scholarly journals Histochemical Expression of Inducible Nitric Oxide Synthase and Inflammatory Cytokines in Alveolar Macrophages in Patients with ARDS.

1997 ◽  
Vol 30 (1) ◽  
pp. 57-61 ◽  
Author(s):  
Atsuko Kobayashi ◽  
Satoru Hashimoto ◽  
Kunihiko Kooguchi ◽  
Yoshifumi Tanaka ◽  
Hideki Onodera ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inflammatory Cytokines ◽  
Inducible Nitric Oxide Synthase ◽  
Alveolar Macrophages ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Expression of Inducible Nitric Oxide Synthase and Inflammatory Cytokines in Alveolar Macrophages of ARDS Following Sepsis

CHEST Journal ◽  
1998 ◽  
Vol 113 (6) ◽  
pp. 1632-1639 ◽  
Author(s):  
Atsuko Kobayashi ◽  
Satoru Hashimoto ◽  
Kunihiko Kooguchi ◽  
Yoshihiro Kitamura ◽  
Hideki Onodera ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inflammatory Cytokines ◽  
Inducible Nitric Oxide Synthase ◽  
Alveolar Macrophages ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Inducible nitric oxide synthase in pulmonary alveolar macrophages from patients with tuberculosis.

1996 ◽  
Vol 183 (5) ◽  
pp. 2293-2302 ◽  
Author(s):  
S Nicholson ◽  
M da G Bonecini-Almeida ◽  
J R Lapa e Silva ◽  
C Nathan ◽  
Q W Xie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mycobacterium Tuberculosis ◽  
Nitric Oxide Synthase ◽  
Bronchoalveolar Lavage ◽  
Inducible Nitric Oxide Synthase ◽  
Alveolar Macrophages ◽  
Mononuclear Phagocytes ◽  
Mycobacterium Tuberculosis Infection ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The high-output pathway of nitric oxide production helps protect mice from infection by several pathogens, including Mycobacterium tuberculosis. However, based on studies of cells cultured from blood, it is controversial whether human mononuclear phagocytes can express the corresponding inducible nitric oxide synthase (iNOS;NOS2). The present study examined alveolar macrophages fixed directly after bronchopulmonary lavage. An average of 65% of the macrophages from 11 of 11 patients with untreated, culture-positive pulmonary tuberculosis reacted with an antibody documented herein to be monospecific for human NOS2. In contrast, a mean of 10% of bronchoalveolar lavage cells were positive from each of five clinically normal subjects. Tuberculosis patients' macrophages displayed diaphorase activity in the same proportion that they stained for NOS2, under assay conditions wherein the diaphorase reaction was strictly dependent on NOS2 expression. Bronchoalveolar lavage specimens also contained NOS2 mRNA. Thus, macrophages in the lungs of people with clinically active Mycobacterium tuberculosis infection often express catalytically competent NOS2.

scholarly journals Activation of Nuclear Factor κB and Induction of Inducible Nitric Oxide Synthase by Ureaplasma urealyticumin Macrophages

2000 ◽  
Vol 68 (12) ◽  
pp. 7087-7093 ◽  
Author(s):  
Y.-H. Li ◽  
Z.-Q. Yan ◽  
J. Skov Jensen ◽  
K. Tullus ◽  
A. Brauner
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Alveolar Macrophages ◽  
Nuclear Factor Κb ◽  
Inos Expression ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

ABSTRACT Chronic lung disease (CLD) of prematurity is an inflammatory disease with a multifactorial etiology. The importance ofUreaplasma urealyticum in the development of CLD is debated, and steroids produce some improvement in neonates with this disease. In the present study, the capability of U. urealyticum to stimulate rat alveolar macrophages to produce nitric oxide (NO), express inducible nitric oxide synthase (iNOS), and activate nuclear factor κB (NF-κB) in vitro was characterized. The effect of NO on the growth of U. urealyticum was also investigated. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found that U. urealyticum antigen (≥4 × 107 color-changing units/ml) stimulated alveolar macrophages to produce NO in a dose- and time-dependent manner (P < 0.05). This effect was further enhanced by gamma interferon (100 IU/ml; P < 0.05) but was attenuated by budesonide and dexamethasone (10−4 to 10−6 M) (P < 0.05). The mRNA and protein levels of iNOS were also induced in response to U. urealyticum and inhibited by steroids.U. urealyticum antigen triggered NF-κB activation, a possible mechanism for the induced iNOS expression, which also was inhibited by steroids. NO induced by U. urealyticum caused a sixfold reduction of its own growth after infection for 10 h. Our findings imply that U. urealyticum may be an important factor in the development of CLD. The host defense response againstU. urealyticum infection may also be influenced by NO. The down-regulatory effect of steroids on NF-κB activation, iNOS expression, and NO production might partly explain the beneficial effect of steroids in neonates with CLD.

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