艾滋病与非艾滋病病例合并卡氏肺孢子菌肺炎的临床特征对比研究

目的:比较艾滋病相关性卡氏肺孢子菌肺炎与非艾滋病相关性卡氏肺孢子菌肺炎的临床特征及辅助检查,以提高临床医师诊疗水平。方法:收集2018年1月至2021年7月在某三甲医院确诊的卡氏肺孢子菌肺炎17例,按照不同基础疾病将病例分为艾滋病组（7例）与非艾滋病组（10例）,比较两组病例的人口学特征、临床表现、实验室检查、病原学以...     

大鼠卡氏肺孢菌肺炎肺泡灌洗液中炎性细胞及TNFα水平变化

为探讨使用糖皮质激素 (GC )患者诱发大鼠卡氏肺孢菌肺炎 (PCP )的炎症反应强度及TNF α对PCP的防御作用 ,采用清洁级SD大鼠 ,皮下注射醋酸可的松配合低蛋白饮食建立免疫抑制诱导的PCP模型。分PCP组、细菌性肺炎组、阴性组、健康对照组 ,支气管肺泡灌洗液 (BALF )沉淀行细胞计数及分类 ,ELISA法测定BALF中TNF α值。结果显示 ,免疫抑制后 ,并发PCP鼠BALF中细胞计数、中性粒细胞比例比未并发PCP鼠高 ,但增高幅度低于并发细菌感染鼠 ;并发PCP鼠的BALF中TNF α明显低于未并发PCP鼠 ,而并发细菌感染后TNF α升高。GC致免疫抑制状态下 ,TNF α分泌减少 ,可能为PC感染创造条件 ,PCP与细菌性肺炎在炎症免疫反应上存在差异。     

制备小鼠支气管肺泡灌洗液方法的改进

<正>支气管肺泡灌洗术是一种通过对支气管肺泡灌洗技术,获取肺泡灌洗液进行免疫细胞、炎症因子和可溶性物质检查的方法,为某些呼吸道疾病的病情观察、诊断和预后判定提供新途径。医学科研工作者经常需要从小鼠动物模型制备支气管肺泡灌洗液,其制备方法非常重要,操作者需要有较好的技术,既要保证灌洗液一定的数量以完成较多细胞因子等测定,又要保证足够的细胞进行计数和分类。传统的方法~([1])是在处死小鼠后,钝性剥离气管,用三通管连接注射器     

大鼠卡氏肺孢菌肺炎肺泡灌洗液中炎性细胞及TNF—α水平变化

为探讨使用糖皮质激素（ＧＣ）患者诱发大鼠卡氏肺孢菌肺炎（ＰＣＰ）的炎症反应强度及ＴＮＦ－α对ＰＣＰ的防御作用,采用清洁级ＳＤ大鼠,皮下注射醋酸可的松配合低蛋白饮食建立免疫抑制诱导的ＰＣＰ模型。分ＰＣＰ组,细菌性肺炎组,阴笥组,健康对照组,支气管肺泡灌洗液沉淀行细胞计数及分类,ＥＬＩＳＡ法测定ＢＡＬＦ中ＴＮＦ－α值。结果显示,免疫抑制后,并发ＰＣＰ鼠ＢＡＬＦ中的细胞计数,中性粒细胞比例比未并发ＰＣＰ     

支气管肺泡灌洗液在鉴别肺良恶性肿瘤中的价值

本文对54例肺疾病患者的肺泡灌洗液及血清进行了CYFRA21-1、CEA水平检测,其中肺良性疾病21例,肺癌33例,同时检测健康人血清41例并加以比较,发现它对早期鉴别肺恶性肿瘤可提供有价值的依据,现报道如下. 1 对象和方法 1.1 对象 `1.1.1 对照组 41例(男31,女10),年龄(31～59)岁,为我院体检中心确认的健康者,各项指标正常,无呼吸、肝、肾、肺等重要器官疾病. 1.1.2 疾病组 54例(男33,女21),年龄(45～71)岁,为我院及另一医院呼吸科住院病人,经临床病理学、细胞学及影像学检查确诊肺癌32例,其中鳞癌17例、腺癌14例、小细胞癌1例.肺良性疾病22例(男14,女8),年龄(32～66)岁.     

