Journal articles: 'Allergic Airways Disease'

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Lew, D. Betty, Kim S. LeMessurier, Maneesha Palipane, Yanyan Lin, and Amali E. Samarasinghe. "Saccharomyces cerevisiae-Derived Mannan Does Not Alter Immune Responses to Aspergillus Allergens." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/3298378.

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Severe asthma with fungal sensitization predominates in the population suffering from allergic asthma, to which there is no cure. While corticosteroids are the mainstay in current treatment, other means of controlling inflammation may be beneficial. Herein, we hypothesized that mannan from Saccharomyces cerevisiae would dampen the characteristics of fungal allergic asthma by altering the pulmonary immune responses. Using wild-type and transgenic mice expressing the human mannose receptor on smooth muscle cells, we explored the outcome of mannan administration during allergen exposure on the pathogenesis of fungal asthma through measurement of cardinal features of disease such as inflammation, goblet cell number, and airway hyperresponsiveness. Mannan treatment did not alter most hallmarks of allergic airways disease in wild-type mice. Transgenic mice treated with mannan during allergen exposure had an equivalent response to non-mannan-treated allergic mice except for a prominent granulocytic influx into airways and cytokine availability. Our studies suggest no role for mannan as an inflammatory regulator during fungal allergy.

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Morianos, Ioannis, and Maria Semitekolou. "Dendritic Cells: Critical Regulators of Allergic Asthma." International Journal of Molecular Sciences 21, no. 21 (October 26, 2020): 7930. http://dx.doi.org/10.3390/ijms21217930.

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Allergic asthma is a chronic inflammatory disease of the airways characterized by airway hyperresponsiveness (AHR), chronic airway inflammation, and excessive T helper (Th) type 2 immune responses against harmless airborne allergens. Dendritic cells (DCs) represent the most potent antigen-presenting cells of the immune system that act as a bridge between innate and adaptive immunity. Pertinent to allergic asthma, distinct DC subsets are known to play a central role in initiating and maintaining allergen driven Th2 immune responses in the airways. Nevertheless, seminal studies have demonstrated that DCs can also restrain excessive asthmatic responses and thus contribute to the resolution of allergic airway inflammation and the maintenance of pulmonary tolerance. Notably, the transfer of tolerogenic DCs in vivo suppresses Th2 allergic responses and protects or even reverses established allergic airway inflammation. Thus, the identification of novel DC subsets that possess immunoregulatory properties and can efficiently control aberrant asthmatic responses is critical for the re-establishment of tolerance and the amelioration of the asthmatic disease phenotype.

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KRISHNA, M. T., I. MUDWAY, F. J. KELLY, A. J. FREW, and S. T. HOLGATE. "Ozone, airways and allergic airways disease." Clinical Experimental Allergy 25, no. 12 (December 1995): 1150–58. http://dx.doi.org/10.1111/j.1365-2222.1995.tb03037.x.

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Carlsten, Chris, Anders Blomberg, Mandy Pui, Thomas Sandstrom, Sze Wing Wong, Neil Alexis, and Jeremy Hirota. "Diesel exhaust augments allergen-induced lower airway inflammation in allergic individuals: a controlled human exposure study." Thorax 71, no. 1 (November 16, 2015): 35–44. http://dx.doi.org/10.1136/thoraxjnl-2015-207399.

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RationaleTraffic-related air pollution has been shown to augment allergy and airway disease. However, the enhancement of allergenic effects by diesel exhaust in particular is unproven in vivo in the human lung, and underlying details of this apparent synergy are poorly understood.ObjectiveTo test the hypothesis that a 2 h inhalation of diesel exhaust augments lower airway inflammation and immune cell activation following segmental allergen challenge in atopic subjects.Methods18 blinded atopic volunteers were exposed to filtered air or 300 µg PM2.5/m3 of diesel exhaust in random fashion. 1 h post-exposure, diluent-controlled segmental allergen challenge was performed; 2 days later, samples from the challenged segments were obtained by bronchoscopic lavage. Samples were analysed for markers and modifiers of allergic inflammation (eosinophils, Th2 cytokines) and adaptive immune cell activation. Mixed effects models with ordinal contrasts compared effects of single and combined exposures on these end points.ResultsDiesel exhaust augmented the allergen-induced increase in airway eosinophils, interleukin 5 (IL-5) and eosinophil cationic protein (ECP) and the GSTT1 null genotype was significantly associated with the augmented IL-5 response. Diesel exhaust alone also augmented markers of non-allergic inflammation and monocyte chemotactic protein (MCP)-1 and suppressed activity of macrophages and myeloid dendritic cells.ConclusionInhalation of diesel exhaust at environmentally relevant concentrations augments allergen-induced allergic inflammation in the lower airways of atopic individuals and the GSTT1 genotype enhances this response. Allergic individuals are a susceptible population to the deleterious airway effects of diesel exhaust.Trial registration numberNCT01792232.

