Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of high oxygen concentrations on lungs of neonatal rats was studied. In addition, some oxygen-exposed animals were treated with either dexamethasone or thalidomide. No gross histologic changes were noted in the lungs following exposure to 95% oxygen nor were there changes in the total number or the phenotypic distribution of BAL cells obtained from these lungs compared to lungs from air exposed (control) neonatal rats. The majority of the BAL cells were CD45+ leukocytes (macrophages). However, when BAL cells were exposed to LPS in vitro, TNF-alpha production was higher in cells from rats exposed to 95% oxygen compared to cells from rats exposed to ambient air. In addition, lung TNF-alpha and IL-6 mRNA levels were increased after exposure to 95% oxygen. In the lungs of animals treated with either dexamethasone or thalidomide, TNF-alpha mRNA levels were reduced, while only dexamethasone treatment also reduced IL-6 mRNA levels.
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PMID:Modulation of hyperoxia-induced TNF-alpha expression in the newborn rat lung by thalidomide and dexamethasone. 1085 Aug 56

The aim of the study was to evaluate the concentrations of TNF-alpha and GM-CSF in double BAL (2 x 120 ml) from two different lung segments: (s.A) from upper lobe with the most and (s.B) from lower lobe with the least extensive involvement estimated by high resolution computed tomography (HRCT). Examined group consisted of 28 non-smoking sarcoid patients with homogenous, regular distribution of nodular opacities in conventional chest X-ray (14 F, 14M aged 19-54). In examined patients 16 had nonhomogenous distribution (ND) and 12 had regular distribution (RD) of HRCT changes. Eleven healthy volunteers served as controls. In patients with sarcoidosis we observed the significantly higher concentrations (p < 0.01) of TNF-alpha (3.18 pg/ml, 2.64 pg/ml) and GM-CSF (1.01 pg/ml, 0.95 pg/ml) respectively in BAL fluid from s.A and s.B in comparison with BAL from s.Abis and s.Bbis in control group (TNF-alpha: 0.46 pg/ml, 0.47 pg/ml and GM-CSF: 0.28 pg/ml, 0.31 pg/ml respectively). Mean concentration of TNF-alpha in BAL from s.A (3.77 pg/ml) in ND group was significantly higher than in BAL from s.B in RD group (2.91 pg/ml). TNF-alpha in BAL from s.A in active sarcoidosis was higher than in BAL from s.A and s.B in non-active sarcoidosis. Concentrations of TNF-alpha in BAL from both s.A and s.B correlated positively with CD4/CD8 ratio, percentage of lymphocytes, lymphocytes HLA-DR+ and absolute number of CD4 cells and negatively with CD8 cells estimated in BAL from these lung segments. In patients with indications to therapy the level of GM-CSF in BAL from s.A (1.44 pg/ml) was significantly higher (p < 0.05) than in BAL from s.A (0.64 pg/ml) in patients without indications to treatment. We conclude that TNF-alpha and GM-CSF may be involved in sarcoidosis pathogenesis and TNF-alpha may be useful in estimation of sarcoidosis activity.
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PMID:[Cytokines TNF-alpha and GM-CSF in BAL from two different segments of lungs defined by high resolution computerized tomography (HRCT) in patients with sarcoidosis]. 1120 Jul 48

To determine the effect of heat stress on histopathology of acute lung injury (ALI) caused by administration of lipopolysaccharide (LPS), and to determine the roles of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, interferon (IFN)-gamma, IL-10 and surfactants in heat-induced tolerance to ALI, we administered either saline or LPS (3 mg/kg of body weight) intravenously to male Sprague-Dawley rats without and with heat pretreatment. Five hours after LPS or saline treatment (23 h after heat-pretreatment), samples were obtained. We found that the histopathologic features of LPS-induced ALI were attenuated by heat-pretreatment. Heat-pretreatment did not decrease the elevated plasma or BAL fluid levels of TNF-alpha, IL-1beta, and IFN-gamma by LPS. The plasma level of IL-10 in LPS-treated rats with heat-pretreatment, however, was increased compared to that of LPS-treated rats without heat-pretreatment (P = 0.001). There were no differences in the BAL fluid concentrations of light or heavy density pulmonary surfactant phospholipids depending on heat-pretreatment in LPS-treated rats. These observations suggest that IL-10 might play a role in decreasing LPS-induced acute lung injury after heat-pretreatment.
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PMID:Effects of heat pretreatment on histopathology, cytokine production, and surfactant in endotoxin-induced acute lung injury. 1140 10

