No abstract available.
Macrophages, Alveolar* ; Mycobacterium tuberculosis* ; Mycobacterium*

No abstract available.
Animals ; Arachidonic Acid* ; Macrophages, Alveolar* ; Rats*

No abstract available.
Animals ; Macrophages, Alveolar* ; Rats* ; Superoxides* ; Verapamil*

Humans ; Lung ; cytology ; Macrophages, Alveolar ; Pulmonary Fibrosis ; pathology ; Silicosis ; pathology

OBJECTIVES: This study was conducted to evaluate the cytotoxicity of gallium arsenide(GaAs), indium phosphide(InP) and indium arsenide(InAs) all of which are used as the semiconductor eletments in semiconductor industry. METHODS: Cytotoxicity in the alveolar macrophage was evaluated by the measurement of in vitro magnetometry, LDH release assay and histological examination. RESULTS: The relaxation curves by the in vitro magnetometry showed that GaAs has the cytotoxicity for the alveolar macrophage which is more significant in the higher dosages, while this cytotoxicity is not appeared in the groups added with InP or InAs or PBS. In the decay constant for two minutes after magnetization, GaAs-added groups showed a significant decrease with increasing doses, but both InP- and InAs-added groups did not show any significance. The LDH release assay showed a dose-dependent increasing tendency in the GaAs-, InP- and InAs-added groups. In terms of cellular morphological changes, GaAs-added groups revealed such severe cellular damages as prominent destructions in cell membranes and their morphological changes of nucleus, while InP- and InAs-added groups remained intact in intracellular structures, except for cytoplasmic degenerations. CONCLUSIONS: It is suggested that GaAs is more influential to cytotoxicity of alveolar macrophages than InP and InAs.
Arsenic* ; Arsenicals* ; Cell Membrane ; Cytoplasm ; Gallium ; Indium ; Macrophages* ; Macrophages, Alveolar ; Magnetometry ; Relaxation ; Semiconductors

Mycobacterium tuberculosis (Mtb) causing tuberculosis as an intracellular pathogen initially infects alveolar macrophages following aerosol inhalation. Thus, macrophages play a critical role in the establishment of Mtb infection and macrophage cell death, a common outcome during Mtb infection, may initiate host- or pathogen-favored immune responses, resulting in facilitating protection or pathogenesis, respectively. In addition, virulent Mtb strains are known to inhibit apoptosis and consequently down-regulates immune response using a variety of strategies. In many recent studies have shown that virulent Mtb can either augment or reduce apoptosis by regulating expression of pro-apoptotic and anti-apoptotic proteins belonging to Bcl-2 family proteins. In this review, we will discuss and dissect the apoptotic pathways of Bcl-2 family proteins in Mtb-infected macrophages.
Apoptosis ; Apoptosis Regulatory Proteins ; Cell Death ; Humans ; Inhalation ; Macrophages* ; Macrophages, Alveolar ; Mycobacterium tuberculosis* ; Mycobacterium* ; Tuberculosis

The aim of this study was to investigate the effects of polarization program on the ability of macrophages to regulate iron metabolism. M1 and M2 macrophages were propagated in vitro from porcine alveolar macrophages 3D4/2 and polarized by cytokines. The 3D4/2 macrophages were treated with 20 ng/mL interferon gamma (IFN-γ) and 10 ng/mL interleukin-4 (IL-4) combined with 10 ng/mL macrophage colony-stimulating factor (M-CSF) to induce polarization to M1 and M2, respectively. After incubation for 24 h, the expression levels of inflammatory factors and iron-metabolism genes were determined using real-time qPCR, Western bot and immunofluorescence. The M1/M2 macrophages culture media supernatant was collected and used to treat porcine intestinal epithelial cells IPEC-J2. The proliferation ability of IPEC-J2 was detected using CCK-8 assay kit. Following exogenous addition of ammonium ferric citrate (FAC) to M1/M2 macrophages, the phagocytic function of macrophages was detected using fluorescein isothiocyanate-dextran (FITC-dextran) and flow cytometry. The results showed that, compared with control, M1 macrophages had higher mRNA levels of iron storage proteins (ferritin heavy and light polypeptide, i.e. FtH and FtL), hepcidin and lipocalin-2, as well as iron content. Moreover, iron enhanced the ability of M1 macrophages to phagocytize FITC-dextran. There was no significant change in these mRNA expression levels in M2 macrophages, but the mRNA expression levels of ferroportin and transferrin receptor were up-regulated. In addition, the conditioned media supernatant from M2 macrophages promoted cell proliferation of IPEC-J2. These findings indicate that M1 macrophages tend to lock iron in the cell and reduce extracellular iron content, thereby inhibiting the proliferation of extracellular bacteria. While M2 macrophages tend to excrete iron, which contributes to the proliferation of surrounding cells and thus promotes tissue repair.
Animals ; Cytokines ; Ferritins ; Iron/metabolism* ; Macrophages/metabolism* ; Macrophages, Alveolar/metabolism* ; Swine

In order to find potential therapeutic agents on lung inflammatory conditions, the extracts of Acanthopanax divaricatus var. albeofructus were prepared and its constituents were isolated. They include lignans such as (+)-syringaresinol (1), acanthoside B (2), salvadoraside (3) and acanthoside D (4), lariciresinol-9-O-beta-D-glucopyranoside (5) and phenylpropanoids such as 4-[(1E)-3-methoxy-1-propenyl]phenol (6), coniferin (7), and methyl caffeate (8). The extracts and several constituents such as compound 1, 6 and 8 inhibited the production of inflammatory markers, IL-6 and nitric oxide, from IL-1beta-treated lung epithelial cells and lipopolysaccharide (LPS)-treated alveolar macrophages. Furthermore, the extracts and compound 4 significantly inhibited lung inflammation in lipolysaccharide-treated acute lung injury in mice by oral administration. Thus it is suggested that A. divaricatus var. albeofructus and its several constituents may be effective against lung inflammation.
Eleutherococcus* ; Acute Lung Injury ; Administration, Oral ; Animals ; Epithelial Cells ; Interleukin-6 ; Lignans ; Lung* ; Macrophages ; Macrophages, Alveolar ; Mice ; Nitric Oxide ; Pneumonia*

