NDLI: Lung environment determines unique phenotype of alveolar macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Guth, Amanda M. Janssen, William J. Bosio, Catharine M. Crouch, Erika C. Henson, Peter M. Dow, Steven W.
Description	Country affiliation: United States Author Affiliation: Guth AM ( Departments of Clinical Sciences, Colorado State University, Ft. Collins, USA.)
Abstract	Alveolar macrophages (AM) are the most abundant antigen-presenting cells in the lungs, and they play a critical role in regulating pulmonary immune responses to inhaled pathogens and to allergens. However, compared with macrophages in other body sites, AM have an unusual phenotype that, in many respects, resembles the phenotype of dendritic cells (DC). Therefore, to more fully define the unique nature of AM, we compared the phenotype and function of AM with the phenotype and function of resident peritoneal lavage-derived macrophages (PLM). We found striking phenotypic differences between AM and PLM, particularly with regard to CD11c expression, and we also observed that AM had a significantly better antigen-presenting capability than PLM. Therefore, we investigated the role of the local airway environment in generation of the unusual phenotype of AM. We carried out cell transfer experiments to compare macrophage differentiation in the airways with that in the peritoneal cavity. We observed significant upregulation of CD11c expression on bone marrow macrophages and peritoneal macrophages when they were adoptively transferred into the airways. In contrast, CD11c expression was not upregulated after cell transfer into the peritoneal cavity, whereas CD11b expression was significantly increased. In vitro, culture of bone marrow-adherent cells with surfactant protein D (SP-D) or granulocyte/macrophage colony-stimulating factor (GM-CSF) induced significant upregulation of CD11c expression, and in vivo GM-CSF concentrations were significantly higher in bronchoalveolar than in peritoneal lavage fluid. Finally, GM-CSF(-/-) mice failed to develop CD11c(+) AM, but CD11c(+) AM were present in SP-D(-/-) mice. However, macrophages from GM-CSF(-/-) bone marrow could upregulate CD11c expression when transferred to the airways of wild-type mice. These results suggest that the airway environment promotes development of macrophages with unique DC-like characteristics and that this unusual phenotype is determined, to a large degree, by locally high concentrations of GM-CSF and, possibly, SP-D.
File Format	HTM / HTML
ISSN	10400605
e-ISSN	15221504
DOI	10.1152/ajplung.90625.2008
Journal	AJP: Lung Cellular and Molecular Physiology
Issue Number	6
Volume Number	296
Language	English
Publisher	American Physiological Society
Publisher Date	2009-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Discipline Physiology Discipline Molecular Biology Discipline Pulmonary Medicine Lung Cytology Immunology Macrophages, Alveolar Adoptive Transfer Animals Antigen Presentation Antigens, Cd11c Metabolism Bone Marrow Cells Bronchoalveolar Lavage Fluid Cell Differentiation Cells, Cultured Dendritic Cells Flow Cytometry Granulocyte-macrophage Colony-stimulating Factor Immunophenotyping Classification Macrophages, Peritoneal Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Inbred Icr Pinocytosis Pulmonary Surfactants Specific Pathogen-free Organisms Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Pulmonary and Respiratory Medicine Cell Biology Physiology Physiology (medical)

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

GM-CSF treatment prevents respiratory syncytial virus-induced pulmonary exacerbation responses in postallergic mice by stimulating alveolar macrophage maturation.

Alveolar macrophage activation and an emphysema-like phenotype in adiponectin-deficient mice.

Surfactant protein a promotes attachment of Mycobacterium tuberculosis to alveolar macrophages during infection with human immunodeficiency virus.

Cellular kinetics and modeling of bronchioalveolar stem cell response during lung regeneration.

Pulmonary alveolar proteinosis: time to shift?

Tubular lysosomes accompany stimulated pinocytosis in macrophages

Diagnosis of pulmonary aspiration: a mouse model using a starch granule test in bronchoalveolar lavage.

Alveolar proteinosis syndrome: pathogenesis, diagnosis, and management.

Metalloelastase in lungs and alveolar macrophages is modulated by extracellular substance P in mice.

Lung environment determines unique phenotype of alveolar macrophages.

Similar Documents

GM-CSF treatment prevents respiratory syncytial virus-induced pulmonary exacerbation responses in postallergic mice by stimulating alveolar macrophage maturation.

Alveolar macrophage activation and an emphysema-like phenotype in adiponectin-deficient mice.

Surfactant protein a promotes attachment of Mycobacterium tuberculosis to alveolar macrophages during infection with human immunodeficiency virus.

Cellular kinetics and modeling of bronchioalveolar stem cell response during lung regeneration.

Pulmonary alveolar proteinosis: time to shift?

Tubular lysosomes accompany stimulated pinocytosis in macrophages

Diagnosis of pulmonary aspiration: a mouse model using a starch granule test in bronchoalveolar lavage.

Alveolar proteinosis syndrome: pathogenesis, diagnosis, and management.

Metalloelastase in lungs and alveolar macrophages is modulated by extracellular substance P in mice.

Lung environment determines unique phenotype of alveolar macrophages.