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TODEA, Doina Adina, Iuliu SUATEAN, Andreea Codruta COMAN, and Loredana Elena ROSCA. "The Effect of Climate Change and Air Pollution on Allergenic Potential of Pollens." Notulae Botanicae Horti Agrobotanici Cluj-Napoca 41, no. 2 (December 6, 2013): 646. http://dx.doi.org/10.15835/nbha4129291.

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Climate change is associated with atmospheric warming due to continuous increase in anthropogenic greenhouse gas concentration following the industrial revolution. The urban areas are more responsible for these changes. Europe for example has experienced a progressive warming +0.9Â°C for 1901-2005. Climate change is unequivocal and represents a possible threat for patients affected by allergic conditions because it is related with an increased distribution and concentration of pollen. Higher temperature, wet condition (especially thunderstorms), wind speed, transition of cold fronts, environmental changes (allergenic pollens arrived in new areas), are mechanisms which involve changes of production, dispersion and allergen content of pollen. Prolonged and more severe pollen seasons are leading to worsened asthma and allergies. The interaction of pollen with urban air pollutants could also lead to an increased effect of aero allergens on allergic patients, with a greater likelihood of the development of an allergic respiratory disease in sensitized subjects and exacerbation of symptomatic patients. Air pollution could induce damage to airways mucosa, thus promoting sensitization of the airways; also it could increase the expression of allergenic proteins (allergen contents of pollen produce by plants is increased by higher temperature and CO2 enriched atmosphere). By increasing pollen concentration or making the airways susceptible to allergens, the climate change and air pollution have a negative impact on human health.

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Haberal, Ilknur, and Jacquelynne P. Corey. "The Role of Leukotrienes in Nasal Allergy." Otolaryngology–Head and Neck Surgery 129, no. 3 (September 2003): 274–79. http://dx.doi.org/10.1016/s0194-5998(03)00601-6.

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OBJECTIVE: This review focuses on the role of cysteinyl leukotrienes (cysLTs) in nasal allergy. The purpose was to provide knowledge of the role of cysLTs in the pathophysiology of nasal allergy and the role of antileukotrienes in the treatment of nasal allergies. MATERIALS AND METHODS: We conducted a literature review. RESULTS: The proinflammatory effects of cysLTs have been well described in asthma. Antileukotrienes have proved to be an effective anti-inflammatory treatment for asthma patients. Similar to pathogenesis of asthma, cysLTs exert potent inflammatory effects in the upper airways and play a role in the pathogenesis of allergic rhinitis and other nasal allergies. CONCLUSION: Antileukotriene treatment appears to be beneficial in nasal allergies. Allergic rhinitis is a complex, IgE-mediated inflammatory disease of the upper airways. It is the most common allergic disease, occurring in 10% to 30% of adults and up to 30% of children. It may be perennial or seasonal. Sneezing, itching, watery rhinorrhea, and nasal obstruction are classic symptoms. It may impair cognition, school/work performance and productivity, behavior, mood, and quality of life. On physical examination, clear secretions, nasal congestion, pink-bluish nasal mucosa, the allergic salute, and allergic shiners may be detected. Allergic rhinitis is a common comorbid condition with asthma, sinusitis, otitis media, nasal polyposis, and respiratory infections.

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Salvador, Laia Castro, Christabelle Chen, and Runa Ali. "Allergic rhinitis and its impact on airways disease." Practice Nursing 33, no. 4 (April 2, 2022): 138–44. http://dx.doi.org/10.12968/pnur.2022.33.4.138.

