Lung surfactant and reactive oxygen-nitrogen species: antimicrobial activity and host-pathogen interactions
1 Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama 35249; 2 Clinical Microbiology Laboratory, University of Colorado Health Sciences Center, Denver 80262; 5 Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colora...
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Published in | American journal of physiology. Lung cellular and molecular physiology Vol. 281; no. 3; pp. 517 - L523 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.09.2001
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Subjects | |
Online Access | Get full text |
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Summary: | 1 Department of Anesthesiology, University of Alabama at
Birmingham, Birmingham, Alabama 35249; 2 Clinical
Microbiology Laboratory, University of Colorado Health Sciences
Center, Denver 80262; 5 Department of Medicine, National Jewish
Center for Immunology and Respiratory Medicine, Denver, Colorado
80206; 3 Department of Microbiology and Immunology, Weill
Medical College of Cornell University, New York, New York 10021;
4 Department of Medicine, Vanderbilt University School of
Medicine, Nashville, Tennessee 37212; and 6 Department of
Cell Biology, Duke University, Durham, North Carolina 27710
Surfactant protein (SP)
A and SP-D are members of the collectin superfamily. They are widely
distributed within the lung, are capable of antigen recognition, and
can discern self versus nonself. SPs recognize bacteria, fungi, and
viruses by binding mannose and N -acetylglucosamine residues
on microbial cell walls. SP-A has been shown to stimulate the
respiratory burst as well as nitric oxide synthase expression by
alveolar macrophages. Although nitric oxide (NO·) is a
well-recognized microbicidal product of macrophages, the mechanism(s)
by which NO· contributes to host defense remains undefined. The
purpose of this symposium was to present current research pertaining to
the specific role of SPs and reactive oxygen-nitrogen species in innate
immunity. The symposium focused on the mechanisms of NO·-mediated
toxicity for bacterial, human, and animal models of SP-A- and
NO·-mediated pathogen killing, microbial defense mechanisms against
reactive oxygen-nitrogen species, specific examples and signaling
pathways involved in the SP-A-mediated killing of pulmonary pathogens,
the structure and binding of SP-A and SP-D to bacterial targets, and
the immunoregulatory functions of SP-A.
collectins; surfactant protein A; nitric oxide; peroxynitrite; innate immunity; macrophages; signal transduction |
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ISSN: | 1040-0605 1522-1504 |
DOI: | 10.1152/ajplung.2001.281.3.L517 |