It is widely known that fungal airways infections may deteriorate the course of bronchial asthma. The mechanism of the phenomenon is still unclear. The aim of our study was to assess the effect of fungal infections on the secretion of selected cytokines by bronchoalveolar leukocytes. Five patients (group FA) with bronchial asthma and Candida albicans or Aspergillus fumigatus airways infections (confirmed by bronchoscopy and culture) were included in the study. All of them were on the chronic treatment with corticosteroids (10-20 mg of prednisone per day) and underwent several courses of therapy with antibiotics. The control groups comprised 5 previously untreated asthmatics without bronchial colonization with fungi (group A) as well as 5 healthy volunteers (group H). Leukocytes were isolated from bronchoalveolar lavage fluid (BALF) and cultured in the presence or absence of cytokine inducers such as phytohemagglutin L (PHA), lipo-polysaccharide (LPS) from E. coli. The activity of TNF-alpha, IL-6 and IFN-gamma were measured in the BAL cell culture supernatants by using specific bioassays. In comparison with healthy controls the spontaneous or induced secretion of cytokines were significantly augmented in patients from group A. In contrast the asthmatics who represented group FA demonstrated normal levels of spontaneous cytokine secretion. However, the tendency to increase LPS and PHA-induced production was observed in BAL leukocytes from the patients. The above results support the view that beneficial effect of corticosteroid treatment in bronchial asthma may act, at least in part, by inhibition of the high spontaneous secretion of proinflammatory cytokines. Nevertheless, fungal airways infections may lead to increase of LPS- or PHA-induced production of TNF-alpha, IL-6 or IFN-gamma (despite prednisone therapy) by prestimulation of the BAL cells with fungi.
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PMID:TNF-alpha, IL-6 and IFN-gamma secreted by bronchoalveolar leukocytes isolated from patients with bronchial asthma, complicated by fungal airways infections. 1171 87

Numerous investigations have been conducted to elucidate mechanisms involved in the initiation and progression of silicosis. However, most of these studies involved bolus exposure of rats to silica, i.e. intratracheal instillation or a short duration inhalation exposure to a high dose of silica. Therefore, the question of pulmonary overload has been an issue in these studies. The objective of the current investigation was to monitor the time course of pulmonary reactions of rats exposed by inhalation to a non-overload level of crystalline silica. To accomplish this, rats were exposed to 15 mg/m3 silica, 6 h/day, 5 days/week for up to 116 days of exposure. At various times (5-116 days exposure), animals were sacrificed and silica lung burden, lung damage, inflammation, NF-KB activation, reactive oxygen species and nitric oxide production, cytokine production, alveolar type II epithelial cell activity, and fibrosis were monitored. Activation of NF-KB/DNA binding in BAL cells was evident after 5 days of silica inhalation and increased linearly with continued exposure. Parameters of pulmonary damage, inflammation and alveolar type II epithelial cell activity rapidly increased to a significantly elevated but stable new level through the first 41 days of exposure and increased at a steep rate thereafter. Pulmonary fibrosis was measurable only after this explosive rise in lung damage and inflammation, as was the steep increase in TNF-alpha and IL-1 production from BAL cells and the dramatic rise in lavageable alveolar macrophages. Indicators of oxidant stress and pulmonary production of nitric oxide exhibited a time course which was similar to that for lung damage and inflammation with the steep rise correlating with initiation of pulmonary fibrosis. Staining for iNOS and nitrotyrosine was localized in granulomatous regions of the lung and bronchial associated lymphoid tissue. Therefore, these data demonstrate that the generation of oxidants and nitric oxide, in particular, is temporally and anatomically associated with the development of lung damage, inflammation, granulomas and fibrosis. This suggests an important role for nitric oxide in the initiation of silicosis.
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PMID:Effect of inhaled crystalline silica in a rat model: time course of pulmonary reactions. 1216 31