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Allergic rhinitis is linked to an increased risk of asthma development. Laia Castro Salvador et al discuss the impact of allergic rhinitis and how it can be managed Allergic rhinitis is characterised by symptoms including rhinorrhoea, sneezing, nasal obstruction and itching, which have a great impact on the patient's quality of life. Allergic rhinitis can be classified depending on the frequency and severity of symptoms, and can be sub-divided into seasonal and perennial. Allergic rhinitis is linked to an increased risk of asthma development and both diseases are believed to be different expressions of the same inflammatory process. The aim of the treatment is improving the patient's quality of life by relieving symptoms. Management of allergic rhinitis will encompass a combination of allergen avoidance, pharmacological therapies and patient education and adherence.

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Redington, Anthony E., and Peter H. Howarth. "Mast Cells, Cytokines and Asthma." Canadian Respiratory Journal 1, no. 2 (1994): 118–27. http://dx.doi.org/10.1155/1994/435781.

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The appreciation that asthma is a chronic inflammatory disorder of the airways has led to a reappraisal of the importance of different cell populations within the bronchial mucosa with respect to their role in the regulation of the cellular events in this disease. While mast cell degranulation has been implicated in the acute allergic bronchoconstrictor response, activation of this cell population has not been considered relevant to either the late phase inflammatory cell influx within the airways following allergen bronchoprovocation or to the mucosa! eosinophilia in chronic clinical disease. As such, attention has focused on the T lymphocyte as an orchestrator of these cellular events on account of its ability to synthesize and release cytokines relevant to the allergic process. It is now, however, realized that many cell populations within the airways are able to generate cytokines comparable with and complimentary to those produced by T lymphocytes and that asthma cannot be considered an inflammatory airway disorder dependent upon activation of one single cell population. This review details the current evidence that airway mast cells synthesize, store and release cytokines relevant to allergic inflammation and considers their potential involvement not only in the cellular influx within the airways but also in the fibrotic structural changes which are evident in chronic disease.

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Haccuria, Amaryllis, Alain Van Muylem, Andrei Malinovschi, Vi Doan, and Alain Michils. "Small airways dysfunction: the link between allergic rhinitis and allergic asthma." European Respiratory Journal 51, no. 2 (February 2018): 1701749. http://dx.doi.org/10.1183/13993003.01749-2017.

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Abnormal airway reactivity and overproduction of nitric oxide (NO) occurring in small airways have been found in asthma. If the “one airway, one disease” concept is consistent, such dysfunctions should also be detected in the peripheral airways of patients suffering from allergic rhinitis.We investigated whether peripheral airway reactivity and NO overproduction could be documented in distal airways in patients with allergic rhinitis. Exhaled NO fraction (FeNO) and the slope (S) of phase III of the single-breath washout test (SBWT) of helium (He) and sulfur hexafluoride (SF6) were measured in 31 patients with allergic asthma, 23 allergic rhinitis patients and 24 controls, before and after sputum induction. SBWT is sensitive to airway calibre change occurring in the lung periphery.The FeNO decrease was more significant in asthma and rhinitis than in controls (−55.1% and −50.0%, respectively, versus −40.8%) (p=0.007 and p=0.029, respectively). SSF6 and SHe increased in all groups. Change in SHe (ΔSHe) > ΔSSF6 was observed in rhinitis (p=0.004) and asthma (p<0.001), whereas ΔSSF6 = ΔSHe in controls (p=0.431).This study provides evidence of peripheral airway dysfunction in patients with allergic rhinitis quite similar to that described in asthma. Furthermore, a large proportion of the increased NO production reported in allergic rhinitis appears to originate in the peripheral airways.

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Jaffar, Zeina, Maria Ferrini, and Kevan Roberts. "Pulmonary NK cells prevent allergic airway sensitization: Regulation by CB2 cannabinoid receptors." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 192.6. http://dx.doi.org/10.4049/jimmunol.196.supp.192.6.

