Premium
Opportunistic Infection, Expression of INOS and Nitrotyrosine in Gp91 Knockout Mice
Author(s) -
Zhang Suhua,
Huang Harer,
Kaminski Pawel M,
Wolin Michael S,
Hintze Thomas H
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1458-b
Subject(s) - nitrotyrosine , knockout mouse , mertk , nadph oxidase , pathology , biology , immunohistochemistry , lung , inflammation , nitric oxide , immunology , medicine , endocrinology , nitric oxide synthase , oxidative stress , receptor , receptor tyrosine kinase
Purpose Gp91 phox is an essential element of NADPH oxidase. Phagocytes of gp91 phox (−/ −) mice have reduced O 2 − production and a lack bactericidaland fungicidal mechanism causing opportunistic infections. This study was to examine the incidence of opportunistic infection and expression of iNOS and nitrotyrosine in gp91 knockout mice. Methods The mice were divided into five groups and examined using histopathology, immunohistochemistry, chemiluminescence and immunoblotting. Results All lungs of gp91knockout mice developed abscesses (fungal) at 12‐week‐old and involved area enlarged gradually. General inflammation was found in 75% gp91knockout mice liver at 14‐week‐old and 100% at 16‐week‐old. O 2 − production was decrease in myocardial cell from gp91knockout mice (p<0.05). The expression of nitrotyrosine was increased in lung, liver, heart and kidney at 16‐week‐old gp91 knockout mice. The location of nitrotyrosine was in phagocytes and cytoplasm of organ parenchyma. The expression of iNOS was obviously increased in lungs and livers in 16‐week‐old gp91 knockout mice (p<0.05). Conclusions These findings suggest that lung is the most common organ for opportunistic infection and liver is second in 12~14 week‐old gp91 knockout mice. Increased expression of nitrotyrosine suggests a mechanism of compensation in gp91knockout. INOS suggests an inflammatory reaction, but not enough of a fungicidal mechanism to compensate for the decrease of superoxide in gp91knockout mice. Supported by HL‐PO1‐43023 grant.