In recent years cases of often fatal pulmonary hemorrhage in infants have been associated with water damaged homes and the toxigenic fungus Stachybotrys chartarum. The fungal spores contain mycotoxins which could be injurious to the rapidly developing lung. In order to understand the developmental pathophysiology of this disease we developed an infant rat model of stachybotrytoxicosis describing the effects of fungal spores on survival, growth, histopathology of the lung and respiration. Conidia of S. chartarum were instilled intratracheally (1.0-8.0 x 10(5)/gm wt.) in 4-d old Sprague-Dawley rat pups. Two control groups received either sterile PBS or a suspension of spores extensively extracted with ethanol to remove toxins. Lethal dose response was determined (LD50 = 2.7 x 10(5) spores/gm wt.). All dead pups had extensively hemorrhagic lungs. Growth of surviving animals was impaired in a dose-dependent manner. Changes of pulmonary function parameters in rats treated with 1.1 x 10(5) spores/g were consistent with an increased respiratory resistance. Histology of lungs revealed fresh hemorrhage, sparse hemosiderin-laden macrophages, and evidence of inflammation including thickened alveolar septa infiltrated by lymphocytes and mononuclear cells and intra-alveolar macrophages. Significant increases (p = 0.001) in numbers of macrophages (2-fold), lymphocytes (5-fold) and neutrophils (7-fold) were found in BAL fluid. Hemoglobin was elevated 2-fold (p = 0.004). Proinflammatory mediator IL-1beta increased more than 6-fold and TNF-alpha 30-fold (p = 0.001). Extracted spores had a minimal effect on all examined parameters in BAL fluid indicating that mycotoxins are primarily responsible for the hemorrhagic and inflammatory response.
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PMID:Infant animal model of pulmonary mycotoxicosis induced by Stachybotrys chartarum. 1217 46

The lipid mediator PAF plays an important role in the phagocytosis of particles, including bacteria, and consequent production of pro-inflammatory cytokines, such as TNF-alpha and IL-8. Using a PAF receptor antagonist (UK-74,505) and PAF receptor knock-out mice, we have investigated the relevance of PAF for the inflammatory changes and lethality after pulmonary infection with the gram-negative bacteria Klebsiella pneumoniae in mice. At an inoculum of 3 x 10(6) bacteria, there was marked pulmonary (bronchoalveolar lavage and lung) neutrophilia that started early (2.5 h after infection) and peaked at 48 h. All animals were dead by day 4 of infection. The chemokine KC and the pro-inflammatory cytokine TNF-alpha increased rapidly and persisted for 48 h in the lungs. Pretreatment with UK-74,505 (30 mg kg(-1) per day, p.o.) had no significant effects on the number of infiltrating neutrophils in BAL fluid or lung tissue, as assessed by histology and measuring myeloperoxidase, or on the concentrations of KC. In contrast, concentrations of TNF-alpha and the number of bacteria inside neutrophils were significantly diminished. In order to support a role for the PAF during K. pneumoniae infection, experiments were also carried out in PAFR-deficient mice. In the latter animals, lethality occurred earlier than in wild-type controls. This was associated with greater number of bacteria in lung tissue and diminished percentage of neutrophils containing bacteria in their cytoplasm. Our results suggest that PAF, acting on its receptor, plays a protective role during infection with K. pneumoniae in mice.
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PMID:Role of the platelet-activating factor (PAF) receptor during pulmonary infection with gram negative bacteria. 1238 75

