肥大细胞在肺部感染性疾病中的作用

肺部肥大细胞主要分布于肺部血管周围,支气管以及粘膜组织。病原体入侵时,肥大细胞通过胞吞作用直接摄取病原体,同时通过激活自身受体促进下游细胞介质的释放,增强炎性细胞的募集,直接和间接杀伤病原体。此外,肺部肥大细胞参与病原体的抗原递呈,介导细胞和体液免疫。肥大细胞对肺部病原体感染具有重要的保护功能。     

肥大细胞在慢性肝病发生中的作用

［摘要］ 目的：探讨肥大细胞(mast cell, MC)在慢性肝病中的作用及乙型肝炎病毒（HBV）感染是否引起慢性肝病中MC数量增加。方法：本研究包括正常组(NL)8例、慢性肝炎组(CH)30例、肝硬化组(LC)43例、肝癌组(HCC)49例。采用甲苯胺蓝染色和免疫组织化学染色观察130 例人肝组织中肥大细胞的密度和分布特征。另外，采用免疫组织化学染色定性检测各组HBsAg，HBcAg的表达。结果：各肝病组中（肝炎组、肝硬化组、肝癌组）肥大细胞密度比正常组显著增加 (P<0.05)；肝硬化组、肝癌组中MC密度均比慢性肝炎组显著增加(P<0.05)；但肝硬化组与肝癌组之间差异无统计学意义（P>0.05）。MC分布以结缔组织区域多见。本组病例中肥大细胞密度与HBV感染无关。结论：肥大细胞可能参与慢性肝病发生发展过程并发挥重要作用，但其数量增加可能与HBV感染无直接关系。     

肥大细胞在单纯和放射复合伤口愈合中的作用

目的:观察肥大细胞(MC)及其亚群在单纯和放射复合伤口中的动态变化,旨在探讨MC在其中的作用及其机制。方法:应用阿里新兰－番红花红(ABS)双染色法,检测MC及其亚群。结果:①伤后2d两组MC总数均出现一致降低,伤后5-7dMC总数迅速升高并逐渐达到峰值,且一直维持到伤后15-28d。②粘膜型MC(MMC)和结缔组织型MC(CTMC)亚群也出现规律性变化。伤后2d,MMC和混合型MC(MixMC)均出现明显降低,此后一直维持在较低水平。而CTMC伤后一直维持在较高水平。③伤照组MixMC在伤后5d、MC总数在伤后5-15d,均明显少于单伤组。结论:MC及其亚群在创伤愈合以及辐射延迟伤口愈合过程中起着重要作用。     

肥大细胞在支气管哮喘中的研究进展

支气管哮喘(哮喘)是呼吸系统的常见病和多发病,肥大细胞是其主要的反应细胞,目前关于肥大细胞在哮喘中作用的研究取得了新的进展,特别是肥大细胞蛋白酶及其抑制剂的深入研究和哮喘患者气道平滑肌束中肥大细胞数量明显增加并呈脱颗粒状态的发现,引起学者们极大的关注,本文将就肥大细胞在哮喘中的研究进展进行综述。     

肥大细胞在辐射后器官纤维化中的作用

用新建立的阿里新蓝－番红花红双染法，抗５－溴脱氧尿苷单抗和图像分析技术，研究肥大细胞在正常和照射大鼠组织内的分布特点及其颗粒活性介质（组胺）对成纤维细胞生长的影响，结果表明了肥大细胞及其亚群在组织内不均匀分布，辐射后的变化趋势以及与辐射后器官纤维化的关系，提示了肥大细胞重要颗粒活性介质－组胺，在辐射后器官纤维化的发生中可能起着不可忽视的作用。     

肥大细胞在感染及免疫中的作用研究进展

既往认为，肥大细胞主要超敏反应特别是在速发型超敏反应中发挥作用，并与许多疾病的病理生理过程有关，近年来发现，肥大细胞在宿主对病原体的防御反应中发挥着重要作用，该细胞除了具有识别，吞噬并杀灭病原微生物的功能外，尚具有加工，提呈抗原及调节机体免疫反应的作用，为此，有必要对肥大细胞的生物学作用进行更深入的研究及重新认识。     

肥大细胞在脂肪组织中的生理与病理作用

脂肪组织可分为白色脂肪组织(white adipose tissue,WAT)与棕色脂肪组织(brown adipose tissue, BAT).WAT行使能量储存功能,将人体多余的能量以化学能形式储存,而BAT则具有产热功能,在寒冷等刺激下将化学能转化为热能,以维持体温.脂肪组织同时还具有内分泌功能,可分泌多种激素...     

