A., Bahl, Christopher D., Bomberger, Jennifer M., Levy, Bruce D., Stanton, Bruce A., Hogan, Deborah A., Madden, Dean R. |
| author_facet | Hvorecny, Kelli L., Dolben, Emily, Moreau-Marquis, Sophie, Hampton, Thomas H., Shabaneh, Tamer B., Flitter, Becca A., Bahl, Christopher D., Bomberger, Jennifer M., Levy, Bruce D., Stanton, Bruce A., Hogan, Deborah A., Madden, Dean R., Hvorecny, Kelli L., Dolben, Emily, Moreau-Marquis, Sophie, Hampton, Thomas H., Shabaneh, Tamer B., Flitter, Becca A., Bahl, Christopher D., Bomberger, Jennifer M., Levy, Bruce D., Stanton, Bruce A., Hogan, Deborah A., Madden, Dean R. |
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| description | <jats:p> The opportunistic pathogen Pseudomonas aeruginosa colonizes the lungs of susceptible individuals by deploying virulence factors targeting host defenses. The secreted factor Cif (cystic fibrosis transmembrane conductance regulator inhibitory factor) dysregulates the endocytic recycling of CFTR and thus reduces CFTR abundance in host epithelial membranes. We have postulated that the decrease in ion secretion mediated by Cif would slow mucociliary transport and decrease bacterial clearance from the lungs. To test this hypothesis, we explored the effects of Cif in cultured epithelia and in the lungs of mice. We developed a strategy to interpret the “hurricane-like” motions observed in reconstituted cultures and identified a Cif-mediated decrease in the velocity of mucus transport in vitro. Presence of Cif also increased the number of bacteria recovered at two time points in an acute mouse model of pneumonia caused by P. aeruginosa. Furthermore, recent work has demonstrated an inverse correlation between the airway concentrations of Cif and 15-epi-lipoxin A<jats:sub>4,</jats:sub> a proresolving lipid mediator important in host defense and the resolution of pathogen-initiated inflammation. Here, we observe elevated levels of 15-epi-lipoxin A<jats:sub>4</jats:sub> in the lungs of mice infected with a strain of P. aeruginosa that expresses only an inactive form of cif compared with those mice infected with wild-type P. aeruginosa. Together these data support the inclusion of Cif on the list of virulence factors that assist P. aeruginosa in colonizing and damaging the airways of compromised patients. Furthermore, this study establishes techniques that enable our groups to explore the underlying mechanisms of Cif effects during respiratory infection. </jats:p> |
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| spelling | Hvorecny, Kelli L. Dolben, Emily Moreau-Marquis, Sophie Hampton, Thomas H. Shabaneh, Tamer B. Flitter, Becca A. Bahl, Christopher D. Bomberger, Jennifer M. Levy, Bruce D. Stanton, Bruce A. Hogan, Deborah A. Madden, Dean R. 1040-0605 1522-1504 American Physiological Society Cell Biology Physiology (medical) Pulmonary and Respiratory Medicine Physiology http://dx.doi.org/10.1152/ajplung.00383.2017 <jats:p> The opportunistic pathogen Pseudomonas aeruginosa colonizes the lungs of susceptible individuals by deploying virulence factors targeting host defenses. The secreted factor Cif (cystic fibrosis transmembrane conductance regulator inhibitory factor) dysregulates the endocytic recycling of CFTR and thus reduces CFTR abundance in host epithelial membranes. We have postulated that the decrease in ion secretion mediated by Cif would slow mucociliary transport and decrease bacterial clearance from the lungs. To test this hypothesis, we explored the effects of Cif in cultured epithelia and in the lungs of mice. We developed a strategy to interpret the “hurricane-like” motions observed in reconstituted cultures and identified a Cif-mediated decrease in the velocity of mucus transport in vitro. Presence of Cif also increased the number of bacteria recovered at two time points in an acute mouse model of pneumonia caused by P. aeruginosa. Furthermore, recent work has demonstrated an inverse correlation between the airway concentrations of Cif and 15-epi-lipoxin A<jats:sub>4,</jats:sub> a proresolving lipid mediator important in host defense and the resolution of pathogen-initiated inflammation. Here, we observe elevated levels of 15-epi-lipoxin A<jats:sub>4</jats:sub> in the lungs of mice infected with a strain of P. aeruginosa that expresses only an inactive form of cif compared with those mice infected with wild-type P. aeruginosa. Together these data support the inclusion of Cif on the list of virulence factors that assist P. aeruginosa in colonizing and damaging the airways of compromised patients. Furthermore, this study establishes techniques that enable our groups to explore the underlying mechanisms of Cif effects during respiratory infection. </jats:p> An epoxide hydrolase secreted by <i>Pseudomonas aeruginosa</i> decreases mucociliary transport and hinders bacterial clearance from the lung American Journal of Physiology-Lung Cellular and Molecular Physiology |
| spellingShingle | Hvorecny, Kelli L., Dolben, Emily, Moreau-Marquis, Sophie, Hampton, Thomas H., Shabaneh, Tamer B., Flitter, Becca A., Bahl, Christopher D., Bomberger, Jennifer M., Levy, Bruce D., Stanton, Bruce A., Hogan, Deborah A., Madden, Dean R., American Journal of Physiology-Lung Cellular and Molecular Physiology, An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung, Cell Biology, Physiology (medical), Pulmonary and Respiratory Medicine, Physiology |
| title | An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_full | An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_fullStr | An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_full_unstemmed | An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_short | An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_sort | an epoxide hydrolase secreted by <i>pseudomonas aeruginosa</i> decreases mucociliary transport and hinders bacterial clearance from the lung |
| title_unstemmed | An epoxide hydrolase secreted by Pseudomonas aeruginosa decreases mucociliary transport and hinders bacterial clearance from the lung |
| topic | Cell Biology, Physiology (medical), Pulmonary and Respiratory Medicine, Physiology |
| url | http://dx.doi.org/10.1152/ajplung.00383.2017 |