Significance of IL-1β and IL-1 receptor antagonist (IL-1Ra) in bronchoalveolar lavage fluid (BALF) in patients with diffuse panbronchiolitis (DPB)

We evaluated the effect of erythromycin therapy on pulmonary function tests and the airway inflammatory response of patients with DPB. The number of neutrophils in BALF obtained from DPB patients was significantly higher than that of healthy volunteers. Treatment with erythromycin (600 mg/day for 12·9 ± 9·5 months (mean ±s.d.)) significantly reduced the total number of cells and neutrophils in the airway, and significantly improved pulmonary function tests. The levels of IL-1β and IL-8 were significantly higher in DPB compared with healthy volunteers (P < 0·05, P < 0·05, respectively). IL-1 Ra in patients is considered to have a weak inhibitory activity for IL-1β, with approximately five-fold concentration of IL-1β compared with that in healthy volunteers (approx. nine-fold concentration of IL-1β). Erythromycin therapy significantly reduced these cytokines to levels comparable to those of healthy volunteers, and produced a trend toward reduction in the level of IL-1Ra in BALF. The level of IL-1β correlated significantly with the concentration of neutrophils in BALF (r = 0·72, P < 0·01), as well as with the level of IL-1Ra (r = 0·688, P < 0·05) and IL-8 (r = 0·653, P < 0·05). A nearly significant or significant correlation was observed between the concentration of neutrophils and levels of IL-1Ra or IL-8 in BALF (r = 0·526, P = 0·053 or r = 0·776, P < 0·01, respectively). There was also a significant relationship between FEV, and the concentration of neutrophils in BALF (r = 0·524, P < 0·05). Our results suggest that the relative amounts of IL-1β and IL-1Ra or IL-8 may contribute, at least in part, to the neutrophil-mediated chronic airway inflammation in patients with chronic airway disease, and long-term erythromycin therapy may down-regulate the vigorous cycle between the cytokine network and neutrophil accumulation, with resultant reduction of neutrophil-mediated inflammatory response.     

Lidocaine in bronchoalveolar lavage fluid (BALF) is an inhibitor of eosinophil-active cytokines

Eosinophils and eosinophil granule proteins may play an important role in the pathogenesis of asthma. BALF from 40 patients with symptomatic asthma were analysed for cytokine activity by the eosinophil survival assay. BALF from 15 patients showed increased survival activity. Survival activities in BALF from four of these patients were almost completely blocked by anti-IL-5 MoAb, and the remaining activities were blocked by anti-granulocyte-macrophage colony-stimulating factor (GM-CSF), anti-IL-3 antibody, or both. Surprisingly, BALF samples from the other 25 patients decreased eosinophil viabilities below the levels of medium control. The inhibitory factor in these BALF was of low molecular weight, was heat-stable, was largely overcome by excess exogenously added cytokines, and was positively correlated with the concentrations of lidocaine in the BALF. Lidocaine itself inhibited eosinophil survival at concentrations less than those present in the BALF. These findings indicate that lidocaine is an inhibitor of cytokines in the eosinophil survival assay, and they suggest the need for caution in analyses of BALF containing lidocaine or other local anaesthetics.     

IL-6和IL-8 mRNA在变态反应性哮喘患者BAL细胞的表达

目的：测定IL-6和IL-8 mRNA在变态反应性哮喘患者支气管肺泡灌洗（BAL）细胞中的表达。方法：采用原位杂交技术，测定变态反应性哮喘患者BAL中表达IL-6和IL-8 mRNA的阳性细胞数。结果：全部哮喘患者BAL细胞对IL-6和IL-8 mRNA探针杂交均呈阳性（阳性率分别为14/14和14/14）。变态反应性哮喘患者BAL中表达IL-6和IL-8 mRNA阳性细胞数明显多于对照（P<0.01）。结论：变态反应性哮喘患者BAL细胞中IL-6和IL-8 mRNA表达增加。     

