The Efficiency of the Translocation of Mycobacterium tuberculosis across a Bilayer of Epithelial and Endothelial Cells as a Model of the Alveolar Wall Is a Consequence of Transport within Mononuclear Phagocytes and Invasion of Alveolar Epithelial Cells

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Published inInfection and Immunity Vol. 70; no. 1; pp. 140 - 146
Main Authors BERMUDEZ, Luiz E, SANGARI, Felix J, KOLONOSKI, Peter, PETROFSKY, Mary, GOODMAN, Joseph
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.01.2002
Subjects
Bacterial diseases
Bacteriology
Biological and medical sciences
Biological Transport
Cell Line
Cell Polarity
Cells, Cultured
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Chemokine CCL2 - biosynthesis
Chemotaxis, Leukocyte - physiology
Endothelium, Vascular - cytology
Endothelium, Vascular - immunology
Endothelium, Vascular - physiology
Epithelial Cells - cytology
Epithelial Cells - immunology
Epithelial Cells - physiology
Experimental bacterial diseases and models
Fundamental and applied biological sciences. Psychology
Humans
Infectious diseases
Interleukin-8 - biosynthesis
Lung - cytology
Lung - immunology
Lung - microbiology
Lung - physiology
Medical sciences
Microbiology
Models, Biological
Monocytes - cytology
Monocytes - immunology
Monocytes - microbiology
Monocytes - physiology
Mycobacterium bovis - physiology
Mycobacterium tuberculosis
Mycobacterium tuberculosis - immunology
Mycobacterium tuberculosis - physiology
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Phagocytes - cytology
Phagocytes - physiology
Pulmonary Alveoli - immunology
Pulmonary Alveoli - microbiology
Pulmonary Alveoli - physiology
Receptors, Cell Surface - metabolism
Receptors, Cell Surface - physiology
Alveolar type II cell
Endothelial cell
Monocyte
Lung
Mycobacterial infection
Respiratory system
Blood
Infection
Tuberculosis
Mycobacterium tuberculosis
Mycobacteriales
Blood vessel
Bacteriosis
Mycobacteriaceae
Bacteria
Epithelial cell
Actinomycetes
Models
Circulatory system
Infected cell
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The mechanism(s) by which Mycobacterium tuberculosis crosses the alveolar wall to establish infection in the lung is not well known. In an attempt to better understand the mechanism of translocation and create a model to study the different stages of bacterial crossing through the alveolar wall, we established a two-layer transwell system. M. tuberculosis H37Rv was evaluated regarding the ability to cross and disrupt the membrane. M. tuberculosis invaded A549 type II alveolar cells with an efficiency of 2 to 3% of the initial inoculum, although it was not efficient in invading endothelial cells. However, bacteria that invaded A549 cells were subsequently able to be taken up by endothelial cells with an efficiency of 5 to 6% of the inoculum. When incubated with a bicellular transwell monolayer (epithelial and endothelial cells), M. tuberculosis translocated into the lower chamber with efficiency (3 to 4%). M. tuberculosis was also able to efficiently translocate across the bicellular layer when inside monocytes. Infected monocytes crossed the barrier with greater efficiency when A549 alveolar cells were infected with M. tuberculosis than when A549 cells were not infected. We identified two potential mechanisms by which M. tuberculosis gains access to deeper tissues, by translocating across epithelial cells and by traveling into the blood vessels within monocytes.
ABSTRACT The mechanism(s) by which Mycobacterium tuberculosis crosses the alveolar wall to establish infection in the lung is not well known. In an attempt to better understand the mechanism of translocation and create a model to study the different stages of bacterial crossing through the alveolar wall, we established a two-layer transwell system. M. tuberculosis H37Rv was evaluated regarding the ability to cross and disrupt the membrane. M. tuberculosis invaded A549 type II alveolar cells with an efficiency of 2 to 3% of the initial inoculum, although it was not efficient in invading endothelial cells. However, bacteria that invaded A549 cells were subsequently able to be taken up by endothelial cells with an efficiency of 5 to 6% of the inoculum. When incubated with a bicellular transwell monolayer (epithelial and endothelial cells), M. tuberculosis translocated into the lower chamber with efficiency (3 to 4%). M. tuberculosis was also able to efficiently translocate across the bicellular layer when inside monocytes. Infected monocytes crossed the barrier with greater efficiency when A549 alveolar cells were infected with M. tuberculosis than when A549 cells were not infected. We identified two potential mechanisms by which M. tuberculosis gains access to deeper tissues, by translocating across epithelial cells and by traveling into the blood vessels within monocytes.
The mechanism(s) by which Mycobacterium tuberculosis crosses the alveolar wall to establish infection in the lung is not well known. In an attempt to better understand the mechanism of translocation and create a model to study the different stages of bacterial crossing through the alveolar wall, we established a two-layer transwell system. M. tuberculosis H37Rv was evaluated regarding the ability to cross and disrupt the membrane. M. tuberculosis invaded A549 type II alveolar cells with an efficiency of 2 to 3% of the initial inoculum, although it was not efficient in invading endothelial cells. However, bacteria that invaded A549 cells were subsequently able to be taken up by endothelial cells with an efficiency of 5 to 6% of the inoculum. When incubated with a bicellular transwell monolayer (epithelial and endothelial cells), M. tuberculosis translocated into the lower chamber with efficiency (3 to 4%). M. tuberculosis was also able to efficiently translocate across the bicellular layer when inside monocytes. Infected monocytes crossed the barrier with greater efficiency when A549 alveolar cells were infected with M. tuberculosis than when A549 cells were not infected. We identified two potential mechanisms by which M. tuberculosis gains access to deeper tissues, by translocating across epithelial cells and by traveling into the blood vessels within monocytes.
