Altered function of pulmonary surfactant in fatty acid lung injury

To determine whether acute fatty acid lung injury impairs pulmonary surfactant function, we studied anesthetized ventilated rabbits given oleic acid (55 mg/kg iv, n = 11) or an equivalent volume of saline (n = 8). Measurements of pulmonary mechanics indicated a decrease in dynamic compliance within 5 min of injury and a decrease in lung volume that was disproportionately large at low pressures, consistent with diminished surfactant activity in vivo. Bronchoalveolar lavage fluid obtained 1 h after injury had significantly increased erythrocytes and total leukocytes, largely polymorphonuclear cells. The phospholipid content and composition of the cell-free fraction had only minor changes from those of controls, but the protein content was increased 35-fold. Measurements of lavage surface activity in vitro showed an increase in average minimum surface tension from 1.3 +/- 0.4 (SE) dyn/cm in controls to 20.2 +/- 3.9 dyn/cm in injured animals. The alterations in static pressure-volume curves and decrease in lavage surface activity suggest a severe alteration of surfactant function in this form of lung injury that occurs despite the presence of normal amounts of surfactant phospholipids.     

Phagocytosis of liposomes by human alveolar macrophages

The ability of cells recovered from lung lavages to phagocytose liposomes has been investigated.Inulin (¹⁴C-labelled), entrapped in multilamellar immunoglobulin-G coated liposomes with ³H-labelled cholesterol as the lipid phase marker, was fed to the recovered cells. Fifteen patients with diffuse interstitial pulmonary disease (DIPD), prior to steroid treatment, and eight normal controls were lavaged for the study. Uptake was found for both groups and it was concluded that the liposomes enter the cells predominantly via endocytosis. Follow-up lavage, three months after the initial lavage, was repeated on three patients receiving 60 mg prednisone per day. A decrease in the uptake of liposomes was observed after steroid treatment.     

Vascular and epithelial damage in the lung of the mouse after X rays or neutrons

The response of the lung was studied in CFLP mice after exposure of the whole thorax to X rays (250 kVp) or cyclotron neutrons (16 MeV deuterons on Be, mean energy 7.5 MeV). To measure blood volume and leakage of plasma proteins, 51Cr-labeled red blood cells and 125I-albumin were injected intravenously and 24 h later lungs were lavaged via the trachea. Radioactivities in lung tissue and lavage fluid were determined to estimate the accumulation of albumin in the interstitial and alveolar spaces indicating damage to blood vessels and alveolar epithelium respectively. Function of type II pneumonocytes was assessed by the amounts of surfactant (assayed as lipid phosphorous) released into the lavage fluid. During the first 6 weeks, lavage protein and surfactant were increased, the neutron relative biological effectiveness (RBE) being unity. During pneumonitis at 12-24 weeks, surfactant levels were normal, blood volume was decreased, and both interstitial and alveolar albumin were increased. Albumin levels then decreased. At late times after exposure (42-64 weeks) alveolar albumin returned to normal but interstitial albumin was still slightly elevated. Values of RBE for changes in blood volume and interstitial and alveolar albumin at 15 weeks and for changes in blood volume and interstitial albumin at 46 weeks were 1.4, comparable with that for animal survival at 180 days. The results indicate that surfactant production is not critical for animal survival. They suggest that changes in blood vessels and alveolar epithelium occur during acute pneumonitis; epithelial repair follows but some vascular damage may persist. The time course of the changes in albumin levels did not correlate with increases in collagen biosynthesis which have been observed as early as 1 month after exposure and persist for up to 1 year. Furthermore, a dose which had no effect on leakage caused a marked increase in collagen biosynthesis. Thus the present results do not support a causal relationship between exudation of vascular protein during pneumonitis and the later development of fibrosis.     