Soluble intercellular adhesion molecule-1 (ICAM-1) in sera and bronchoalveolar lavage fluid of patients with idiopathic pulmonary fibrosis and pulmonary sarcoidosis

ICAM-1 plays an important role in inflammatory diseases. To assess level of soluble ICAM-1 in the circulation and inflamed lesions, we measured levels of soluble ICAM-1 in the circulation and bronchoalveolar lavage fluid (BALF) of patients with idiopathic pulmonary fibrosis (IPF) and with pulmonary sarcoidosis (PS) and of healthy volunteers (HV), and we also analysed ICAM-1 expression of BALF cells in some patients and HV. IPF patients had significantly higher levels of circulating ICAM-1 than HV, while PS patients did not. By contrast, significantly increased levels of BALF soluble ICAM-1 were found in PS patients copared with those of HV, but not in IPF patients. There were no significant differences in the proportions of ICAM-1⁺BALF lymphocytes in IPF patients, PS patients and HV, whereas significantly increased proportions of ICAM-1⁺ pulmonary alveolar macrophages were found in PS patients compared with those of HV, but not in IPF patients. There was a significant positive correlation of BALF soluble ICAM-1 levels to BALF lymphocyte proportions in PS patients. Although the source of BALF soluble ICAM-1 is unclear, BALF soluble ICAM-1 appears to reflect the grade of local activity of sarcoidosis. An interesting discrepancy between soluble ICAM-1 levels in the circulation and BALF was found in IPF patients, and this might be an important clue to an understanding of this disorder.     

Measurement of interleukin-6 in bronchoalveolar lavage fluid by radioimmunoassay: differences between patients with interstitial lung disease and control subjects.

Bronchoalveolar lavage fluid (BALF) from subjects with a variety of interstitial lung diseases (active sarcoidosis, pigeon breeders' disease (PBD), asymptomatic pigeon breeders, patients with idiopathic pulmonary fibrosis) and from control subjects were assayed for interleukin-6 (IL-6) using a novel radioimmunoassay system. IL-6 was detectable in BALF from all groups, with disease groups showing significantly increased IL-6 levels compared with controls (P less than 0.01 in all cases). When these results were standardized, using urea to compensate for dilution effects in the BALF, only the asymptomatic pigeon breeders had significantly higher IL-6 levels than the controls (P less than 0.025), with all other groups showing no difference. When albumin was used for standardization, both the PBD group (P less than 0.001) and the sarcoidosis patients (P less than 0.01) had considerably lower levels of IL-6 than the control subjects. Using either albumin or urea for standardization, the PBD patients had significantly lower levels of IL-6 than do their asymptomatic counterparts (P less than 0.001 in both cases). This is contrasted by the finding of greatly elevated levels of IgG in the BALF of the PBD patients compared with asymptomatics (P less than 0.001). There was, however, no relation between IL-6 and IgG in any patient group, although the PBD patients had the lowest IL-6 and highest IgG as a group. These findings may suggest a mechanism by which asymptomatic subjects remain free from clinical complaints.     

Identification of IL-16 as the lymphocyte chemotactic activity in the bronchoalveolar lavage fluid of histamine-challenged asthmatic patients

Objective: We have previously demonstrated that the earliest lymphocyte chemotactic factors present in bronchoalveolar lavage fluid (BALF) of subjects with atopic asthma after subsegmental antigen challenge are IL-16 and MIP-1α, of which IL-16 appears to contribute a majority of the chemotactic activity. Because IL-16 is released in vitro after histamine stimulation of CD8⁺ T cells and epithelial cells, we evaluated the potential role of histamine in the release of IL-16 into the airways of allergic asthmatics in vivo. Methods: Eight allergic asthmatic subjects, six normal subjects, and six atopic nonasthmatic subjects were challenged with saline in the lingula and with serial concentrations of histamine (1 × 10^-7 to 5 × 10^-5 mol/L) in the right middle lobe followed by bronchoalveolar lavage (BAL) 15 minutes and 6 hours later. Results: The BALF from saline- and histamine-challenged lobes of normal subjects and atopic nonasthmatic subjects contained no significant lymphocyte chemoattractant activity. In six of the eight atopic asthmatic subjects, the histamine-challenged but not saline-challenged segment contained IL-16 chemotactic activity but no other identifiable lymphocyte chemoattractant activities at 6 hours. Conclusions: IL-16 appears in the airways after histamine challenge and therefore could contribute to the earliest infiltration of CD4⁺T cells and eosinophils observed after antigen challenge due to histamine release from mast cells. (J Allergy Clin Immunol 1998;101:786-792.)     

