Abstract
The formation of intrapulmonary immune complexes in mice generates a vigorous inflammatory response characterized by microvascular permeability and polymorphonuclear neutrophil influx. Gene-targeted disruption of the substance P receptor (NK-1R) protected the lung from immune complex injury, as did disruption of the C5a anaphylatoxin receptor. Immunoreactive substance P was measurable in fluids lining the lung at time points before neutrophil influx and may thus be involved in an early step in the inflammatory response to immune complexes in the lung.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Antigen-Antibody Complex / immunology*
-
Antigens, CD / genetics
-
Antigens, CD / physiology
-
Bronchoalveolar Lavage Fluid / chemistry
-
Capillary Permeability
-
Complement C5a / physiology*
-
Female
-
Gene Targeting
-
Immune Complex Diseases / immunology
-
Immune Complex Diseases / metabolism*
-
Immune Complex Diseases / pathology
-
Inflammation / immunology
-
Inflammation / metabolism
-
Inflammation / pathology
-
Lung / chemistry
-
Lung / pathology
-
Lung Diseases / immunology
-
Lung Diseases / metabolism*
-
Lung Diseases / pathology
-
Male
-
Mice
-
Mice, Inbred C57BL
-
Neutrophils
-
Receptor, Anaphylatoxin C5a
-
Receptors, Complement / genetics
-
Receptors, Complement / physiology
-
Receptors, Neurokinin-1 / genetics
-
Receptors, Neurokinin-1 / physiology
-
Substance P / analysis
-
Substance P / physiology*
-
Tumor Necrosis Factor-alpha / analysis
Substances
-
Antigen-Antibody Complex
-
Antigens, CD
-
Receptor, Anaphylatoxin C5a
-
Receptors, Complement
-
Receptors, Neurokinin-1
-
Tumor Necrosis Factor-alpha
-
Substance P
-
Complement C5a