BACKGROUND: The confirmative diagnosis of pulmonary tuberculosis(Tb) can be made by the isolation of Mycobacterium Tuberculosis(MTb) in the culture of the sputum, respiratory secretions or tissues of the patients, but positive result could not always be obtained in pulmonary Tb cases. Although there are many indirect ways of the diagnosis of Tb, clinicians still experience the difficulty in the diagnosis of Tb because each method has its own limitation. Therefore development of a new diagnostic tool is clinically urgent. It was reported that silica cause some lysosomal enzymes to be released from macrophages in vitro and one of these enzymes is elevated in workers exposed to silica dust and in silicotic subjects. In pulmonary Tb, alveolar macrophages are known to be activated after ingestion of MTb. Activated macrophages can kill MTb through oxygen free radical species and digestive enzymes of lysosome. But if macrophages allow the bacilli to grow intracellularly, the macrophages will die finally and local lesion will enlarge. Then it is assumed that the lysosomal enzymes would be released from the dead macrophages. The goal of this investigation was to determine if there are differences in the plasma activities of lysosomal enzymes, beta-glucuronidase(GLU) and beta-N- acetyl glucosaminidase(NAG), among the groups of active and inactive pulmonary Tb and healthy control, and to see if there is any possibility that the plasma activity of GLU and NAG can be used as diagnostic indicies of active pulmonary Tb. METHODS: The plasma were obtained from 20 patients with bacteriologically proven active pulmonary Tb, 15 persons with inactive Tb and 20 normal controls. In 10 patients with active pulmonary Tb, serial samples after 2 months of anti-Tb medications were obtained. Plasma GLU and NAG activities were measured by the fluorometric methods using 4-methylumbelliferyl sub- strates. All data are expressed as the mean +/-the standard error of the mean. RESULTS: The activites of GLU and NAG in plasma of the patients with active Tb were 21.52 +/-3.01 and 325.4+/-23.37(nmol product/h/ ml of plasma), respectively. Those of inactive pulmonary Tb were 24.87+/-3.78, 362.36+/-33.92 and those of healthy control were 25.45 +/-4.05, 324.44+/-28.66 (nmol product/ h/ml of plasma), respectively. There were no significant differences in the plasma activities of both enzymes among 3 groups. The plasma activities of GLU at 2 months after anti-Tb medications were increased(42.18+/-5.94 nmol product/h/ ml of plasma) in the patients with active pulmonary Tb compared with that at the diagnosis of Tb(P-value <0.05). CONCLUSION: The results of the present investigation suggest that the measurement of the plasma activities of GLU and NAG in the patients with active pulmonary Tb could not be a useful method for the diagnosis of active Tb. Further investigation is necessary to define the reasons why the plasma activities of the GLU was increased in the patients with active pulmonary Tb after Tb therapy.
Diagnosis ; Dust ; Eating ; Glucuronidase ; Humans ; Lysosomes ; Macrophages ; Macrophages, Alveolar ; Mycobacterium ; Oxygen ; Plasma* ; Silicon Dioxide ; Sputum ; Tuberculosis ; Tuberculosis, Pulmonary*

BACKGROUND: Eosinophilic airway inflammation is a characteristic feature of bronchial asthma. Recent studies showed that increased production and release of eosinophils from bone marrow(BM) might be the essential step in the development of eosinophilic airway inflammation. To testify the hypothesis that increase in BM eosinophil production may be an important determinant of the severity of airway eosinophilia, their relationship was studied in a mouse model of allergic airway inflammation. METHODS: BALB/c mice were sensitized with intraperitoneal ovalbumin adsorbed to aluminum potassium sulfate, followed by challenges with intranasal ovalbumin on two consecutive days. Saline was used for sensitization and challenge in control mice. Bronchoalveolar lavage(BAL) was performed at 24 h after last nasal challenge, immediately followed by BM cell harvest from the femurs. The severity of airway inflammation was assessed as BAL eosinophilia, and the capacity of BM eosinophil production was assessed as BM eosinophil colony forming units(Eo-CFUs) using a semisolid culture assay. RESULTS: There was a significant increase in the percentage of BAL eosinophils and lymphocytes with a resultant decrease in the percentage of alveolar macrophages in the ovalbumin- treated mice, compared with the saline-treated mice(p<0.05, respectively). Change in the percentage of neutrophils was not statistically significant. Compared with the saline-treated mice, the number of BM Eo-CFUs was significantly increased in the ovalbumin- treated mice(p<0.05). But the number of BM Eo-CFUs was not correlated significantly with the number of eosinophils in BAL fluid in the ovalbumin-treated mice. CONCLUSION: Respiratory exposure to allergen induced not only airway eosinophilia but also BM eosinophilopoiesis in this mice model of asthma. However there was no direct relationship between BM eosinophilopoiesis and airway eosinophilia, suggesting that the capacity of eosino-phil production in BM may not an important determinant of severity of airway eosinophilia.
Aluminum ; Animals ; Asthma* ; Bone Marrow* ; Eosinophilia ; Eosinophils* ; Femur ; Inflammation ; Lymphocytes ; Macrophages, Alveolar ; Mice* ; Neutrophils ; Ovalbumin ; Potassium