Th1 cytokine pattern in sarcoidosis is expressed by bronchoalveolar CD4+ and CD8+ T cells

The pathogenesis of pulmonary sarcoidosis has been related to an increased production of Th1-like cytokines. However, cytokine expression in sarcoidosis has not been systematically studied at a single-cell level. We therefore investigated the expression of IL-2, IL-4, IL-13, tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) intracellularly in bronchoalveolar lavage (BAL) and peripheral blood CD3+ T lymphocytes from patients with pulmonary sarcoidosis (radiologic stage II-III, n = 8) and normal controls (n = 9) by flow cytometry. In contrast to IL-4 and IL-13, the percentage of T lymphocytes expressing intracellular IL-2 (49.3 +/- 21.3% versus 14.5 +/- 15.6%), IFN-gamma (75.5 +/- 14.9% versus 32.6 +/- 18.7%) and TNF-alpha (68.3 +/- 18.7% versus 36.8 +/- 20.8%) was significantly higher in patients with sarcoidosis than in normal controls (each P < 0.005). In contrast to BAL lymphocytes, expression of these cytokines in peripheral blood lymphocytes did not differ between patients with sarcoidosis and normal controls. Close correlations were observed between the percentages of BAL lymphocytes expressing intracellular IL-2, IFN-gamma and TNF-alpha, but not for IL-4 or IL-13. Analysis of the expression of these cytokines in T lymphocyte subsets revealed IL-2, IFN-gamma, and TNF-alpha in CD4+ as well as CD8+ T lymphocytes, suggesting a contribution of TC1 cells to the production of proinflammatory cytokines in sarcoidosis. We conclude that a Th1-like cytokine pattern can be observed in CD4+ as well as in CD8+ BAL T lymphocytes in patients with pulmonary sarcoidosis.     

Evaluation of soluble IL-6 receptor concentration in serum and epithelial lining fluid from patients with interstitial lung diseases.

We measured soluble IL-6 receptor (sIL-6R) levels in serum and bronchoalveolar lavage fluids (BALF) from patients with interstitial pneumonia of unknown etiology (IP) (n = 17), sarcoidosis (n = 8) and normal control subjects (n = 10), to investigate its role in pulmonary diseases. Soluble IL-6R was determined by an ELISA. The volume of epithelial lining fluid (ELF) in BALF was estimated using an urea method. We found that levels of sIL-6R in serum, BALF, and ELF from patients with IP or sarcoidosis were significantly higher than those from normal subjects. Furthermore, levels of sIL-6R in BALF or ELF were significantly correlated with those of albumin, indicating that sIL-6R, together with albumin, may enter ELF as a result of the increased permeability caused by pulmonary inflammation. Thus most of the sIL-6R in ELF would be from serum, and relatively small amounts of it might be produced locally. However, sIL-6R levels in ELF, but neither serum nor BALF, were significantly correlated with levels of C-reactive protein in patients with IP. These results suggest that both systemic and local production of sIL-6R are increased, and raised sIL-6R is involved in the modulation of systemic and local inflammatory responses in patients with IP and sarcoidosis.     