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Abstract Allergic asthma is a chronic inflammatory disease involving the interaction between the innate and adaptive immune response. Endogenously generated cannabinoids, acting via CB receptors play important roles in both homeostatic and inflammatory processes. CB2-active compounds are known to impact innate immunity including responses by monocytes and NK cells. However, the contribution of pulmonary NK cells and CB2-active endocannabinoids to the innate events preceding sensitization of the airways to the common house dust mite (HDM) allergen is unclear. We investigated the significance of CB2 activation during allergen-triggered pulmonary inflammation and NK cell effector function. Allergic airway inflammation was induced in mice by sensitization via the airways by intranasal HDM instillation, and responses in wild type (WT) and CB2-deficient (CB2−/−) mice were compared. Mice lacking CB2 receptor exhibited elevated numbers of pulmonary NK cells yet were resistant to the induction of allergic inflammation and showed diminished airway hyperreactivity, pulmonary eosinophilia, TH2 cytokine production and mucus secretion after allergen inhalation. Cellular depletion and adoptive transfer studies were undertaken to dissect the mechanisms involved. Depletion of NK cells restored HDM responsiveness. Conversely, transfer of CB2−/− NK cells into WT mice suppressed the allergic airway inflammation and was associated with a reduction in monocyte-derived dendritic cells but elevated CX3CL1 release and recruitment of Ly6C−CX3CR1+ monocytes. These studies established a crucial role for CB2 activation in allergic lung disease via regulation of NK cell function and identified novel therapeutic targets for treatment of asthma.

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de Freitas Alves, Claudiney, Giovanna Natalia Angeli, Daniely Cornélio Favarin, Edinéia Lemos de Andrade, Javier Emilio Lazo Chica, Lúcia Helena Faccioli, Paulo Roberto da Silva, and Alexandre de Paula Rogerio. "The Effects of Proresolution of Ellagic Acid in an Experimental Model of Allergic Airway Inflammation." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/863198.

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Asthma is a disease of airway inflammation characterized by airway hyperresponsiveness, eosinophilic inflammation, and hypersecretion of mucus. Ellagic acid, a compound derived from medicinal plants and fruits, has shown anti-inflammatory activity in several experimental disease models. We used the classical experimental model, in BALB/c mice, of sensibilization with ovalbumin to determine the effect of ellagic acid (10 mg/kg; oral route) in the resolution of allergic airways response. Dexamethasone (1 mg/kg; subcutaneous route) was used as a positive control. The control group consisted of nonimmunized mice that received challenge with ovalbumin. Ellagic acid and dexamethasone or vehicle (water) were administered before or after intranasal allergen challenge. Ellagic acid accelerated the resolution of airways inflammation by decreasing total leukocytes and eosinophils numbers in the bronchoalveolar lavage fluid (BALF), the mucus production and lung inflammation in part by reducing IL-5 concentration, eosinophil peroxidase (EPO) activity, and P-selectin expression, but not activator protein 1 (AP-1) and nuclear factor kappa B (NF-κB) pathways. In addition, ellagic acid enhanced alveolar macrophage phagocytosis of IgG-OVA-coated beadsex vivo, a new proresolving mechanism for the clearance of allergen from the airways. Together, these findings identify ellagic acid as a potential therapeutic agent for accelerating the resolution of allergic airways inflammation.

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Bentabol-Ramos, Guillermo, Rocio Saenz de Santa Maria-Garcia, Monica Vidal-Diaz, Ibon Eguiluz-Gracia, and Almudena Testera-Montes. "The Utility of Nasal Challenges to Phenotype Asthma Patients." International Journal of Molecular Sciences 23, no. 9 (April 27, 2022): 4838. http://dx.doi.org/10.3390/ijms23094838.

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Asthma is a heterogeneous disease in terms of both phenotype and response to therapy. Therefore, there is a great need for clinically applicable tools allowing for improved patient classification, and selection for specific management approaches. Some interventions are highly helpful in selected patients (e.g., allergen immunotherapy or aspirin desensitization), but they are costly and/or difficult to implement. Currently available biomarkers measurable in peripheral blood or exhaled air display many limitations for asthma phenotyping and cannot identify properly the specific triggers of the disease (e.g., aeroallergens or NSAID). The united airway concept illustrates the relevant epidemiological and pathophysiological links between the upper and lower airways. This concept has been largely applied to patient management and treatment, but its diagnostic implications have been less often explored. Of note, a recent document by the European Academy of Allergy and Clinical Immunology proposes the use of nasal allergen challenge to confirm the diagnosis of allergic asthma. Similarly, the nasal challenge with lysine acetylsalicylate (L-ASA) can be used to identify aspirin-sensitive asthma patients. In this review, we will summarize the main features of allergic asthma and aspirin-exacerbated respiratory disease and will discuss the methodology of nasal allergen and L-ASA challenges with a focus on their capacity to phenotype the inflammatory disease affecting both the upper and lower airways.

