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The prevalence of asthma has markedly increased in recent decades. Asthma affects approximately ten percent of the population of the United States, and is the leading cause of childhood hospitalization. This epidemic has been attributed to air pollution, childhood immunizations and a more sanitary living environment. Allergic asthma is clinically characterized by airway hyperreactivity (AHR), increased mucus production and airway remodeling. On the cellular level, pulmonary eosinophilic infiltration and augmented levels of serum IgE arise as a consequence of a CD4+ Th2 cell response in the airway following exposure to allergen. It has been proposed that the chronic inflammation and associated airway events evident in this disease stem from a failure to regulate the underlying immune response. How these events are regulated in the healthy lung is yet unclear. In studies to investigate the mechanisms underlying such regulation we found that firstly, co-transfer of expanded natural CD4+ CD25+ Foxp3+ regulatory T cells (nTregs) mediated regulation of CD4+ Th17 effector cells as exemplified by diminished levels of IL-17 and decreased neutrophilic infiltration in the airways. In contrast, co-transfer of nTregs did not attenuate the lung inflammation elicited by CD4+ Th2 or Th1 polarized cells. Interestingly, using the C129. IL4GFP mice we found that nTregs have the capacity to inhibit IL-4 production and Th2 differentiation in vitro. Secondly, mice with genetically disrupted receptors (IP-/- ) for the lipid-mediator prostacyclin (PGI2), demonstrated increased airway inflammation, eosinophilic infiltration and airway hyperreactivity following immunization and repeated aerosol challenge with ovalbumin. Moreover these mice displayed reduced serum immunoglobulin levels. In summary, nTregs serve a specific function in controlling Th17 cell effector functions, but not Th1 or Th2 inflammation. Additionally, PGI2-IP signaling is an important pathway for inhibiting allergic pulmonary inflammation by controlling CD4+ Th2 cell effector functions.
Eosinophils represent approximately 1% of peripheral blood leukocytes and play a central proinflammatory and immunoregulatory role in various immune disorders. This volume provides the reader with a comprehensive survey of the major aspects of human eosinophilic biology and immunology as well as the most clinically relevant aspects of eosinophil-related disorders. Expert contributions cover the ultrastructural and phenotypic characteristics of human eosinophils, and their fundamental biochemical features including receptors for IgE and chemokines. The production of cytokines and their role in the activation of eosinophils are reviewed. Furthermore, the classic eosinophil-related disorders such as hypereosinophilia, drug reactions, allergic disorders and some cardiovascular diseases are described. Each of the chapters is written by an investigator actively engaged in research on the topic under consideration. The well-edited and stimulating material compiled in this volume will be of interest to all those working in allergology, immunology, biochemistry and pulmonary medicine.
Among the topics reviewed are T and B cell tolerance, clonal deletion, suppressor cells, mechanisms of immune privileged sites and experimental models of tumor immunity. Oral tolerance, ultraviolet radiation and photosensitized effects on immunity, allograft management, T cell vaccination and regulation of immunity with T cell epitopes are discussed from the point of view of possible therapeutic application.
Over the last half century, a dramatic increase in allergic diseases has been observed throughout industrialized nations, which has resulted in significant worldwide socio-economic challenges. In Mouse Models of Allergic Disease: Methods and Protocols, a wide range of expert contributors provide detailed protocols for the design and execution of experiments to thoroughly analyze critical elements associated with a diverse range of allergic diseases, all through the lens of mouse models that accurately recapitulate clinically relevant aspects of the respective human disease. The volume opens with a section featuring techniques essential for effective ex vivo cell isolation and evaluation of specific cell types relevant to a diverse range of allergic diseases, and the book then moves on to cover in vivo protocols to evaluate prevalent mouse models of human allergic diseases, including mouse models of systemic anaphylaxis, contact hypersensitivity, allergic rhinitis, and asthma, as well as a collection of chapters on in vivo and ex vivo protocols used to assess indirect mediators of allergic diseases, such as the nervous system, non-hematopoietic cells, and the composition of the gut microbiome. Written in the highly successful Methods in Molecular Biology series, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Timely and authoritative, Mouse Models of Allergic Disease: Methods and Protocols serves as an essential collection of protocols that allow both novice and expert researchers the ability to accurately develop, evaluate, and characterize the mechanisms associated with these disorders.
