肺结核合并肺癌患者的临床分析

目的：探讨肺结核合并肺癌的临床特点,提高临床医师诊断肺结核合并肺癌的警惕性。方法：对2000年1月至2009年12月在我院诊断为肺结核、肺结核合并肺癌、肺癌患者各40例进行回顾性分析。结果：三组之间的临床表现与实验室检查进行相互比较,发现其临床表现并无统计学差异,影像学与支气管镜检查有明显统计学差异外,其他实验室检查无差异。结论：结核合并肺癌与肺结核、肺癌等临床表现、实验室检查近似,易造成漏诊、误诊,临床医师应提高警惕,及时行影像学及支气管镜等检查。     

结核分枝杆菌潜伏感染诊断方法的新进展

每年有超过8百万人感染结核,其中绝大部分没有发展为活动性结核病,而是表现为潜伏性结核感染。大多数活动性结核病是潜伏感染的结核杆菌重新被激活所致,因此结核潜伏感染者成为结核患者的重要来源。及早诊断和治疗结核潜伏感染者是控制结核传播的最有效手段之一。我们较要综述了目前国内外结核潜伏感染的诊断方法及其新进展。     

肺结核合并肺癌患者的临床分析

目的:探讨肺结核合并肺癌的临床特点,提高临床医师诊断肺结核合并肺癌的警惕性.方法:对2000年1月至2009年12月在我院诊断为肺结核、肺结核合并肺癌、肺癌患者各40例进行回顾性分析.结果:三组之间的临床表现与实验室检查进行相互比较,发现其临床表现并无统计学差异,影像学与支气管镜检查有明显统计学差异外,其他实验室检查无差异.结论:结核合并肺癌与肺结核、肺癌等临床表现、实验室检查近似,易造成漏诊、误诊,临床医师应提高警惕,及时行影像学及支气管镜等检查.     

肺结核合并下呼吸道感染患者CT影像特点及IL-23R水平表达的临床意义

摘要 目的：探讨肺结核合并下呼吸道感染患者CT影像特点及IL-23R水平表达的临床意义。方法：选取2015年1月-2018年8月于我院就诊的123例肺结核患者,将所选取的患者按是否合并下呼吸道感染分为单纯肺结核组73例和肺结核合并下呼吸道感染组50例。分析两组组患者临床表现、CT影像学图片、CT影像学表现、血清IL-23R的表达水平的差异。结果：单纯肺结核组患者出现14例低热、11例胸闷、17例消瘦、14例气短、18例痰中带血、14例颈部淋巴结肿大、23例咳嗽、21例胸痛。肺结核合并下呼吸道感染组患者出现16例低热、13例胸闷、21例消瘦、19例气短、20例痰中带血、15例颈部淋巴结肿大、26例咳嗽、23例胸痛,两组患者临床表现差异均无统计学意义（P＞0.05）。单纯肺结核组CT影像学图片显示可见结节影或包块影,呈明显分叶征、短毛刺征、空泡征并发肺不张、棘状突起,边缘较清晰,增强扫描后明显强化。肺结核合并下呼吸道感染组CT影像学图片显示有分叶、毛刺,同时肺内肿物周边存在晕征、血管聚集征、卫星灶征、胸膜凹陷等表现,此外伴纵膈及肺门淋巴结明显肿大,胸壁侵犯。肺结核合并下呼吸道感染组CT影像中毛刺状结节、胸膜凹陷、空洞、分叶征、肿块、条索影比例均高于单纯肺结核组,差异有统计学意义（P＜0.05）。肺结核合并下呼吸道感染组患者IL-23R水平明显高于单纯肺结核组,差异有统计学意义（P＜0.05）。结论：与单纯肺结核患者相比较,肺结核合并下呼吸道感染患者临床表现更为严重,CT影像学特点更为明显,患者血清中IL-23R表达水平明显升高,临床可通过CT影像学结合血清IL-23R检测,以提高肺结核合并下呼吸道感染患者的临床诊断。     