Author Luiz E. Bermudez
Joseph Goodman
Mary Petrofsky
Felix J. Sangari
Peter Kolonoski
AuthorAffiliation Kuzell Institute for Arthritis & Infectious Diseases, California Pacific Medical Center Research Institute, 1 Laboratory of Pediatrics Electron Microscopy, Department of Pediatrics, University of California, San Francisco, San Francisco, California 2
AuthorAffiliation_xml – name: Kuzell Institute for Arthritis & Infectious Diseases, California Pacific Medical Center Research Institute, 1 Laboratory of Pediatrics Electron Microscopy, Department of Pediatrics, University of California, San Francisco, San Francisco, California 2
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  givenname: Felix J
  surname: SANGARI
  fullname: SANGARI, Felix J
  organization: Kuzell Institute for Arthritis & Infectious Diseases, California Pacific Medical Center Research Institute, San Francisco, California, United States
– sequence: 3
  givenname: Peter
  surname: KOLONOSKI
  fullname: KOLONOSKI, Peter
  organization: Kuzell Institute for Arthritis & Infectious Diseases, California Pacific Medical Center Research Institute, San Francisco, California, United States
– sequence: 4
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  surname: PETROFSKY
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  surname: GOODMAN
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  organization: Laboratory of Pediatrics Electron Microscopy, Department of Pediatrics, University of California, San Francisco, San Francisco, California, United States
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Issue 1
Keywords Alveolar type II cell
Endothelial cell
Monocyte
Lung
Mycobacterial infection
Respiratory system
Blood
Infection
Tuberculosis
Mycobacterium tuberculosis
Mycobacteriales
Blood vessel
Bacteriosis
Mycobacteriaceae
Bacteria
Epithelial cell
Actinomycetes
Models
Circulatory system
Infected cell
Language English
License CC BY 4.0
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Editor: S. H. E. Kaufmann
Present address: Department of Pathology, Veterans Administration Hospital of Palo Alto, Palo Alto, Calif.
Present address: Department of Molecular Biology, University of Cantabria, Santander, Spain.
Corresponding author. Mailing address: Kuzell Institute, Suite 305, 2200 Webster St., San Francisco, CA 94115. Phone: (415) 561-1624. Fax: (415) 441-8548. E-mail: luizb@cooper.cpmc.org.
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The mechanism(s) by which Mycobacterium tuberculosis crosses the alveolar wall to establish infection in the lung is not well known. In an attempt to better...
ABSTRACT The mechanism(s) by which Mycobacterium tuberculosis crosses the alveolar wall to establish infection in the lung is not well known. In an attempt to...
The mechanism(s) by which Mycobacterium tuberculosis crosses the alveolar wall to establish infection in the lung is not well known. In an attempt to better...
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StartPage 140
SubjectTerms Bacterial diseases
Bacteriology
Biological and medical sciences
Biological Transport
Cell Line
Cell Polarity
Cells, Cultured
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Chemokine CCL2 - biosynthesis
Chemotaxis, Leukocyte - physiology
Endothelium, Vascular - cytology
Endothelium, Vascular - immunology
Endothelium, Vascular - physiology
Epithelial Cells - cytology
Epithelial Cells - immunology
Epithelial Cells - physiology
Experimental bacterial diseases and models
Fundamental and applied biological sciences. Psychology
Humans
Infectious diseases
Interleukin-8 - biosynthesis
Lung - cytology
Lung - immunology
Lung - microbiology
Lung - physiology
Medical sciences
Microbiology
Models, Biological
Monocytes - cytology
Monocytes - immunology
Monocytes - microbiology
Monocytes - physiology
Mycobacterium bovis - physiology
Mycobacterium tuberculosis
Mycobacterium tuberculosis - immunology
Mycobacterium tuberculosis - physiology
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Phagocytes - cytology
Phagocytes - physiology
Pulmonary Alveoli - immunology
Pulmonary Alveoli - microbiology
Pulmonary Alveoli - physiology
Receptors, Cell Surface - metabolism
Receptors, Cell Surface - physiology
Title The Efficiency of the Translocation of Mycobacterium tuberculosis across a Bilayer of Epithelial and Endothelial Cells as a Model of the Alveolar Wall Is a Consequence of Transport within Mononuclear Phagocytes and Invasion of Alveolar Epithelial Cells
URI http://iai.asm.org/content/70/1/140.abstract
https://www.ncbi.nlm.nih.gov/pubmed/11748175
https://search.proquest.com/docview/18219412
https://search.proquest.com/docview/71381571
https://pubmed.ncbi.nlm.nih.gov/PMC127600
Volume 70
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