Elevated levels of beta-chemokines in bronchoalveolar lavage fluid (BALF) of individuals infected with human T lymphotropic virus type-1 (HTLV-1)

Pulmonary complications are known to develop in HTLV-1 carriers, including T lymphocytic alveolitis, and increased IL-2 receptor alpha (CD25)-bearing T cells have been found in BALF. Several chemokines may contribute to accumulation of T lymphocytes in the lungs of HTLV-1 carriers. Here, we compared the distribution of T lymphocyte subsets and beta-chemokines, such as macrophage inflammatory peptide-1alpha (MIP-1alpha), regulated on activation normal T expressed and secreted (RANTES), and macrophage chemoattractant protein-1 (MCP-1), in BALF and peripheral blood between HTLV-1 carriers and non-infected healthy normal subjects. Flow cytometric analysis with MoAbs to cell surface antigens was used to identify T lymphocyte subsets in BALF samples from HTLV-1 carriers (n = 13) and non-infected healthy controls (n = 10). The levels of different beta-chemokines were estimated by ELISA. High percentages of CD3+ cells, CD3 expressing HLA-DR antigen and CD3+CD25+ cells were detected in BALF of HTLV-1 carriers compared with non-infected controls. The concentration of MIP-1alpha in BALF of patients was significantly higher than in non-infected healthy controls and correlated well with the percentage of CD3+CD25+ cells. The level of RANTES in BALF was also significantly high in HTLV-1 carriers, but did not correlate with the percentage of CD3+CD25+ cells. On the other hand, the level of MCP-1 in BALF of HTLV-1 carriers was not different from that of controls. Our results suggest a possible interaction between activated T cells bearing CD25 and beta-chemokines, especially MIP-1alpha, which may contribute to the pulmonary involvement in HTLV-1 carriers.     

Detection of IL-5 and IL-1 receptor antagonist in bronchoalveolar lavage fluid in acute eosinophilic pneumonia

BACKGROUND: Acute eosinophilic pneumonia is an idiopathic cause of respiratory failure, characterized by very high numbers of alveolar eosinophils without significant blood eosinophilia. OBJECTIVE: The purpose of this study was to determine which cytokines are associated with acute eosinophilic pneumonia. METHODS: Soluble IL-1 type II receptor and the cytokines IL-1β, IL-1ra, IL-3, IL-5, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α were measured in serum and in bronchoalveolar lavage fluid from two patients with acute eosinophilic pneumonia during both acute and convalescent phases. RESULTS: Compared with patients with adult respiratory distress syndrome, the patients with acute eosinophilic pneumonia had high bronchoalveolar lavage fluid levels of IL-5, IL-1ra, and soluble type II IL-1 receptor but not IL-1β, tumor necrosis factor-α>, IL-3, or granulocyte-macrophage colony-stimulating factor. Bronchoalveolar lavage fluid levels of IL-5 and IL-1ra fell after resolution of symptoms. In the serum of patients with acute eosinophilic pneumonia, IL-5 was not detectable, and IL-1ra was initially high but fell after corticosteroid treatment. CONCLUSION: Acute eosinophilic pneumonia is characterized by locally high levels of IL-5, IL-1ra, and soluble type II IL-1 receptor in the alveolar space. (J ALLERGY CLIN IMMUNOL 1996;97:1366-74.)     

Total and specific IgE in serum, bronchial lavage and bronchoalveolar lavage of asthmatic patients

Total and specific IgE were assessed in serum, bronchial lavage (BL) and broncho-alveolar lavage (BAL) of allergic asthmatics and healthy controls. Serum total IgE were found to be correlated with total IgE in BAL but not in BL. Total IgE/K⁺ ratio in serum and BL was higher in asthmatics than in controls, while the total IgE/albumin ratio was significantly higher in asthmatics than in controls in serum but not in BL and BAL. The mean of specific IgE in serum and BL was significantly higher in the group of patients with positive specific bronchial provocation test (sBPT) than in the group with negative sBPT. Similar results were observed between specific IgE serum level and BL and prick tests (PT). which show that BL does not always reflect the total IgE level of serum; in asthmatics, albumin can not be used to determine the degree of dilution in the recovered fluids; as in the serum, there is agreement between specific IgE in BL and PT or sBPT results.     