肥大细胞在感染及免疫中的作用研究进展

既往认为，肥大细胞主要在超敏反应特别是在速发型超敏反应中发挥作用，并与许多疾病的病理生理过程有关。近年来发现，肥大细胞在宿主对病原体的防御反应中发挥着重要作用。该细胞除了具有识别、吞噬并杀灭病原微生物的功能外，尚具有加工、提呈抗原及调节机体免疫反应的作用。为此，有必要对肥大细胞的生物学作用进行更深入的研究及重新认识。     

肥大细胞在高血压大鼠心肌纤维化中的作用

目的观察高血压大鼠心肌纤维化过程中是否有肥大细胞参与。方法应用自发性卒中型高血压大鼠（ＳＨＲｓｐ，Ｓ组，６只）及年龄匹配的ＷＫＹ（Ｗ组，５只），用Ｍａｓｏｎ染色及图像分析方法，电镜及Ｔｏｌｕｉｄｉｎｅｂｌｕｅ染色和增殖细胞核抗原（ＰＣＮＡ）免疫染色观察心肌间质纤维化的程度、肥大细胞和细胞增殖。结果Ｓ组较Ｗ组肥大细胞数增加３９倍，ＰＣＮＡ阳性细胞（ＰＣＮＡＰ）增加３９倍，肥大细胞与心肌间质胶原容积百分比（ＩＣＶＦ），血管周围胶原面积比（ＰＶＣＡ／ＶＬＣＡ）及ＰＣＮＡＰ显著正相关（ｒ分别为０４７，Ｐ＜００５；０５９，Ｐ＜０００１及０６８，Ｐ＜０００１）。电镜示心肌间质增生胶原间的肥大细胞呈特征性的缓慢脱颗粒，异于过敏反应中的一次性脱颗粒。结论肥大细胞在高血压心肌间质纤维化过程中起一定的作用     

降钙素原定量检测在鉴别细菌和病毒感染中的诊断意义

目的:检测降钙素原(PCT)定量检测在鉴别细菌和病毒感染中的诊断价值,为PCT在感染性疾病中的应用提供实验依据.方法:采用定量固相免疫测定119例患者的PCT浓度,其中87例细菌感染患者、5例脓毒症患者、27例病毒感染患者和30例正常体检者,同时测定C反应蛋白(CRP)的浓度.以此分析PCT和CRP感染指标在病毒感染和细菌感染中的浓度变化.结果:细菌感染组、脓毒症组、病毒感染组和健康组的PCT水平分布存在统计学差异(P<0.01);细菌感染组显著高于病毒感染组和健康组(P<0.01);脓毒症组显著高于病毒感染组和健康组(P<0.01);但病毒感染组与健康组之间无统计学意义(P>0.05).结论:PCT定量检测对于细菌性感染是一个敏感的新指标,比CRP体现出更好的灵敏度及特异性.而在病毒感染的患者中,PCT结果始终处于比较低的浓度水平.     

The role of mast cells and eosinophils in chronic gastritis

Abstract The role of mast cells and eosinophils in influencing the pathology of chronic gastritis remains unclear. We attempted to study the relationship between endoscopy and the mast cell and eosinophil infiltrate. We also studied the role of gene polymorphisms, Helicobacter pylori density and the CagA antibody status in influencing the mast cell and eosinophil infiltrate. One hundred and twenty consecutive patients were studied. Endoscopic evaluation was done and 3 antral biopsies were taken from each patient and were assessed for eosinophilic and mast cell infiltration, H. pylori density and the density of the other inflammatory cells as per the revised Sydney system. Cytokine gene polymorphisms (IL-1β, IL-1RA and TNF-α) were done on the DNA extracted from the peripheral blood by PCR-RFLP. ELISA was done on the patients’ serum for the anti-CagA antibody titres. Nodularity is strongly associated with the presence and density of eosinophils on biopsy (P< 0.05). Eosinophil density is strongly associated with the density of H. pylori, neutrophils, lymphocytes, plasma cells, atrophy, ulceration, foveolitis and lymphoid follicles. The mast cell density is not associated with any of the other histopathological variables. Gene polymorphisms and the CagA antibody titres have no relationship to the mast cell and eosinophil density. Eighty-one patients showed positive anti-CagA antibody titres but there was no association with the eosinophilic or the mast cell infiltrate. It is likely that eosinophilic infiltration is influenced by the H. pylori density but the CagA protein has no role to play in influencing the grade of the eosinophilic infiltrate in the Indian context. Cytokine gene proinflammatory polymorphisms have no role to play in influencing the eosinophilic or the mast cell response. It is likely that other mediators are involved in the inflammatory cell responses.     

The contribution of mast cells to bacterial and fungal infection immunity

Mast cells are hematopoietic progenitor-derived, granule-containing immune cells that are widely distributed in tissues that interact with the external environment, such as the skin and mucosal tissues. It is well-known that mast cells are significantly involved in IgE-mediated allergic reactions, but because of their location, it has also been long hypothesized that mast cells can act as sentinel cells that sense pathogens and initiate protective immune responses. Using mast cell or mast cell protease-deficient murine models, recent studies by our groups and others indicate that mast cells have pleiotropic regulatory roles in immunological responses against pathogens. In this review, we discuss studies that demonstrate that mast cells can either promote host resistance to infections caused by bacteria and fungi or contribute to dysregulated immune responses that can increase host morbidity and mortality. Overall, these studies indicate that mast cells can influence innate immune responses against bacterial and fungal infections via multiple mechanisms. Importantly, the contribution of mast cells to infection outcomes depends in part on the infection model, including the genetic approach used to assess the influence of mast cells on host immunity, hence highlighting the complexity of mast cell biology in the context of innate immune responses.     