Expression of insulin-like growth factor-I (IGF-I) in alveolar macrophages and lymphocytes obtained by bronchoalveolar lavage (BAL) in interstitial lung diseases (ILD). Assessment of IGF-I as a potential local mitogen and antiapoptotic cytokine

Little is known about IGF-I expression in the alveolar lymphocytes (AL), and about local role of IGF-I in physiological conditions and in interstitial lung diseases. Bronchoalveolar lavage was carried out in patients with silicosis, asbestosis, idiopathic pulmonary fibrosis (IPF) and sarcoidosis, as well as in control subjects (n = 13, 9, 12, 56, 15, resp). Alveolar macrophages (AM) and lymphocytes (AL) were studied for (1) IGF-I, BCL-2, Fas and Fas Ligand expression and (2) cell cycle (incl. sub-G1 peak of late apoptosis) with propidium iodide (PI). Flow cytometry (FC) and immunocytochemistry were used. AL early apoptosis was detected by Annexin V FITC/PI staining. IGF-I was present in AL of all tested groups. The number of IGF-I positive AL was significantly higher in IPF (52 +/- 6.7%) and in later (II and III) stages of sarcoidosis (39 +/- 7.8 vs 16 +/- 4.0% in controls, p < 0.05). Increased BCL-2 expression in AL was detected in IPF and sarcoidosis. In all tested groups, AL were almost exclusively Fas+ T cells. Generally, a low number of AL entered apoptosis; no significant differences were found between patient groups, except decreased apoptosis rate in sarcoidosis (0.60 +/- 0.17 vs 1.15 +/- 0.33% in controls, p < 0.05). Proportion of AL positive for IGF-I was significantly correlated with parameters reflecting AL and AM cell proliferation and BCL-2 expression (e.g. AL IGF-I+ vs AM in S phase of cell cycle: r(S) = +0.50, p = 0.001), but not with apoptosis. The results show that human alveolar lymphocytes express IGF-I in normal conditions, as well as in ILD. The proportion of IGF-I+ lymphocytes was significantly increased in IPF and at later stages of sarcoidosis. In our material there was no evidence for profibrogenic or antiapoptotic activity of IGF-I. We suggest that IGF-I originating from AL may be locally active as a mitogen for alveolar macrophages and lymphocytes in ILD.     

Cytoplasmic enzyme patterns in isolated hamster pulmonary alveolar type II cells

Three cytoplasmic enzyme patterns were studied in pulmonary alveolar type II cells isolated from normal adult hamster lung: lactate dehydrogenase (total and isoenzymes), peroxidase, and beta-N-acetylglucosaminidase. Enzyme patterns of freshly-isolated type II cells were found to be different from those of freshly-isolated pulmonary hamster fibroblasts. After both types of cells had been cultured for seven days, no difference in cytoplasmic enzyme patterns remained. Lactate dehydrogenase isoenzyme patterns for type II cells were different from those obtained from polymorphonuclear leukocytes and alveolar macrophages. These data may be useful in detecting sources of lung injury by assessment of enzyme patterns in bronchoalveolar lavage fluid.     

Familial pulmonary alveolar microlithiasis diagnosed by bronchoalveolar lavage. A case report

BACKGROUND: Familial alveolar microlithiasis is a rare lung disease. In this study we describe the cytologic features of this disease in bronchoalveolar lavage. CASE: A 10-year-old girl and her uncle, a 50-year-old man, had dyspnea and diffuse interstitial pattern on chest radiograph with no defined cause at a period of 10 years apart. Open lung biopsy in the girl and transbronchial lung biopsy plus bronchoalveolar lavage (BAL) in the man were per-formed to determine the diagnosis. In cyopen lung biopsy the diagnosis was alveolar microlithiasis. BAL revealed rehtypical microliths (calcospherites), and th transbronchial lung biopsy performed in the same patient failed to disclose superficially reset any significant pathology. In cytologic a smears, extracellular and intracellular concentrically layered purple-brown, round-to-oval microliths were clearly seen. Cyanophilic periodic acid-Schiff positive intracytoplasmic amorphous material was also frequently seen in alveolar macrophages. CONCLUSION: Familial alveolar microlithiasis is a rare interstitial lung disease that can be easily diagnosed by BAL. This procedure is a very useful tool in diagnosing and classifying some interstitial lung diseases.     