肺结节病支气管肺泡灌洗液和血清补体活化研究

作者对肺结节病患者血清和支气管肺泡灌洗液(BALF)中补体经典途径(CCP)活化和C_2活化进行研究。研究对象分为4组:第1组肺结节病患者27例;第2组治愈心肺结节病组4例;第3组原发性肺纤维样变组7例;第4组正常对照组8例。     

慢性支气管炎患者支气管肺泡灌洗液癌胚抗原含量的探讨

<正> 癌胚抗原(CEA)最初认为是某些癌瘤所特有的抗原。进一步研究发现在良性疾患病人血清和体液中也存在。本文对慢性支气管炎(慢支)病人的支气管肺泡灌洗液(洗液)进行了CEA含量测定,结果报告如下。 材料和方法 一、研究对象:慢支病人38例,其中吸烟者21例,不吸烟者17例。 二、标本采取:(1)血清:取空腹血清0.5ml测定。(2)洗液:经鼻腔插入OLympus B:型纤维支气管镜直到右肺中叶开口,然后将导管进入中叶内或外段支气管,先灌入37℃无菌生理盐水10ml,再用6.7～13.4KPa负压回吸,如此灌洗3次,总灌入     

VAP患者支气管肺泡灌洗液IL-8、IL-13检测的临床分析

呼吸机相关性肺炎（Ventilator—associated pneumonia,VAP）是机械通气的常见并发症之一,文献显示,机械通气患者发生VAP的危险是一般患者的（3～21）倍,其病死率比一般患者高24％-50％,有高危因素者甚至高达76％。目前关于VAP的危险因素研究多着重于流行病学研究,甚少从免疫学方面加以关注。本文通过检测我院ICU呼吸机治疗发生VAP患者支气管灌洗液中的IL-8、IL-13含量,探讨IL-8、IL-13在VAP发生中的临床意义,现报道如下。     

支气管肺泡灌洗液乳铁蛋白测定的临床意义初探

当前,肺结核和肺癌的鉴别诊断仍为临床一难题。传统的x线摄片、痰细胞学检查及采用先进的纤维支气管镜检查术为主要的诊断手段,可使相当一部分患者确诊。但对痰细胞学细菌学检查阴性,x线胸片病灶类似的病例,要确诊仍非易事。我们分别检测了肺结核、肺癌患者血清及支气管肺泡灌洗液乳铁蛋白的含量,初步探讨了它的诊断价值和鉴别诊断的意义。     

Application of immunoblotting to detect soluble Pneumocystis carinii antigen(s) in bronchoalveolar lavage of patients with Pneumocystis pneumonia and AIDS.

The technique of immunoblotting for detecting soluble Pneumocystis carinii antigen(s) in bronchoalveolar lavage fluid specimens from patients with AIDS and Pneumocystis pneumonia was evaluated. A soluble 67 kilodalton polypeptide that was immunoreactive with an anti-P carinii monoclonal antibody (2G2) was found in the supernatants of 26 lavage samples from patients with pneumocystosis. Intact organisms in lavage sediments were detected by methenamine silver or immunofluorescence staining procedures. The diagnostic use of this technique was shown in four cases in which lavage sediments proved negative for intact Pneumocystis carinii organisms on first examination; 2G2 reactive soluble antigen, however, was identified in the immunoblots of the supernatants from the same samples. It is concluded that immunoblotting of bronchoalveolar lavage specimens using 2G2 monoclonal antibody as a detection probe may be a useful adjunct to the morphological demonstration of organisms by special staining procedures.     

Use of a monoclonal antibody to detect Pneumocystis carinii in induced sputum and bronchoalveolar lavage fluid by immunoperoxidase staining

We evaluated the utility of a monoclonal antibody that recognizes Pneumocystis carinii as a diagnostic tool in specimens of bronchoalveolar lavage fluid and sputum from patients in whom a diagnosis of P carinii pneumonia was being considered. In addition to routine processing for diagnosis by morphologic recognition of P carinii on a Diff-Quik-stained specimen, the specimen was reacted with a monoclonal antibody to P carinii and visualized in an avidin-biotin horseradish peroxidase technique. Of 50 specimens evaluated, there was 94% agreement between results of conventional Diff-Quik staining and immunoperoxidase staining. Two Diff-Quik-positive specimens were negative by immunoperoxidase staining, and one Diff-Quik-negative specimen was positive by immunoperoxidase staining. These discrepancies are most likely attributable to random distribution of P carinii onto smears. The monoclonal antibody used in this study can accurately detect P carinii in induced sputum and bronchoalveolar lavage fluid specimens.     

Type I reactions directed against Pneumocystis carinii in AIDS patients

Type I allergy directed against Pneumocystis carinii (PC) has been investigated in 14 patients with AIDS. The Pneumocystis carinii pneumonia often shows a rapid and severe course, and type I allergy against the parasite might be a pathogenic co-factor in the interstitial lung inflammation. In twelve of the AIDS patients the clinical symptoms and course of illness indicated a PC pneumonia. The basophil histamine release test was used as a sensitive test to detect type I allergy against PC. Eight of the patients showed significant histamine release when stimulated with PC. In contrast, only two patients in the group of 12 HIV antibody-positive homosexual men and none in the control group of 13 heterosexual men released histamine. The histamine release was mediated by an immunological reaction, since the release was abolished and regained by removal from and refixation to the cell surface of the cell-bound immunoglobulins before the antigen challenge. The results suggest an involvement of type I allergy as a pathogenic co-factor in Pneumocystis carinii pneumonia.     