IL-4 is required for defense against mycobacterial infection

Although the involvement of T helper (Th1) cells is central to protection against intracellular bacteria, including Mycobacterium tuberculosis, the involvement of Th2 cells, characterized by potent interleukin (IL)-4 secretion in mycobacterial infection is still unclear. In order to clarify the role of IL-4 in murine tuberculosis, IL-4-deficient mutant mice, IL-4 knockout (IL-4 KO) mice, were utilized. The mice were infected with H37Rv, Kurono or BCG Pasteur via an airborne infection route by placing them in the exposure chamber of a Middlebrook airborne infection apparatus. Their capacity to control mycobacterial growth, granuloma formation, cytokine secretion, and nitric oxide (NO) production were examined. These mice developed large granulomas, but not necrotic lesions in the lungs, liver or spleen (P<0.05). This was consistent with a significant increase in lung colony-forming units (CFU). Compared with levels in wild-type mice, upon stimulation with mycobacteria, splenic IL-10 levels were low and IL-6 levels were intermediate, but interferon (IFN)-gamma and IL-12 levels were significantly higher. IL-18 levels were within the normal range. The level of NO production by alveolar macrophages of the IL-4 KO mice was similar to that of the wild-type mice. Granulomatous lesion development by IL-4 KO mice was inhibited significantly by treatment with exogenous recombinant IL-4. These findings were not specific to the IL-4 KO mice used. Our data show that IL-4 may play a protective role in defense against mycobacteria, although IFN-gamma and TNF-alpha play major roles in it. Our data do not rule out an IFN-gamma-independent function of IL-4 in controlling tuberculosis.     

肺部菌群与呼吸道疾病的相互关系

由于呼吸道黏膜免疫系统具有很好的防御保护作用和强大的清除病原体的能力,过去学术界曾经一度认为健康机体的肺是无菌的。随着不依赖于体外培养的第二代测序技术的发展,关于肺部共生微生物的结构组成及其免疫调节功能的研究越来越受重视。肺部菌群的结构组成与出生方式、饮食结构、生活环境和抗生素使用等多种因素有关,生命早期的肺部菌群的形成和发育会影响全生命周期的呼吸道疾病的发生和发展。肺部菌群通过与宿主免疫系统相互作用调节肺部免疫稳态,还可以与肠道菌群、呼吸道病毒相互作用影响呼吸道感染。因此,干预生命早期肺部菌群的结构组成可以成为预防和控制呼吸道疾病的有效策略和新靶点。     

多层螺旋CT对肺结核合并肺癌患者的诊断价值

目的:研究多层螺旋CT对肺结核合并肺癌的鉴别诊断价值。方法:选择2013年3月至2015年9月在我院确诊的肺结核合并肺癌患者32例和单纯肺结核患者39例应用多层螺旋CT扫描患者肺部病变情况。结果:肺结核合并肺癌组:陈旧性肺结核28例、活动性肺结核4例;病灶位置经典部位29例、非经典部位3例,合并鳞癌11例、腺癌13例、小细胞癌5例、未分化癌3例;10例结核病灶与肺癌病灶不同侧、13例结核病灶与肺癌病灶同侧不同叶、9例结核病灶于肺癌病灶同侧同叶。单纯性肺结核组胨旧性肺结核36例、活动性肺结核3例;病灶位置经典部位34例(上叶尖段11例、后段9例、下叶背段14例)、非经典部位5例。肺结核合并肺癌组患者分叶征、毛刺征、胸膜凹陷征、阻塞性肺炎及肺不张以及棘状突起比例高于单纯肺结核组,而空泡影比例低于单纯肺结核组,差异具有统计学意义(P0.05);两组钙化、斑片条索影、结节影以及空洞或空腔比较,差异无统计学意义(P0.05)。结论:多层螺旋CT对肺结核合并肺癌具有较高的临床鉴别诊断价值。     

The role of vitamin D in pulmonary disease: COPD,asthma, infection,and cancer

The role of vitamin D (VitD) in calcium and bone homeostasis is well described. In the last years, it has been recognized that in addition to this classical function, VitD modulates a variety of processes and regulatory systems including host defense, inflammation, immunity, and repair. VitD deficiency appears to be frequent in industrialized countries. Especially patients with lung diseases have often low VitD serum levels. Epidemiological data indicate that low levels of serum VitD is associated with impaired pulmonary function, increased incidence of inflammatory, infectious or neoplastic diseases. Several lung diseases, all inflammatory in nature, may be related to activities of VitD including asthma, COPD and cancer. The exact mechanisms underlying these data are unknown, however, VitD appears to impact on the function of inflammatory and structural cells, including dendritic cells, lymphocytes, monocytes, and epithelial cells. This review summarizes the knowledge on the classical and newly discovered functions of VitD, the molecular and cellular mechanism of action and the available data on the relationship between lung disease and VitD status.     