The role of macrophages and mast cells in lymphangiogenesis and angiogenesis in cervical carcinogenesis

During carcinogenesis it is known that growth factors and cytokines from stromal and inflammatory cells from the microenvironment promote angiogenesis and lymphangiogenesis. However, the participation of macrophages and mast cells in these processes is not well understood. The aim of this study was to evaluate the relationship between mast cell and macrophage density with blood and lymphatic vessels in various stages of carcinoma of the uterine cervix. Tissue sections from archival paraffin-embedded samples from cases with cervical intraepithelial neoplasias (CIN) 1, 2, 3, carcinoma in situ, and invasive carcinoma were used. Immunohistochemical staining was done using the following antibodies: anti-LYVE-1; anti-CD31; anti-CD68, and anti-tryptase. Our results showed a significant increase in the number of macrophages in carcinoma in situ, a correlation between lymphatic vessels and macrophages in premalignant lesions CIN 2, and a correlation between mast cells and blood vessels in both CIN 2 and carcinoma in situ. In conclusion, our data underscore the importance of the recruitment of macrophages and mast cells in the development of tumor-associated blood and lymphatic capillaries.     

The role of the mast cell in acute inflammatory responses of copper-deficient rats

Macromolecular leakage associated with mast cell degranulation was studied in the cremaster muscle microcirculation of copper-deficient rats. Male Sprague-Dawley rats were fed a purified diet either adequate for copper (6 g copper/gram diet) or deficient (no added copper) 4 weeks prior to experimentation. The rats were anesthetized and the cremasters (with nerve and blood supply intact) were spread in a tissue bath filled with Kreb's solution.In vivo television microscopy was used to observe the microcirculation. Intravascular fluorescein isothiocyanate conjugated to bovine serum albumin was injected and interstitial fluorescent emission intensity was used as an index of macromolecular leakage. Topical administration of the mast cell degranulator compound 48/80 (1.0 and 10.0 g/ml) induced a significantly greater macromolecular leakage in the copper-deficient animals. The compound 48/80 leakage was blocked in both groups of rats by pretreatment with diphenhydramine which is a histamine H₁ receptor blocker. Topical administration of the inflammatory mediators histamine, serotonin, and bradykinin all induced macromolecular leakage which was not significantly different between groups. These results suggest that copper deficiency increases macromolecular leakage associated with mast cell degranulation by a primary effect on the mast cell rather than on the endothelium.This material is based upon work supported by the Cooperative State Research Service, U.S. Department of Agriculture, under Agreement No. 92-37200-7676. Mention of a trademark of proprietary product does not constitute a guarantee or warranty of the product by the U.S. Department of Agriculture, and does not imply its approval to the exclusion of other products that may also be suitable.     

The history of the controversial relationship between mast cells and basophils

Work on mast cells and basophils began with their identification by Paul Ehrlich at the end of the 19th century. Mast cells and basophils were immediately perceived as closely linked cells and early nomenclature formulated by Ehrlich himself, i.e., tissue “Mastzellen” and blood “Mastzellen”, reflected this unifying viewpoint. With time, important functional affinities but also substantial diversities were recognized. This review article focuses on the historical development of the concept of mast cell/basophil specificity, from the initial identification of these cells to current studies.     

The role of mast cells and angiogenesis in benign and malignant neoplasms of the uterus

In this study, we looked for a relationship between the extent of angiogenesis and mast cell density (MCD) in human leiomyomas and endometrial carcinomas (EC), and investigated the clinicopathological relevance of mast cells (MCs) in EC. Specimens of 15 control, 20 leiomyoma, and 23 EC patients were investigated immunohistochemically using anti-CD31 and anti-tryptase antibodies. In EC, both stromal and myometrial expressions of CD31 were significantly higher than in the controls (p < 0.01 and p = 0.013; respectively). Stromal tryptase expression was not significantly lower than that of leiomyoma. In addition, in the leiomyoma group, CD31 and tryptase expressions were not much different compared to the controls. Moreover, a correlation was detected between cancer histological grade and both stromal and myometrial expressions of CD31 (p = 0.017 and p = 0.005; respectively). The findings show that high grade EC has a higher degree of vascularization than EC of lower grade, but MCD does not increase in parallel with the histological grade. This study has demonstrated that MCD does not correlate with angiogenesis and progression of grade in EC. Moreover, MCD in EC was found to be lower than in benign lesions of the uterus. In conclusion, MCs may not account for the angiogenic process which facilitates tumor growth.     

Functional heterogeneity of mast cells from different species and tissues

Summary The systemic responses of different animals to a number of histamine liberators and the effects of these compounds on isolated tissue mast cells in vitro are examined. Mast cells from different species and even from individual tissues within a single animal are shown to vary markedly in their response to given inducers. On this basis, the usefulness of animal models in predicting whether a particular compound may act as a histamine liberator in man is discussed.