Search for human herpesvirus 6 and human cytomegalovirus in bronchoalveolar lavage from patients with human immunodeficiency virus-1 and respiratory disorders

Virus isolation and viral DNA detection by the polymerase chain reaction were used to investigate the presence of human herpesvirus 6 (HHV-6) and human cytomegalovirus (HCMV) in bronchoalveolar lavage from 34 human immunodeficiency virus-1 (HIV-1)-infected patients with respiratory disorders. The aim was to assess the presence of reactivated HHV-6 in lung tissues for a subsequent evaluation of the frequency of virus involvement in respiratory clinical manifestations in the course of HIV-1 infection. Bronchoalveolar lavage samples were tested for the presence of HCMV, as a routine investigation within a protocol monitoring opportunistic infections in symptomatic HIV-1 patients. Whereas HCMV DNA was detected by the polymerase chain reaction in 12 bronchoalveolar lavage specimens, 10 of which were also positive for virus isolation, all samples were negative for HHV-6 by both virological procedures. The HHV-6 DNA finding in bronchoalveolar lavage from an HIV-1-seronegative patient with renal carcinoma, investigated accidentally together with the bronchoalveolar lavage specimens from HIV-1 seropositive patients, stressed the HHV-6 polymerase chain reaction-negative results in the bronchoalveolar lavage samples under study. It is concluded that the lung may be a target organ for HCMV infection in HIV-1-seropositive patients affected by respiratory symptoms but that this does not seem to be the case for HHV-6. © 1996 Wiley-Liss, Inc.     

Elevated interleukin-18 levels in bronchoalveolar lavage fluid of patients with eosinophilic pneumonia

BACKGROUND: Interleukin (IL)-18 can induce Th2 cytokine production particularly in collaboration with IL-2. Accumulation of Th2 cells and increased levels of Th2 cytokines are found in bronchoalveolar lavage fluid (BALF) from patients with eosinophilic pneumonia (EP). To evaluate the role of IL-18 in the pathogenesis of EP, we measured the concentration of IL-2, IL-12, IL-18, and Th2 cytokines in BALF from patients with EP. METHODS: The concentrations of interferon (IFN)-gamma, IL-2, IL-5, IL-10, IL-12, IL-13, and IL-18 in BALF were measured in patients with idiopathic acute eosinophilic pneumonia (AEP), with idiopathic chronic eosinophilic pneumonia (CEP), with sarcoidosis and healthy volunteers (HV). RESULTS: The BALF concentrations of Th2 cytokines, IL-5, IL-10, and IL-13, were higher in patients with EP than in sarcoidosis and control. The IL-2 level in BALF was higher in EP than in sarcoidosis and control. The IL-18 and IL-12 (p40 + p70) levels were higher in patients with EP than sarcoidosis, while the level of IL-12 (p70) was below the detection limit in patients with EP. There was a significant correlation between IL-2 level and both IL-5 and IL-13 in BALF of patients with EP. CONCLUSIONS: Our findings suggest that IL-18 may contribute to Th2 cytokine-dominant responses in patients with EP in collaboration with IL-2.     

Phenotypic characterization of T cells in bronchoalveolar lavage fluid (BALF) and peripheral blood of patients with diffuse panbronchiolitis; the importance of cytotoxic T cells