A critical evaluation of bronchoalveolar lavage. Criteria for identifying unsatisfactory specimens

In a multicenter, city-wide study of the use of bronchoalveolar lavage for the evaluation of diffuse interstitial lung diseases, the occurrence of specimens unsuitable for analysis was evaluated. Using a standardized bronchoscopy technique, 26 physicians obtained 1,588 lavage specimens from 787 patients over a 52-month period. After transport to and processing in one laboratory using standardized procedures, all specimens were interpreted by one pathologist. Specimens were considered unsatisfactory if they contained: (1) a paucity of alveolar macrophages (i.e., less than ten alveolar macrophages/high-power field), (2) excessive numbers of airway-derived cells (i.e., more than the alveolar macrophages present), (3) a mucopurulent exudate, (4) cells altered by degeneration or (5) laboratory artifacts. Using these criteria, 30.4% of the specimens were considered unsuitable for analysis. There were no significant differences in the frequency of unsatisfactory specimens among participating physicians and institutions or between smoking and nonsmoking patients. Appraisal of alveolar inflammatory and immune effector cells in bronchoalveolar lavage specimens from patients with interstitial lung disease should include an assessment for contamination from airways proximal to the terminal bronchioles before conclusions are drawn about the activity of alveolar inflammation.     

Bronchoalveolar lavage fluid differential cell count. How many cells should be counted?

OBJECTIVE: To investigate the number of cells to be counted in cytocentrifuged bronchoalveolar lavage (BAL) fluid preparations in order to reach a reliable enumeration of each cell type. STUDY DESIGN: A total of 136 BAL fluid samples for patients with suspected pneumonia or interstitial lung disease were investigated. Differential cell counts were performed on May-Grünwald-Giemsa-stained cytocentrifuged preparations by 2 observers, each differentiating 500 cells. Reliability for the enumeration of each cell type was expressed as phi value, as calculated in generalizability theory. RESULTS: For polymorphonuclear neutrophils (PMNs), alveolar macrophages, lymphocytes and eosinophils, an acceptable phi value of > or = .95 was reached at a count of 300 cells by 1 observer. Mast cells reached a phi value of only .674 at a count of 500 cells by 1 observer, precluding a reliable count. At a count of 500 cells by 1 observer, squamous epithelial cells, bronchial epithelial cells and plasma cells displayed phi values of .868, .903 and .816, respectively. CONCLUSION: At a count of 300 cells, PMNs, alveolar macrophages, lymphocytes and eosinophils are reliably enumerated in cytocentrifuged BAL fluid samples.     

Electron microscopy and autoradiography study of bronchoalveolar lavage cells in nonspecific pneumonia

Cells obtained by bronchoalveolar lavage from patients with chronic nonspecific pulmonary inflammatory diseases were studied using light and electron microscopy and radioautography. Five morphological forms of alveolar macrophages, distinct in their structure and 3H-uridine content were described. A higher level of RNA synthesis has been revealed in alveolar macrophage forms 2 and 3 than in forms 1, 4 and 5; with it being lower in polymorphonuclear leukocytes and lymphocytes. It was shown that changes in the number of lavage cells and the structure-to-function characteristics in each cellular population depended on the phase of the inflammatory process. It was postulated that structural and metabolic heterogeneity of alveolar macrophages reflected the successive stages of cellular development from cell-precursors (through activation of protein synthesis) to cells with complete lysosomal cycle and the following phagocytosis.     