Systemic and mucosal immunity to respiratory syncytial virus induced by recombinant Streptococcus gordonii surface-displaying a domain of viral glycoprotein G

A conserved fragment comprising amino acid residues 130-230 of the G glycoprotein of human respiratory syncytial virus subtype A was expressed in the commensal bacterium Streptococcus gordonii. Recombinant streptococci displaying the G domain at the cell surface were used to immunize mice via both parenteral and mucosal routes. Subcutaneous immunization induced respiratory syncytial virus-specific serum immunoglobin G (IgG) capable of partially controlling virus replication in the lungs. Intranasal immunization with live bacteria stimulated the production of IgA against both the whole virus and the G domain in serum and bronchoalveolar fluid. Upon challenge, immunized animals had significantly lower virus titres in the lungs than the controls. Our results show for the first time that the G domain-expressing S. gordonii strain elicits both systemic and mucosal immunity that reduced respiratory syncytial virus replication in the lungs of mice.     

QuantiFERON-TB Gold Plus Test in Diagnostics of Latent Tuberculosis Infection in Children Aged 1–14 in a Country with a Low Tuberculosis Incidence

The aim of the study was to evaluate the QuantiFERON-TB Gold Plus (QFT-Plus) test usability in the identification of latent tuberculosis infection (LTBI) in children and the determination of features associated with tuberculin skin test (TST) and QFT-Plus-positive results concerning LTBI. Two-hundred thirteen children aged 1–14 were screened for LTBI due to household contact with TB, suspected TB, or were qualified for biological therapy. The objective of this study was to evaluate the QFT-Plus affectivity as a diagnostic test in the absence of a gold standard (GS) test for the diagnosis of LTBI. The children were diagnosed with QFT-Plus, TST, and culture of TB. The QFT-Plus results were analyzed depending on the children’s age, TST size, and type. In children aged 1–4, the positive predictive value of QFT-Plus was 1, the negative predictive value was 0.94, QFT-Plus sensitivity was 75%, and specificity was 100%. It was observed that in children aged 5–14 years, the level of agreement decreased to the substantial, i.e., 87.2%. Moreover, the negative predictive value was 0.83. QFT-Plus sensitivity was 64%, and specificity was 100%. Statistical analysis of QFT-Plus and TST results showed substantial and almost perfect agreements. Our study suggests that QFT-Plus is helpful in a pediatric practice showing good sensitivity and specificity for LTBI. The BCG vaccine, infections, and concomitant morbidities do not affect QFT-Plus results.     

Toll样受体与抗结核感染免疫

结核分枝杆菌(MTB)是结核病的致病菌,其发病机制仍未阐明。Toll样受体(TLR)蛋白家族属于动物模式识别受体家族。研究表明,TLR对先天免疫和获得性免疫都有调控作用,与抗结核感染免疫有关的主要是TLR2和TLR4。对TLR的研究为MTB诱导先天免疫反应机制的阐明以及治疗方法的进步提供了新的思路。     

Further Search for Small Molecular Inactivants Capable of Eliciting Respiratory Mucosal Immunogenicity by Modifying Sendai Virus Core RNA

