Contributions to microbiology最新文献_第4页

General introduction to innate immunity: Dr. Jekyl/Mr. Hyde quality of the innate immune system. 先天免疫概述:Jekyl博士/Mr。海德品质的先天免疫系统。

Contributions to microbiology Pub Date : 2008-01-01 DOI: 10.1159/000135683

Kurt S Zänker

{"title":"General introduction to innate immunity: Dr. Jekyl/Mr. Hyde quality of the innate immune system.","authors":"Kurt S Zänker","doi":"10.1159/000135683","DOIUrl":"https://doi.org/10.1159/000135683","url":null,"abstract":"The innate immunity plays a critical role in host protection against pathogens and transformed cells. It relies amongst others on pattern recognition receptors such as Toll-like receptors, C-type lectin receptors, and nucleotide-binding oligomerization domain proteins to alert and activate defense pathways including the activation of the complement system. Innate immunity represents a trait common to plants and animals, and besides the humoral factors different cell types e.g. subspecies of dendritic cells (plasmacytoid dendritic cells), phagocytic cells, mast cells, glia cells, Kupffer cells, neutrophils and natural killer cells are involved to orchestrate the anti-infectious and antitumor response. Studies in plants, in fruit flies and in mammals reveal that the defensive strategies of invertebrates and vertebrates are highly conserved at the molecular level, which raises the exciting prospects of an increased understanding of innate immunity in a healthy or diseased organism. However, the molecular machinery, e.g. cytokines and chemokines, which triggers, amplifies, and sustains the different phases of the innate immune response could also promote a substantial imbalance between danger and inflammatory response when an infectious challenge is either chronic or not properly declining.","PeriodicalId":79855,"journal":{"name":"Contributions to microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000135683","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27468382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 11

Aging and impairment of innate immunity. 衰老和先天免疫功能受损。

Contributions to microbiology Pub Date : 2008-01-01 DOI: 10.1159/000136358

Vanessa Nomellini, Christian R Gomez, Elizabeth J Kovacs

引用次数: 43

Antimicrobial peptides in innate immune responses. 天然免疫反应中的抗菌肽。

Contributions to microbiology Pub Date : 2008-01-01 DOI: 10.1159/000136315

Ole E Sørensen, Niels Borregaard, Alexander M Cole

引用次数: 76

Allergen inhalation challenge: a human model of asthma exacerbation. 过敏原吸入挑战:哮喘加重的人类模型。

Contributions to microbiology Pub Date : 2007-01-01 DOI: 10.1159/000107052

Gail M Gauvreau, Michelle Y Evans

{"title":"Allergen inhalation challenge: a human model of asthma exacerbation.","authors":"Gail M Gauvreau, Michelle Y Evans","doi":"10.1159/000107052","DOIUrl":"https://doi.org/10.1159/000107052","url":null,"abstract":"Allergen challenge by inhalation is a very useful clinical and research tool for evaluating allergic airway disease. Inhalation of allergen leads to cross-linking of allergen-specific IgE bound to IgE receptors on mast cells and basophils. This is followed by activation of secretory pathways to release preformed and newly generated mediators of bronchoconstriction and vascular permeability. The onset of bronchoconstriction, representing the early phase of the asthmatic response, can be detected within 10 min of the inhalation, reaches a maximum within 30 min, and resolves within 3 h. The late-phase asthmatic response starts between 4 and 8 h, and is characterized by cellular inflammation of the airway, increased bronchiovascular permeability, and mucus secretion. The late-phase asthmatic response is also associated with increased airway responsiveness to nonallergic stimuli. Approximately half of the allergic asthmatic patients develop a late-phase response after allergen inhalation challenge. There has been a tremendous interest in trying to understand the differences between the pathways leading to the dual response and those leading to the early response alone. The current hypotheses are discussed in this chapter. Our understanding of the allergen inhalation challenge model and the complex interplay between leukocytes, tissue and inflammatory mediators will doubtlessly help to define novel and relevant targets for new drugs for the treatment of allergic asthma.","PeriodicalId":79855,"journal":{"name":"Contributions to microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26874353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 41

Respiratory syncytial virus-induced pulmonary disease and exacerbation of allergic asthma. 呼吸道合胞病毒诱发的肺部疾病和过敏性哮喘的加重。

Contributions to microbiology Pub Date : 2007-01-01 DOI: 10.1159/000107055

Nicholas W Lukacs, Joost Smit, Dennis Lindell, Matthew Schaller

引用次数: 13

Animal models of chronic obstructive pulmonary disease exacerbations. 慢性阻塞性肺疾病急性加重的动物模型。

Contributions to microbiology Pub Date : 2007-01-01 DOI: 10.1159/000107059

Gordon J Gaschler, Carla M T Bauer, Caleb C J Zavitz, Martin R Stämpfli

引用次数: 24

A human rhinovirus model of chronic obstructive pulmonary disease exacerbations. 慢性阻塞性肺疾病加重的人鼻病毒模型