Influence of refractory ceramic fibres - asbestos substitute - on the selected parameters of bronchoalveolar lavage 6 months after intratracheal instillation to W-rats

Industrial fibrous dusts are applied in many industrial branches and represent adverse factors in occupational and environmental area. Refractory ceramic fibers (RCFs) - amorphous alumina silicates - are used as one kind of asbestos substitutes. Because RCFs are relatively durable and some RCFs are respirable, they may present a potential health hazard by inhalation. The aim of present work was to find out the subchronic effect of RCFs on selected parameters of bronchoalveolar lavage (BAL) in W-rats, confirm the biopersistence of RCFs after 6 month instillation and contribute to the understanding of the pathomechanism of lung injury after fibrous dust exposure. Wistar rats were intratracheally instilled with 4 mg/animal of RCFs - exposed group and with 0.4 ml saline solution/animal - control group. Animals were sacrificed after 6 month exposure. Bronchoalveolar lavage (BAL) was performed and selected BAL parameters (mainly inflammatory and cytotoxic) were examined. After treatment with RCFs the following changes were observed: statistically significant increase in proportion of lymphocytes and polymorphonuclears as well as in % of immature alveolar macrophages (AM) and phagocytic activity of AM; statistically significant decrease in viability of AM and proportion of AM (from the differential cell count) in comparison with the control group. The results of this study indicated that RCFs even 6 months after intratracheal instillation very significantly changed the majority of examined BAL parameters. The presence of inflammatory and cytotoxic response in lung may signalize beginning or developing disease process.     

The modifications produced in allergic alveolitis and in Goodpasture's syndrome due to exposure to cigarette smoke.

Two groups of rats with experimental alveolitis were exposed to cigarette smoke. After comparing the results, the possible muffling effect of the cigarette smoke related to interstitial lung disease was discussed. 180 rats were divided into 6 groups of 30 animals each: Group 1: untreated controls; Group 2: exposed to cigarette smoke for 2 months; Group 3: sensitized with bovine albumin (BA) and exposed to an atmosphere with this antigen for two months, to reproduce a type of extrinsic allergic alveolitis (EAA); Group 4: treated with a single daily dose of anti-lung serum for three days followed by two days without treatment, to reproduce a type of Goodpasture's syndrome; Group 5: exposed to cigarette smoke and to BA; Group 6: exposed to cigarette smoke and treated with anti-lung serum. The animals were sacrificed and their lungs were treated for: Bronchoalveolar lavage (BAL), percentage lymphocyte count, polymorphonuclear (PMN) and alveolar macrophages (AM); semiquantitative and morphometric histological study. The semiquantitative study determined the area of the studied lung incision, affected by granulomae, increased alveolar aerial spaces, thickened alveolar walls and haemosiderine lung area. The morphometric study, based on the linear integration method, evaluated: the distance between two alveolar walls, the amount of interstice per field; and the number of AM with haemosiderine per field was counted. From the results we point out that the treated animals had significantly higher lymphocyte and BAL PMN counts than the untreated ones; no significant differences were found between the singly and doubly treated animals. The animals exposed to cigarette smoke and treated with anti-lung serum were those that showed the least number of lymphocytes and PMN of all the treated animals. The semiquantitative variables studied were all increased in comparison to the control group, most of the increases being significant. The morphometric variables revealed significant differences with respect to the untreated group, except for the animals which were treated with anti-lung serum and cigarette smoke, which showed a minimum decrease in the alveolar size and a slight increase of the interstitial tissue. Only one morphometric variable showed a significant difference between the group treated with anti-lung serum and the one treated with anti-lung serum and cigarette smoke: the number of AM with haemosiderine in the lung.(ABSTRACT TRUNCATED AT 400 WORDS)     

Alveolar macrophages regulate neutrophil recruitment in endotoxin-induced lung injury

Background

Alveolar macrophages play an important role during the development of acute inflammatory lung injury. In the present study, in vivo alveolar macrophage depletion was performed by intratracheal application of dichloromethylene diphosphonate-liposomes in order to study the role of these effector cells in the early endotoxin-induced lung injury.