The pulmonary granulomatous diseases may be staged using clinical examination, pulmonary function tests, ⁶⁷Ga scans, chest X-rays, BAL and serum ACE levels; furthermore, these disorders are clearly associated to changes in lymphocyte subpopulations, CD4+/CD8+ ratio and surface receptors; in particular, T cell activation characterizes early alveolitis phase, while activated macrophages and related cytokines prevail in granulomata and fibrosis development. In this study, we dosed the serum and blood concentrations of IL-6 (a well-known pro-inflammatory cytokine), sIL-2R (marker of T-cell activation), TNF-alpha and IFN-gamma (associated with the granuloma development), in patients affected by active or inactive sarcoidosis, primary tuberculosis, idiopathic pulmonary fibrosis and healthy control subjects, using the ELISA method. Cytokines assay showed significant changes only in subjects with primary tuberculosis and active sarcoidosis; infact, primary tuberculosis was characterized by high values of IL-6 and IFN-gamma both in peripheral blood and in BAL, with high values of sIL-2R in BAL; patients with active sarcoidosis showed high levels of IFN-gamma and TNF-alpha both in BAL and in peripheral blood, associated to an increase of serum sIL-2R levels. Our data confirm that the compared assay of these cytokines in peripheral blood and BAL specimens, may be useful to diagnose and to assess the disease activity in pulmonary granulomatous diseases; in particular, the levels of sIL-2R are a marker of the alveolitis phase, while TNF-alpha and IL-6 levels discriminate patients with sarcoidosis or tuberculosis granulomata, respectively.
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PMID:Cytokines assay in peripheral blood and bronchoalveolar lavage in the diagnosis and staging of pulmonary granulomatous diseases. 1265 92

To elucidate the mechanism of anti-inflammatory effect of partial liquid ventilation (PLV), cytokine concentration, surface CD11b, and macrophage expression were investigated in BALF. The 30-minutes group was treated with gas ventilation (GV) for 30 minutes after intratracheal LPS administration. The GV group was prepared in the same manner as the 30-minutes group, then the GV was continued for the following 2 hours. The PLV group was treated in the same manner as the 30-minutes group, and then received PLV with perflubron for the following 2 hours. Animals were euthanized to receive BAL. The PLV group showed a tendency to have a higher concentration than the GV group of TNF-alpha, MIP-2, and CINC-1 as measured by ELISA, although there were no significant differences. The ratio of expressions of CD11b and macrophages to total leukocytes were determined by flow-cytometry. There were no significant differences in the ratio of CD11b-positive expression to acquired cells (GV: 63.6 +/- 8.4%, PLV: 60.5+/-5.4%, P=0.73). However, the proportion of macrophages was significantly increased (GV: 5.6 +/-1.5, PLV: 14.0+/-1.3, P=0.006). These results suggest that the anti-inflammatory effect of PLV is not caused by the change in CD11b expression, and that PLV affects the proportion of macrophage among BALF cells.
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PMID:Partial liquid ventilation does not affect BALF TNF-, MIP-2, CINC-1 concentrations, or CD11b cell surface expression, but does increase macrophage proportion among BALF cells in the acute phase of rat LPS-induced lung injury. 1290 11

A variety of studies have demonstrated that organ-to-organ communication circuits are established during various disease states. For example, an activated liver may release high levels of cytokines, which are carried to the lung and activate this organ. In the present study, we have examined the inflammation occurring as the liver-lung interact during the initiation of acetaminophen-induced toxicity. An overnight fast followed by an intraperitoneal acetaminophen challenge was required to elicit liver injury. In these animals, lung injury was most pronounced at 24 h post-challenge and was characterized by necrosis, edema and inflammation. Interestingly, the non-fasted/fed animals that received acetaminophen had only minor liver injury, but still presented with significant pathologic changes of the lung. BAL fluid contained increased neutrophils after acetaminophen challenge in the fasted (26%) and the fed (35%) animal groups. A significant vascular leak was found in the fasted, but not the fed, acetaminophen challenged animals. However, lung levels of the chemokine, eotaxin, and the cytokine, IL-12, were significantly elevated in the acetaminophen challenged animals that were fed, but not in the fasted group. The immunoneutralization of eotaxin, but not IL-12 or TNF-alpha, improved the histological appearance of the lung in fed mice challenged with acetaminophen.
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PMID:Alterations in cytokine/chemokine expression during organ-to-organ communication established via acetaminophen-induced toxicity. 1461 9


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