We investigated the contribution of T cells in diffuse panbronchiolitis (DPB) by identifying T cell subsets in BALF of 36 patients with DPB, before and after long-term treatment with macrolide antibiotics, and 16 healthy control subjects. The percentages of lymphocytes and CD3⁺γδ⁺ cells in BALF of DPB patients and control subjects were similar, but the absolute number of these cells was higher in DPB patients. Treatment resulted in a significant reduction in the absolute number of these cells. A further two-colour analysis of T cell subsets in BALF showed a significantly higher ratio and number of CD8⁺HLA-DR⁺ cells in DPB patients. Treatment resulted in a significant reduction of activated T cells. Most BALF CD8⁺ cells were CD8⁺CD11b⁻ cytotoxic T cells. The number of these cells in BALF of DPB patients (26.69 ± 5.86 × 10³/ml) was higher than the control (2.02 ± 0.38 × 10³/ml; P< 0.001), and a significant reduction was observed after treatment (7.69 ± 2.59 × 10³/ml; P< 0.01). The number of CD4⁺ cells was also higher in DPB patients than in controls, and most were CD4⁺CD29⁺ memory T cells. However, treatment did not influence the number of these cells. The number of lymphocytes, CD3⁺γδ⁺, CD8⁺CD11b⁻, CD8⁺HLA-DR⁺, and CD4⁺CD29⁺ cells was higher in patients with bacterial infection than in those without bacterial infection, and interestingly, macrolide therapy reduced the number of lymphocytes, CD3⁺γδ⁺, CD8⁺CD11b⁻ and CD8⁺HLA-DR⁺ cells, irrespective of bacterial infection. In peripheral blood, the percentage of CD8⁺HLA-DR⁺ cells was also higher in DPB patients than in healthy subjects, and significantly decreased after treatment. The percentage of CD8⁺CD11b⁻ cells in peripheral blood was similar in DPB patients and normal subjects, and treatment significantly reduced the percentage of these cells. Finally, the expression of the adhesion molecules CD11a/CD18 (α/β-chains of LFA-1) on lung CD3⁺ cells and CD49d (α-chain of VLA) on lung CD4⁺ cells was enhanced compared with that on peripheral blood in DPB patients. Our results suggest that elevation of memory T cells and activation of CD8⁺ cells, mainly cytotoxic T cells, in the airway lumen of DPB patients may contribute to chronic bronchial inflammation, possibly through up-regulation of adhesion molecules. Our findings also indicate that macrolide antibiotics may have a direct or indirect suppressive effect on cytotoxic T cells, and as such, reduce inflammation and improve clinical condition.     

白细胞介素6(IL-6)和IL-8mRNA在变应原诱导的鼻粘膜晚期反应标本的表达

目的测定IL-6和IL-8变应原诱导的鼻粘膜晚期反应标本中mRNA的表达。方法采用原位杂交技术,测定变应原诱导的10例变态反应性鼻炎病人的鼻粘膜标本表达IL-6和IL-8mRNA阳性细胞数。结果在10例标本中,2种细胞因子的阳性表达率分别为9/10和10/10。与对照相比,变应原诱导的鼻粘膜标本表达IL-6和IL-8mRNA阳性细胞数明显增加(P＜0.05和P＜0.01)。结论IL-6和IL-8mRNA表达增加可作为变态反应性鼻炎晚期的标志。     

有创机械通气的危重症患者支气管肺泡灌洗临床观察

目的观察经纤维支气管镜支气管肺泡灌洗和经吸痰管注水后吸出方式灌洗的临床效果。方法93例行机械通气的危重症患者,其中男性59例,女性34例,年龄18～92岁;随机分为两组。进行经纤维支气管镜支气管肺泡灌洗（A组）和经吸痰管注水后吸出方式灌洗（B组）。观察并比较两组对象灌洗前后的气道峰压（PIP）、内源性PEEP（PEEPi）、动脉氧分压（PaO2）、动脉二氧化碳分压（PaCO2）及有创机械通气时间、重症监护病房（ICU）入住时间和病死率。结果两组的PIP和PEEPi较灌洗前均有明显下降;两组组间APIP、APEEPi比较,A组大于B组;两组的PaCO2较灌洗前有明显下降,两组的PaO2均较灌洗前有明显升高;A组分别在PaCO2降低和PaO2升高的程度上优于B组;A组有创机械通气时间和ICU入住时间均较B组明显缩短;以上比较差异均有统计学意义。但两组病死率差异无统计学意义。结论对有创机械通气的危重症患者进行经纤维支气管镜支气管肺泡灌洗或经吸痰管注水后吸出方式灌洗,均可以改善呼吸力学参数和血气参数。经纤维支气管镜支气管肺泡灌洗效果优于经吸痰管注水后吸出方式灌洗,值得广泛开展。     