Methods

Lipopolysaccharide was applied intratracheally and the inflammatory reaction was assessed 4 hours later. Neutrophil accumulation and expression of inflammatory mediators were determined. To further analyze in vivo observations, in vitro experiments with alveolar epithelial cells and alveolar macrophages were performed.

Results

A 320% increase of polymorphonuclear leukocytes in bronchoalveolar lavage fluid was observed in macrophage-depleted compared to macrophage-competent lipopolysaccharide-animals. This neutrophil recruitment was also confirmed in the interstitial space. Monocyte chemoattractant protein-1 concentration in bronchoalveolar lavage fluid was significantly increased in the absence of alveolar macrophages. This phenomenon was underlined by in vitro experiments with alveolar epithelial cells and alveolar macrophages. Neutralizing monocyte chemoattractant protein-1 in the airways diminished neutrophil accumulation.

Conclusion

These data suggest that alveolar macorphages play an important role in early endotoxin-induced lung injury. They prevent neutrophil influx by controlling monocyte chemoattractant protein-1 production through alveolar epithelial cells. Alveolar macrophages might therefore possess robust anti-inflammatory effects.     

Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos.

Exposure of phagocytic cells to asbestos in vitro results in an augmented production of reactive oxygen metabolites and increased peroxidation of lipids. The aim of this investigation was to assess the extent of lipid peroxidation both in cells and fluid obtained from bronchoalveolar lavage (BAL), and in lungs of rats exposed to crocidolite asbestos or titanium dioxide (TiO2), a nonfibrous particulate control. In comparison to sham and TiO2-exposed rats, the BAL fluid and cells of crocidolite-exposed animals contained significantly elevated levels of malondialdehyde (MDA), a breakdown product of lipid peroxidation detected using high-pressure liquid chromatography (HPLC). In contrast, no significant differences in MDA were detected in lavaged lung tissue from these animals. Inhalation of crocidolite caused an early inflammatory response characterized by elevated numbers of polymorphonuclear leukocytes and lymphocytes, as well as enhanced total protein in BAL. Pulmonary fibrosis and increased lung hydroxyproline also were observed after 20 days of exposure. Exposure to TiO2 did not cause inflammation, pulmonary fibrosis, or elevated amounts of hydroxyproline in the lung. Our results show that exposure to the fibrogenic and inflammatory mineral, crocidolite, results in an enhanced lipid peroxidation in BAL cells and fluid not observed after inhalation of the particulate TiO2. These novel observations suggest that MDA in BAL may be useful as a biomarker of exposure to inhaled asbestos or other oxidants.     

Changes in the composition of canine respiratory cells obtained by bronchial lavage following irradiation or drug immunosuppression.

Canine respiratory cells, obtained by bronchial lavage, and blood leukocytes were monitored to observe cellular changes following acute and chronic immunosuppression. Irradiation (350 R) produced bone marrow suppression and prompt peripheral blood leukopenia, but did not affect recovery of pulmonary alveolar macrophages or lymphocytes for 12 days after. Treatment for 6 weeks with daily methylprednisolone (1 mg/kg) caused a progressive decrease in the number of recoverable respiratory lymphocytes, whereas alternate day methylprednisolone (2 mg/kg) had less effect. Cyclophosphamide in combination with steroids generally augmented the progressive loss of blood and respiratiory lymphocytes. Recovery of alveolar macrophages was not changed appreciably. Thus, the population of lung macrophages, sampled by pulmonary lavage, withstood acute and chronic forms of immunosuppression very well. In contrast, canine lymphocytes seem more susceptible to injury, especially to drug regimens containing steroids.     

