cUMP elicits interendothelial gap formation during Pseudomonas aeruginosa infection

Author:

deWeever Althea12ORCID,Paudel Sunita S.12ORCID,Zhou Chun12,Francis C. Michael12ORCID,Tambe Dhananjay T.32ORCID,Frank Dara W.45,Balczon Ron62,Stevens Troy172ORCID

Affiliation:

1. Department of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama, United States

2. Center for Lung Biology, University of South Alabama, Mobile, Alabama, United States

3. Department of Mechanical, Aerospace and Biomedical Engineering, University of South Alabama, Mobile, Alabama, United States

4. Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

5. Center for Infectious Disease Research, Medical College of Wisconsin, Milwaukee, Wisconsin, United States

6. Department of Biochemistry and Molecular Biology, University of South Alabama, Mobile, Alabama, United States

7. Department of Internal Medicine, University of South Alabama, Mobile, Alabama, United States

Abstract

During pneumonia, bacteria utilize a virulence arsenal to communicate with host cells. The Pseudomonas aeruginosa T3SS directly introduces virulence molecules into the host cell cytoplasm. These molecules are enzymes that trigger interkingdom communication. One of the exoenzymes is a nucleotidyl cyclase that produces noncanonical cyclic nucleotides like cUMP. Little is known about how cUMP acts in the cell. Here we found that cUMP instigates pulmonary edema during Pseudomonas aeruginosa infection of the lung.

Funder

HHS | NIH | NIAID | Division of Microbiology and Infectious Diseases

HHS | NIH | National Heart, Lung, and Blood Institute

Publisher

American Physiological Society

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