Changes in lung immune cells related to clinical outcome during treatment with infliximab for sarcoidosis

Pulmonary sarcoidosis is characterized by an exaggerated CD4⁺ T cell response and formation of non-necrotizing granulomas. Tumour necrosis factor α (TNF-α) is regarded as crucial for granuloma formation and TNF-α inhibitors offer a third-line treatment option for patients not responding to conventional treatment. However, not all patients benefit from treatment, and an optimal dose and treatment duration have not been established. Insight into the influence of TNF-α inhibitors on lung immune cells may provide clues as to what drives inflammation in sarcoidosis and improve our understanding of treatment outcomes. To evaluate the effects of treatment with the TNF-α inhibitor infliximab on lung immune cells and clinical features of the patients, 13 patients with sarcoidosis refractory to conventional treatment were assessed with bronchoalveolar lavage (BAL), spirometry and computerized tomography (CT) scan closely adjacent to the start of infliximab treatment. These investigations were repeated after 6 months of treatment. Treatment with TNF-α inhibitor infliximab was well tolerated with no adverse events, except for one patient who developed a probable adverse event with liver toxicity. Ten patients were classified as responders, having a reduced CD4/CD8 ratio, a decreased percentage of CD4⁺ T cells expressing the activation marker CD69 and number of mast cells (P < 0·05 for all). The percentage of T regulatory cells (T_regs), defined as forkhead box P3⁺ CD4⁺ T cells decreased in most patients. In conclusion, six months of infliximab treatment in patients with sarcoidosis led to signs of decreased CD4⁺ T cell alveolitis and decreased mastocytosis in the lungs of responders.     

T-cell subtypes in bronchoalveolar lavage fluid and in peripheral blood from patients with primary lung cancer

The changes in local immunology play an important role in lung cancer development. We used bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) for the analysis of cell profiles in patients with primary lung cancer. Twenty-one patients with confirmed primary lung cancer and 13 healthy volunteers were investigated. All persons were smokers. The analysis of T-cell subsets was performed with a flow cytometry method and with the following antibodies: anti CD3, CD4, CD8, CD16, CD25, CD45, CD56, and HLA-DR. We found differences in the proportion of lymphocytes between BALF and PB, and a higher proportion of T cells and a lower proportion of B and natural-killer (NK) cells in BALF. There was a significant difference in the proportion of T-cytotoxic/suppressor lymphocytes, which was elevated in the BALF of patients and decreased in patients' PB. The T-helper:T-cytotoxic/suppressor (Th:Tc/s) ratio was significantly lower in the BALF of patients. These changes were visible in patients with a small cell type. The percentage of T cells with the alpha chain of receptor to IL-2 (IL -R) was lower in the BALF of patients than in the control group. Our observations reflect local changes in lung environment in patients affected with lung cancer.     

卵巢癌细胞IL-6、IL-8及其受体表达的研究

目的分析比较五种常见的上皮性卵巢癌细胞系IL-6、IL-8及其受体表达的差异。方法IL-6、IL-8的表达分别采用RT-PCR和ELISA法进行检测,IL-6受体（IL-6Rα和gp130）及IL-8受体（IL-8RA和IL-8RB）的表达采用免疫印迹技术进行测定。结果①五种上皮性卵巢癌细胞均组成性表达IL-6和IL-8。IL-6和IL-8在CAOV-3细胞中的表达水平均最高,而在HO-8910PM细胞中的表达水平均最低,IL-6在SKOV-3、HO-8910、OVCAR-3细胞中的表达水平依次降低,IL-8在OVCAR-3、SKOV-3、HO-8910细胞中的表达水平依次降低。②五种上皮性卵巢癌细胞均表达IL-6Rα、gp130及IL-8RA;除CAOV-3细胞外,其它细胞均表达IL-8RB。结论本研究旨在筛选表达IL-6和IL-8及其相应受体的细胞株,为研究IL-6、IL-8与卵巢癌发生、发展关系奠定基础,同时也为今后卵巢癌的免疫治疗提供一个新的思路。