More than 50 million Americans, one out of five, suffer from hay fever, asthma, and other allergic diseases. Many of these conditions are caused by exposure to allergens in indoor environments such as the house, work, and schoolâ€"where we spend as much as 98 percent of our time. Developed by medical, public health, and engineering professionals working together, this unique volume summarizes what is known about indoor allergens, how they affect human health, the magnitude of their effect on various populations, and how they can be controlled. The book addresses controversies, recommends research directions, and suggests how to assist and educate allergy patients, as well as professionals. Indoor Allergens presents a wealth of information about common indoor allergens and their varying effects, from significant hay fever to life-threatening asthma. The volume discusses sources of allergens, from fungi and dust mites to allergenic chemicals, plants, and animals, and examines practical measures for their control. Indoor Allergens discusses how the human airway and immune system respond to inhaled allergens and assesses patient testing methods, covering the importance of the patient's medical history and outlining procedures and approaches to interpretation for skin tests, in vitro diagnostic tests, and tests of patients' pulmonary function. This comprehensive and practical volume will be important to allergists and other health care providers; public health professionals; specialists in building design, construction, and maintenance; faculty and students in public health; and interested allergy patients.
Animal models are indispensable for studies requiring an intact immune system, especially for studying the pathogenic mechanisms in atopic diseases, regulation of IgE production, and related biologic effects. Mice are particularly suitable and have been used extensively for such studies because their immune system is well characterized. Further, large numbers of mutants or inbred strains of mice are available that express deficiencies of individual immunologic processes, inflammatory cells, or mediator systems. By comparing reactions in such mice with appropriate control animals, the unique roles of individual cells or mediators may be characterized more precisely in the pathogenesis of atopic respiratory diseases including asthma. However, given that asthma in humans is characterized by the presence of airway hyperresponsiveness to specific and nonspecific stimuli, it is important that animal models of this disease exhibit similar physiologic abnormalities. In the past, the size of the mouse has limited its versatility in this regard. However, recent studies indicate the feasibility of measuring pulmonary responses in living mice, thus facilitating the physiologic evaluation of putative mouse models of human asthma that have been well charcterized at the immunologic and patholigic level. Future work will provide details of the morphometry of the methacholine-induced bronchoconstriction and will further seek to determine the relationship between cigarette smoke exposure and the development of NS-AHR in the transgenic mouse model.
Asthma is one of the most common noncommunicable diseases affecting over 300 million people worldwide (To et al., 2012; Vos et al., 2017). Asthma is particularly common among children aged 0 to 17 with a global prevalence of approximately 8% (Akinbami, Simon, & Rossen, 2016). However, studies of asthma in very young children are limited, and few pharmacotherapy options are available for children under the age of 5. To better understand asthma development in young children, we utilized a model of allergic asthma in mice at post-natal day 21 with the goal of examining hypothalamic-pituitary-adrenal (HPA) axis regulation and arginase-1 (ARG-1) gene expression in the lungs. We created asthma symptoms in male and female BALB/cJ mice (n=95) with intranasal house dust mite protein (HDM) to produce chronic airway inflammation and aerosolized methacholine (MCH) to produce acute bronchoconstriction. At three timepoints (immediate, 4-hours and 24-hours) following final HDM and MCH exposure, lung and blood samples were collected and analyzed for ARG-1 expression changes and serum corticosterone levels. Results indicated that serum corticosterone concentrations were highest in all treatment groups at the immediate timepoints. Experimental groups that received HDM or MCH had higher serum corticosterone levels compared to controls at the immediate timepoint. HDM-exposure was associated with a significant increase in ARG-1 expression in lungs immediately and at 24-hours after HDM exposure, with marginal changes at 4-hours. No sex-dependent differences in gene expression or serum corticosterone data were observed. These results help validate our mouse model of developmental asthma while also providing a foundation for future work investigating asthma mechanisms and treatment options in very young children.