Pneumocystis carinii Meningoradiculitis in a patient with AIDS

Pneumocystis carinii is a common opportunistic pathogen in patients infected with the human immunodeficiency virus (HIV).Pneumocystis carinii pneumonia is common, while extrapulmonary infections withPneumocystis carinii have been reported sparingly. The clinical features are frequently nonspecific. The detection ofPneumocystis carinii in cerebrospinal fluid (CSF) has not been reported thus far. In this report, an unusual case ofPneumocystis carinii meningoradiculitis in an HIV-infected patient who had previously received primary prophylaxis with trimethoprimsulfamethoxazole is presented.     

Phospholipase activities of bronchoalveolar lavage fluid in rat Pneumocystis carinii pneumonia

Respiratory distress, main clinical symptom of P. carinii pneumonia, is unexplained. We wondered if it could be linked with a lung surfactant anomaly. We have shown in the bronchoalveolar fluid lavage of P. carinii-infected rats: a very significant decrease of the phospholipid content; a lowering of the phospholipid/protein ratio; and an increase in phospholipase activities, partly due to the activation of an inactive phospholipase into the active form. We conclude that, in P. carinii-infected rats, there is an increased catabolism of lung surfactant.     

Detection of antibodies to Pneumocystis carinii in bronchoalveolar lavage fluid by immunoreactivity to Pneumocystis carinii within alveoli, granulomas, and disseminated sites.

Although Pneumocystis carinii pneumonia (PCP) is the most common major opportunistic infection in the acquired immunodeficiency syndrome (AIDS), its immunopathogenesis is not fully understood. It is known that anti-pneumocystis antibodies are present in the sera of individuals with and without PCP. In order to determine whether anti-pneumocystis antibodies are also present in bronchoalveolar lavage fluid (BAL), we looked for them, by immunoreactivity with tissue sections of intra-alveolar P. carinii, in the BAL of (a) HIV-seropositive patients with PCP (n = 18); (b) HIV-seropositive patients without PCP (n = 11); and (c) HIV-seronegative patients with nonpneumocystis lung disease (n = 5). BALs from 19 of 29 HIV-seropositive patients were deficient in at least one isotype (13 with PCP, six without PCP), while only one of five HIV-seronegative patients was deficient. Despite the considerable documentation of atypical presentations of disease caused by P. carinii, little is known concerning the mechanisms involved. To determine whether there is any relationship between BAL anti-pneumocystis antibodies and diverse host responses, we studied antibody binding to P. carinii in different settings. IgG antibodies in BAL bound P. carinii within spleen, liver, skin, and muscle, as well as within pulmonary alveoli and granulomas. However, IgA antibodies in BAL bound intraalveolar and disseminated P. carinii but did not bind to P. carinii within pulmonary granulomas.(ABSTRACT TRUNCATED AT 250 WORDS)     

Decreased production of local immunoglobulin A to Pneumocystis carinii in bronchoalveolar lavage fluid from human immunodeficiency virus-positive patients

An enzyme-linked immunosorbent assay and a Western blot analysis were developed to study the antibody response to Pneumocystis carinii in serum and bronchoalveolar lavage fluid from 27 human immunodeficiency virus 27 (HIV)-infected patients with P. carinii pneumonia (Pcp), 32 patients without Pcp, and 51 HIV-negative controls. Urea was used for the correct dilution of epithelial lining fluid, and albumin was used to evaluate transudation from plasma for the assessment of local production of antibodies to P. carinii. By contrast with those of immunoglobulin G (IgG), IgA responses to P. carinii were increased in serum from HIV-positive patients compared to negative controls. Local production of antibodies to P. carinii, especially IgA, was decreased in patients with Pcp. In a study of 10 patients of each group, IgG and IgA responses to gp116 from P. carinii were lower in patients with Pcp than in other groups. These results suggest that, in addition to alveolar macrophages, local antibodies may play a role in host defense against P. carinii.     

Phospholipase activities of bronchoalveolar lavage fluid in rat Pneumocystis carinii pneumonia.

Respiratory distress, main clinical symptom of P. carinii pneumonia, is unexplained. We wondered if it could be linked with a lung surfactant anomaly. We have shown in the bronchoalveolar fluid lavage of P. carinii-infected rats: a very significant decrease of the phospholipid content; a lowering of the phospholipid/protein ratio; and an increase in phospholipase activities, partly due to the activation of an inactive phospholipase into the active form. We conclude that, in P. carinii-infected rats, there is an increased catabolism of lung surfactant.