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Inhibition of Phagocytosis and Interleukin‐1 Production in Pulmonary Macrophages From Rats With Sialodacryoadenitis Virus Infection
Author(s) -
Boschert K.R.,
Schoeb T.R.,
Chandler D.B.,
Dillehay D.L.
Publication year - 1988
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.44.2.87
Subject(s) - phagocytosis , zymosan , macrophage , biology , alveolar macrophage , opsonin , lipopolysaccharide , pulmonary alveolus , immunology , microbiology and biotechnology , respiratory tract , respiratory system , in vitro , biochemistry , anatomy
To test whether or not sialodacryoadenitis virus (SDAV) infection in rats affects pulmonary macrophage function, we intranasally inoculated pathogen‐free F344 rats with SDAV and collected alveolar and interstitial macrophages 5 d later. We assessed Fc receptor‐mediated attachment and phagocytosis by phase‐contrast microscopic examination of monolayers of alveolar and interstitial macrophages incubated with zymosan, nonopsonized sheep erythrocytes, or erythrocytes opsonized with rabbit antisheeperythrocyte IgG. Alveolar macrophages from virus‐infected rats had significantly ( P ≤ .05) lower indices of attachment and phagocytosis of opsonized erythrocytes than control macrophages, but there was no difference in attachment of zymosan particles. Interstitial macrophages were not affected. Alveolar macrophages from SDAV‐infected rats produced significantly less interleukin‐1 than those from control rats, as assessed by testing supematants from lipopolysaccharide‐stimulated macrophage cultures for induction of mouse thymocytes to take up tritiated thymidine. Effects of SDAV infection on lung macrophages could increase host susceptibility to other pathogens or complicate studies of respiratory tract immunity.