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Salvi, Sundeep. "Pollution and allergic airways disease." Current Opinion in Allergy and Clinical Immunology 1, no. 1 (February 1, 2001): 35–41. http://dx.doi.org/10.1097/01.all.0000010982.31993.84.

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Salvi, Sundeep. "Pollution and allergic airways disease." Current Opinion in Allergy and Clinical Immunology 1, no. 1 (February 2001): 35–41. http://dx.doi.org/10.1097/00130832-200102000-00007.

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Muluk, Nuray Bayar. "The united airway disease." Romanian Journal of Rhinology 9, no. 33 (March 1, 2019): 21–26. http://dx.doi.org/10.2478/rjr-2019-0002.

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Abstract OBJECTIVES. The aim of this paper is to review the united airway concept. MATERIAL AND METHODS. We searched Pubmed, Google, Google Scholar and Proquest Central database of Kırıkkale University. RESULTS. Upper and lower airways are thought as a morphological and functional unit. There is a link between rhinitis and asthma. Over 80% of asthmatics have rhinitis and 10-40% of rhinitis patients have asthma. Rhinosinusitis is related to asthma in 34-50% of the patients. The relationship between rhinosinusitis and asthma may include “nasobronchial reflex, pharyngobronchial reflex, inhalation of dry, cold air and environmental pollutants inhalation”. CONCLUSION. The united airway concept suggests that upper and lower airways are thought as a morphological and functional unit. It has been commonly accepted in recent years. Allergic rhinitis (AR) is a risk factor for asthma; and Allergic Rhinitis and Asthma (ARIA) suggest bronchial involvement in AR patients.

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Finkelman, Fred D., Charles Perkins, George Smulian, Lucy Gildea, Tatyana Orekov, Crystal Potter, Frank Brombacher, and Marsha Wills-Karp. "Selective stimulation of IL-4 receptor on smooth muscle induces airway hyperresponsiveness in mice (79.9)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 79.9. http://dx.doi.org/10.4049/jimmunol.182.supp.79.9.

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Abstract Hyperresponsiveness to cholinergic stimulation of increased airway resistance is a defining characteristic of asthma. Both IL-4 and IL-13 activate Stat6 via IL-4Rα to induce airway hyperresponsiveness (AHR) in mouse models of asthma and increase mouse and human smooth muscle contractility in vitro. However, the relatively small size of mouse vs. human airways, differences in airway smooth muscle cell distribution between mouse and human, and observations that selective IL-13 stimulation of Stat6 in airway epithelium is sufficient to induce AHR in mice have raised questions about the importance of direct IL-4/IL-13 effects on smooth muscle in murine models of allergic airway disease and whether these models are appropriate for studying AHR in human asthma. To determine whether direct effects of IL-4/IL-13 on smooth muscle contribute to murine allergic airway disease, we produced mice that express IL-4Rα only on smooth muscle and evaluated the effects of intratracheal IL-4, IL-13 and allergen on their airways. We demonstrate that IL-4 and IL-13 induce AHR in these mice, without stimulating goblet cell hyperplasia or airway eosinophilia. Similar results were observed following airway inoculation of these mice with a potent allergen. Thus, allergen-stimulated IL-4/IL-13 can induce AHR in mice through direct effects on airway smooth muscle.

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Schuh, Jane M., and Scott A. Hoselton. "Aerosol allergen challenge results in airway hyperresponsiveness, inflammation, goblet cell metaplasia, and fibrosis in a murine model of fungal allergic airways disease (79.15)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 79.15. http://dx.doi.org/10.4049/jimmunol.182.supp.79.15.

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Abstract Allergic asthma is a chronic syndrome punctuated by acute respiratory distress that can result in irreversible remodeling of the airways. Experimental models that represent both acute and chronic dysfunction may provide insights into the pathology of asthma and a platform to test therapeutics. OBJECTIVE: To provide an allergic airway disease model that more closely reflects the human asthma syndrome. METHODS: BALB/c mice were sensitized with soluble Aspergillus fumigatus antigens over 5 weeks and were then challenged with a 10-min nose-only aerosol exposure to A. fumigatus spores. RESULTS: Airway hyperresponsiveness was observed through day 28 following allergen challenge. Goblet cell metaplasia and mucus hypersecretion peaked at day 7 after challenge. Eosinophil and lymphocyte recruitment peaked 7 and 14 days after allergen challenge, respectively, although persistent inflammation was still observed 35 days after challenge. Increased peribronchial and perivascular collagen deposition was first noted at day 14 after challenge in some animals and was consistently noted in lungs by day 35 post-challenge as compared to naïve animals. Visual evidence suggested that smooth muscle mass may also be increased at these time points. CONCLUSION: Aerosol delivery of fungal conidia provides a model that reflects both the acute and chronic outcomes of the allergic airways syndrome.