Contributions to microbiology Pub Date : 2007-01-01 DOI: 10.1159/000107057

Marco Contoli, Gaetano Caramori, Patrick Mallia, Alberto Papi, Sebastian L Johnston

{"title":"A human rhinovirus model of chronic obstructive pulmonary disease exacerbations.","authors":"Marco Contoli, Gaetano Caramori, Patrick Mallia, Alberto Papi, Sebastian L Johnston","doi":"10.1159/000107057","DOIUrl":"https://doi.org/10.1159/000107057","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) exacerbations are common events that punctuate the natural history of COPD contributing to disease severity progression and being the major cause of COPD-related morbidity and mortality. Currently available pharmacological strategies are only partially effective at reducing or preventing COPD exacerbations. Viral infections are the most frequent cause of COPD exacerbations. The recent development of a human experimental model of rhinovirus-induced COPD exacerbations represents an innovative tool with the potential to increase our understanding of the inflammatory and immunological mechanisms that lead COPD patients to exacerbate after respiratory virus infections. Moreover this model will provide the opportunity to test, in a carefully controlled setting, novel pharmacological compounds with a potential for treating and preventing COPD exacerbations. In this chapter we will focus on the role of viral infections in COPD exacerbations and will discuss preliminary reports regarding the development of this human model of virus-induced COPD exacerbation.","PeriodicalId":79855,"journal":{"name":"Contributions to microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26874358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Modeling responses to respiratory house dust mite exposure. 模拟呼吸性屋尘螨暴露的反应。

Contributions to microbiology Pub Date : 2007-01-01 DOI: 10.1159/000107054

Elizabeth C Cates, Ramzi Fattouh, Jill R Johnson, Alba Llop-Guevara, Manel Jordana

{"title":"Modeling responses to respiratory house dust mite exposure.","authors":"Elizabeth C Cates, Ramzi Fattouh, Jill R Johnson, Alba Llop-Guevara, Manel Jordana","doi":"10.1159/000107054","DOIUrl":"https://doi.org/10.1159/000107054","url":null,"abstract":"House dust mite (HDM) is the most pervasive indoor aeroallergen source worldwide. Allergens derived from HDM are associated with sensitization and allergic asthma. Allergic asthma is an immunologically driven disease characterized by a Th2-polarized immune response, eosinophilic inflammation, airway hyperreactivity, and remodeling. Animal models of asthma utilizing ovalbumin (OVA) exposure have afforded us considerable insight with respect to the mediators and cell types involved in allergic airway inflammation. However, OVA preparations and HDM are two vastly different materials. This chapter is specifically concerned with modeling responses to HDM exposure in mice. These studies have furnished new information and unlocked new lines of inquiry regarding biological responses to common aeroallergens. The complexity of HDM as an allergen source, with its plethora of protein and nonprotein immunogenic components, may influence the mechanisms underlying sensitization, inflammation and remodeling. Here, we will discuss this issue, along with giving critical thought to the use of experimental models.","PeriodicalId":79855,"journal":{"name":"Contributions to microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107054","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26874355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 67

Lipopolysaccharide challenge of humans as a model for chronic obstructive lung disease exacerbations. 人类脂多糖挑战作为慢性阻塞性肺疾病恶化的模型。

Contributions to microbiology Pub Date : 2007-01-01 DOI: 10.1159/000107056

Sergei A Kharitonov, Ulf Sjöbring

引用次数: 49

Animal models of cigarette smoke-induced chronic obstructive lung disease. 香烟所致慢性阻塞性肺疾病的动物模型。

Contributions to microbiology Pub Date : 2007-01-01 DOI: 10.1159/000107058

Andrew Churg, Joanne L Wright

{"title":"Animal models of cigarette smoke-induced chronic obstructive lung disease.","authors":"Andrew Churg, Joanne L Wright","doi":"10.1159/000107058","DOIUrl":"https://doi.org/10.1159/000107058","url":null,"abstract":"Recent years have seen an explosion of animal models of cigarette smoke-induced chronic obstructive lung disease (COPD). Almost all of these have concentrated on the induction and prevention of emphysema. Neutrophils and neutrophil elastase, macrophages and macrophage-derived metalloproteases, lymphocytes, TNF-alpha, and oxidants have all been shown to play a role in the pathogenesis of emphysema in animal models, and interventions using either knockout mice or drugs have indicated possible preventive/therapeutic avenues. There is less in the way of models of smoke-induced small airway remodeling and almost nothing is known of its pathogenesis. Cigarette smoke has been shown to induce vascular remodeling and pulmonary hypertension in laboratory animals, and these mechanisms are beginning to be understood. A major limitation of existing animal models is that most produce relatively mild disease (no more severe than corresponding to the GOLD 2 stage of human COPD), and none of the models show the smoke-independent progressive disease seen in humans with GOLD 3 or 4 COPD. There are no models of cigarette smoke-induced chronic bronchitis in animals and there are no models of acute exacerbations of COPD.","PeriodicalId":79855,"journal":{"name":"Contributions to microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107058","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26874359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 38