Five groups of 32 chemicals were examined regarding their immunological functions as modifier inactivants to make inactivated Sendai nasal vaccine using a contact exposure experiment, direct immunofluorescent method, and serum HI titer. (1) Five of the nine reactive groups of reactive dyes (2-chloropyridine, 2, 4, 6-trichloropyrimidine, vinylsulfonic acid, epichlorohydrin and beta-chloroethylamine) induced complete or almost complete defense in the entire respiratory tract, and the four other vaccines brought about slight infection in the respiratory tracts. There was no marked rise in serum HI titers post-exposure, despite uneven development. (2) Of the four sizable substituted AS naphthol vaccines, naphthol AS-IRG and AS-G vaccines elicited nearly complete defense, but the two other vaccines, inactivated with more elongated molecules, invited rare and successive infections. The three immune groups produced invariably high serum HI titers. (3) Of the six naphthalene derivative vaccines, two (3-hydroxy-2-naphthoic acid methylester and 2-naphthol-6-sulfonic acid) induced complete or almost complete protection. But two vaccines brought about less protection, and the remaining two vaccines caused heavy infections. (4) Of the six benzene derivative vaccines, both m-nitrobenzenesulfonic acid and isatoic anhydride induced complete protection. Three vaccines permitted slight infections but 2, 4, 6-trinitrobenzenesulfonic acid vaccine caused severe infection. (5) Of the seven food dye vaccines, only orange I induced complete or nearly complete defense, while the other dye vaccines were inferior. In effect, twelve inactivated Sendai nasal vaccines modified the ribose and/or phosphate groups of the virus core RNA through five groups of small-sized molecules with specially fixed side chains, and elicited complete or almost complete respiratory mucosal defense. The viral stabilization requiring the least alteration of the configuration will be involved in the chemical modification.     

Immunological Mechanisms by Which Concomitant Helminth Infections Predispose to the Development of Human Tuberculosis

Helminthic infections afflict over 1.5 billion people worldwide, while Mycobacterium tuberculosis infects one third of the world''s population, resulting in 2 million deaths per year. Although tuberculosis and helminthic infections coexist in many parts of the world, and it has been demonstrated that the T-helper 2 and T-regulatory cell responses elicited by helminths can affect the ability of the host to control mycobacterial infection, it is still unclear whether helminth infections in fact affect tuberculosis disease. In this review article, current progress in the knowledge about the immunomodulation induced by helminths to diminish the protective immune responses to bacille Calmette-Guerin vaccination is reviewed, and the knowledge about the types of immune responses modulated by helminths and the consequences for tuberculosis are summarized. In addition, recent data supporting the significant reduction of both M. tuberculosis antigen-specific Toll-like receptor (TLR) 2 and TLR9 expression, and pro-inflammatory cytokine responses to TLR2 and TLR9 ligands in individuals with M. tuberculosis and helminth co-infection were discussed. This examination will allow to improve understanding of the immune responses to mycobacterial infection and also be of great relevance in combating human tuberculosis.     

Candida albicans is able to use M cells as a portal of entry across the intestinal barrier in vitro

Candida albicans is the most frequent yeast responsible for systemic infections in humans. These infections mainly originate from the gastrointestinal tract where C. albicans can invade the gut epithelial barrier to gain access to the bloodstream. Along the gut, pathogens can use Microfold (M) cells as a portal of entry to cross the epithelial barrier. M cells are specialized cells mainly located in the follicule‐associated epithelium of Peyer patches. In this study, we used scanning electron and fluorescence microscopy, adhesion and invasion assays and fungal mutants to investigate the interactions of C. albicans with M cells obtained in an established in vitro model whereby enterocyte‐like Caco‐2 cells co‐cultured with the Raji B cell line undergo a phenotypic switch to morphologically and functionally resembling M cells. Our data demonstrate that C. albicans co‐localizes with and invades preferentially M cells, providing evidence that the fungus can use M cells as a portal of entry into the intestinal barrier. In addition to active penetration, F‐actin dependent endocytosis contributes to internalization of the fungus into M cells through a mechanism involving hypha‐associated invasins including Ssa1 and Als3.     

Tuberculosis: Pathogenesis,immune response,and host genetics

Tuberculosis is a chronic infectious disease that predominantly affects the lungs. The hallmark of tuberculosis infection is the formation of granulomas in the vicinity of infectious foci. Tuberculous granulomas are highly organized bodies with a complex cell composition and well-orchestrated biochemical pathways. Granuloma development plays a dual role. The process restricts the infection dissemination and forms a battlefield for protective immunity but simultaneously may compromise the lung function, threatening host health. The susceptibility to the infection per se, the degree of lung failure, and disease severity are under genetic control. Tuberculosis genetics is complex and poorly understood, but current knowledge indicates that intracellular infections are controlled by a network of biochemical reactions, many of which were not suspected to be involved until recently.     