Identification of calcium-dependent phospholipid-binding proteins (annexins) from guinea pig alveolar type II cells

A new group of calcium-regulating proteins, called annexins or Ca⁺⁺-dependent phospholipid-binding proteins (PLBP), have been detected in different species, organs and cell types. In the present study, we have identified and quantitated PLBP from guinea pig lung, lavage fluid and alveolar type II cells to elucidate the possible role of PLBP in lung surfactant biogenesis and secretion. Lungs were lavaged and type II cells from lavaged lung were isolated by elastase digestion and purified by centrifugal elutriation. For the quantitative identification of PLBP, we performed ELISA assays and Western blot analysis by using an antiserum raised in guinea pigs against a pure rabbit lung 36 kDa PLBP. The lavage fluid, cytosol from lung and type II cells contained 784,167 and 435 ng per mg protein, respectively, of PLBP. The SDS-PAGE electrophoretic pattern and Western blot confirmed that all lung samples have band corresponding to a 36 kDa protein. This indicates that both alveolar type II cells and lavage fluid have higher levels of PLBP than whole lung cytosol.     

In vivo toxicity and pulmonary effects of promazine and chlorpromazine in rats

Cationic amphiphilic drugs induce a phospholipid storage disorder known as phospholipidosis. Halogenated analogs of the drugs are more potent inducers of phospholipidosis when compared to nonhalogenated analogs. Two such antipsychotic drugs, promazine and chlorpromazine, are effectively taken up by the lungs and induce lamellar inclusions in vitro. We compared the in vivo toxicity and efficacy of promazine and chlorpromazine to induce phospholipidosis in the lung and in pulmonary alveolar macrophages. Male Sprague-Dawley rats were given promazine or chlorpromazine (25 mg/kg/day, P.O., in water) for 5 weeks. Food intake was decreased in promazine- and chlorpromazine-treated rats, chlorpromazine rats being affected more than promazine rats. To minimize experimental error due to starvation, control rats were pair-fed. The body weight gain was decreased in chlorpromazine rats in comparison to pair-fed controls. Chlorpromazine-treated rats, but not promazine-treated rats, showed increased mortality over the 5-week treatment period. Histopathologic examination of lung revealed loss of alveolar macrophages with no other gross abnormalities in chlorpromazine-treated rats. Quantitative analysis of lung lavage also showed significant reduction in the number of macrophages. This finding is in contrast to other cationic amphiphilic drugs, which induce phospholipidosis as well as accumulation of alveolar macrophages. Phospholipid level increased in alveolar macrophages but not in lavaged lung following chlorpromazine treatment. Acid phosphatase activity in lavaged lung homogenate and macrophages of promazine- and chlorpromazine-treated rats, taken as an index of toxicity to cells, did not differ significantly from control rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

The cellular composition of the bronchoalveolar washing in experimental anthracosis

Bronchoalveolar lavage (BAL) was performed in albino random-bred adult male rats with pneumoconiosis. Fibrotic reaction in the lungs was induced by inhalation coal dust during 6 months. BAL comprised 90.9 +/- 1.2% of macrophages; 4.4 +/- 0.8% of neutrophils and 4.5 +/- 1.0% of lymphocytes. The total cell number in BAL was higher (over 59%) in animals with pneumoconiosis. The number of cells on alveolar surface of the lungs was also higher. Fibrotic reaction in the lungs is probably directly related with the increased number of vital macrophages in the lung.     

Procoagulant,Tissue Factor-Bearing Microparticles in Bronchoalveolar Lavage of Interstitial Lung Disease Patients: An Observational Study

Coagulation factor Xa appears involved in the pathogenesis of pulmonary fibrosis. Through its interaction with protease activated receptor-1, this protease signals myofibroblast differentiation in lung fibroblasts. Although fibrogenic stimuli induce factor X synthesis by alveolar cells, the mechanisms of local posttranslational factor X activation are not fully understood. Cell-derived microparticles are submicron vesicles involved in different physiological processes, including blood coagulation; they potentially activate factor X due to the exposure on their outer membrane of both phosphatidylserine and tissue factor. We postulated a role for procoagulant microparticles in the pathogenesis of interstitial lung diseases. Nineteen patients with interstitial lung diseases and 11 controls were studied. All subjects underwent bronchoalveolar lavage; interstitial lung disease patients also underwent pulmonary function tests and high resolution CT scan. Microparticles were enumerated in the bronchoalveolar lavage fluid with a solid-phase assay based on thrombin generation. Microparticles were also tested for tissue factor activity. In vitro shedding of microparticles upon incubation with H₂O₂ was assessed in the human alveolar cell line, A549 and in normal bronchial epithelial cells. Tissue factor synthesis was quantitated by real-time PCR. Total microparticle number and microparticle-associated tissue factor activity were increased in interstitial lung disease patients compared to controls (84±8 vs. 39±3 nM phosphatidylserine; 293±37 vs. 105±21 arbitrary units of tissue factor activity; mean±SEM; p<.05 for both comparisons). Microparticle-bound tissue factor activity was inversely correlated with lung function as assessed by both diffusion capacity and forced vital capacity (r² = .27 and .31, respectively; p<.05 for both correlations). Exposure of lung epithelial cells to H₂O₂ caused an increase in microparticle-bound tissue factor without affecting tissue factor mRNA.Procoagulant microparticles are increased in interstitial lung diseases and correlate with functional impairment. These structures might contribute to the activation of factor X and to the factor Xa-mediated fibrotic response in lung injury.     

低血压灌注对无心跳大鼠肺支气管肺泡灌洗液中不同白细胞及HMGB1 的影响

目的:研究低血压灌注对无心跳大鼠肺支气管肺泡灌洗液中不同白细胞及HMGB1的影响。方法:将32只180-200g SD雄性大鼠随机分成对照组[sham]、缺血30min组[30I]、缺血60 min组[60I]和缺血90 min组[90I](n=8),4组大鼠分别接受麻醉后持续机械通气,测定并统计各组支气管肺泡灌洗液中总白细胞计数及不同白细胞计数,免疫印迹法检测支气管肺泡灌洗液中HMGB1蛋白的表达。结果:总白细胞、巨噬细胞、淋巴细胞计数及HMGB1蛋白表达均随着低血压灌注时间的延长而逐渐增加,尤其在[60I]和[90I]两组,灌洗液中巨噬细胞和淋巴细胞计数有显著增高,并且巨噬细胞和淋巴细胞与HMGB1蛋白表达呈正相关。结论:本研究证实HMGB1蛋白表达和巨噬细胞,淋巴细胞计数在低血压灌注缺血期内升高,提示HMGB1蛋白可能具有驱动炎症反应的作用。     

Expression of Fas antigen in the cells from bronchoalveolar lavage fluid (BALF)

Fas antigen is a cell surface receptor protein that mediates apoptosis expressed in various cells. In this study Fas expression was examined in cells of patients with lung diseases in which changes in the lung immunology were documented. We have performed bronchoalveolar lavage (BAL) in 24 patients with sarcoidosis (8), lung fibrosis (9), primary lung cancer (7), and we compared expression of Fas in BALF cells from all groups and healthy volunteers (6). Fas protein was detected by immunocytochemistry using APAAP technique with an LSAB 2 kit (Dako). Positive reactions for Fas were found in the cytoplasm of epithelial cells, macrophages, neutrophils and lymphocytes (according to the intensity). There were some differences in proportion of positive cells and intensity of reaction between patients with interstitial lung diseases, healthy volunteers as well as patients with lung cancer. Higher expression of Fas in alveolar macrophages was observed in patients with sarcoidosis, lower in patients with lung cancer, lung fibrosis and the lowest in healthy persons. The analysis of Fas antigen expression in the BALF cells may be useful in evaluation of the role of apoptosis in lung homeostasis and pathology.