BCG Educates Hematopoietic Stem Cells to Generate Protective Innate Immunity against Tuberculosis

1. Download high-res image (251KB)
2. Download full-size image

     

反复呼吸道感染患儿血清微量元素及体液免疫水平测定及临床意义

目的:探讨反复呼吸道感染患儿血清微量元素及体液免疫水平测定及其临床意义。方法:选取2016年1月至2017年1月在我院接受治疗的反复呼吸道感染患儿64例作为观察组,另外选取同期来我院体检的健康儿童60例作为对照组,比较两组儿童血清微量元素钙(Ca)、铁(Fe)、铜(Cu)、锌(Zn)、镁(Mg)等的水平、体液免疫因子免疫球蛋白A(IgA)、免疫球蛋白M(IgM)、免疫球蛋白G(IgG)水平及血清补体C3、C4、C5水平,并分析其相关性。结果:观察组患儿血清Ca、Fe、Zn水平显著低于对照组儿童(P0.05),两组儿童血清Cu、Mg水平比较差异无统计学意义(P0.05)。观察组患儿血清IgA、IgM、IgG水平低于对照组儿童(P0.05)。两组儿童血清补体C3、C4、C5水平比较差异无统计学意义(P0.05)。经Pearson相关性分析可得:反复呼吸道感染患儿血清Ca、Fe、Zn与血清IgA、IgM、IgG水平呈正相关(P0.05)。结论:反复呼吸道感染患儿存在血清Ca、Fe、Zn微量元素缺乏及血清IgA、IgM、IgG水平降低现象,且它们之间具有正相关关系,可能共同促进反复呼吸道感染的发生。     

768例肺结核患者下呼吸道感染致病菌耐药性探讨

目的探讨肺结核患者合并下呼吸道感染的致病菌及其耐药性。方法对768例确诊的肺结核患者进行痰和／或支气管肺泡灌洗液进行细菌培养。结果革兰阴性菌596株,占58．1％,对哌拉西林／舒巴坦及头孢哌N／舒巴坦耐药率在5．7％-14．3％。革兰阳性菌201株,占19．6％,对万古霉素耐药率为0。真菌228株,占22．2％,对伊曲康唑耐药,耐药率为10．6％。结论肺结核患者下呼吸道感染,以革兰阴性菌为主,真菌比例呈上升趋势。     

Antimicrobial peptides and proteins, exercise and innate mucosal immunity

This review examines the question of whether exercise can be used as an experimental model to further our understanding of innate antimicrobial peptides and proteins (AMPs) and their role in susceptibility to infection at mucosal surfaces. There is strong evidence to suggest that AMPs, in combination with cellular and physical factors, play an important role in preventing infection. Although AMPs act directly on microorganisms, there is increasing recognition that they also exert their protective effect via immunomodulatory mechanisms, especially in noninflammatory conditions. Further studies that manipulate physiologically relevant concentrations of AMPs are required to shed light on the role they play in reducing susceptibility to infection. Evidence shows that in various form prolonged and/or exhaustive exercise is a potent modulator of the immune system, which can either sharpen or blunt the immune response to pathogens. The intensity and duration of exercise can be readily controlled in experimental settings to manipulate the degree of physical stress. This would allow for an investigation into a potential dose-response effect between exercise and AMPs. In addition, the use of controlled exercise could provide an experimental model by which to examine whether changes in the concentration of AMPs alters susceptibility to illness.     

结核分枝杆菌感染小鼠的脾脏和肺脏组织荷菌量与病理变化

目的分析结核急性感染小鼠脾脏和肺脏的组织荷菌量以及病理的动态变化。方法以3×105CFU结核分枝杆菌标准株H37Rv尾静脉途径感染雌性C57BL/6J小鼠,测定感染后1 d、1周、2周、3周、4周、6周和8周肺脏及脾脏组织的荷菌量,脾脏和肺脏组织经HE染色分析病理变化。结果感染动物的脾脏荷菌量在前3周逐步提高,在4～8周脾脏荷菌量维持稳定,肺脏组织在2～8周组织荷菌量逐步升高。病理分析显示动物感染3周后肺脏和脾脏出现肉芽肿,在6～8周病理损伤加重。结论小鼠经尾静脉感染高剂量结核分枝杆菌在8周前表现为急性感染状态,适用于抗结核药物的体内药效学评价。