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Royce, Simon G., Anna M. Tominaga, Matthew Shen, Krupesh P. Patel, Brooke M. Huuskes, Rebecca Lim, Sharon D. Ricardo, and Chrishan S. Samuel. "Serelaxin improves the therapeutic efficacy of RXFP1-expressing human amnion epithelial cells in experimental allergic airway disease." Clinical Science 130, no. 23 (October 20, 2016): 2151–65. http://dx.doi.org/10.1042/cs20160328.

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We have identified combination cell-based therapies that effectively treat the airway inflammation and airway remodelling (structural changes) that contribute to airway obstruction and related airway hyperresponsiveness in murine chronic allergic airways.

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Muraro, A., W. J. Fokkens, S. Pietikainen, D. Borrelli, I. Agache, J. Bousquet, V. Costigliola, et al. "European symposium on precision medicine in allergy and airways diseases: report of the European Union parliament symposium (October 14, 2015)." Rhinology journal 53, no. 4 (December 1, 2015): 303–7. http://dx.doi.org/10.4193/rhino15.400.

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On 14 October 2015, the European Academy of Allergy and Clinical Immunology (EAACI), the European Rhinologic Society (ERS) and the European Medical Association (EMA) organized a symposium in the European Parliament in Brussels on Precision Medicine in Allergy and Airways Diseases, hosted by MEP David Borrelli and with active participation of the European Respiratory Society (ERS), the European Federations of Allergy and Airways Diseases Patients Associations (EFA), the Global Allergy and Asthma European Network (Ga2len), Allergic Rhinitis and Its Impact on Asthma (ARIA) and the Respiratory Effectiveness Group (REG). MEP Sirpa Pietikainen, Chair of the European Parliament Interest Group on Allergy and Asthma, underlined the importance of the need for a better diagnostic and therapeutic approach for patients with Allergies and Chronic Airways Diseases, and encouraged a joint initiative to control the epidemic of Allergy and Asthma in Europe. The socio-economic impact of allergies and chronic airways diseases cannot be underestimated, as they represent the most frequently diagnosed chronic non-communicable diseases in the EU. Despite the fact that 30% of the total European population is nowadays suffering from allergies and asthma, more than half of these patients are deprived from adequate diagnosis and treatment. Precision Medicine represents a novel approach in medicine, embracing 4 key features: personalized care based on molecular, immunologic and functional endotyping of the disease, with participation of the patient in the decision making process of therapeutic actions, and taking into account predictive and preventive aspects of the treatment. Implementation of Precision Medicine into clinical practice may help to achieve the arrest of the Epidemic of Allergies and Chronic Airways Diseases. This report summarizes the key messages delivered during the symposium by the speakers, including the EU Commissioner for Health and Food Safety Vitenys Andriukaitis. The Commissioner underscored the need for optimal patient care in Europe, supporting joint action plans for disease prevention, patient empowerment and cost-effective treatment strategies leading to a better health status of European citizens.

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Royce, Simon G., Yu R. Miao, Melissa Lee, Chrishan S. Samuel, Geoffrey W. Tregear, and Mimi L. K. Tang. "Relaxin Reverses Airway Remodeling and Airway Dysfunction in Allergic Airways Disease." Endocrinology 150, no. 6 (February 12, 2009): 2692–99. http://dx.doi.org/10.1210/en.2008-1457.

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Mice deficient in the antifibrotic hormone relaxin develop structural changes in the airway that resemble airway remodeling, and demonstrate exaggerated remodeling changes in models of allergic airways disease (AAD). Relaxin expression in asthma has not been previously studied. We evaluated the efficacy of relaxin in the treatment of established airway remodeling in a mouse model of AAD. Relaxin expression in mouse AAD was also examined by immunohistochemistry and real-time PCR. BALB/c mice with established AAD were treated with relaxin or vehicle control (sc for 14 d), and effects on airway remodeling, airway inflammation, and airway hyperresponsiveness (AHR) were assessed. Relaxin expression was significantly reduced in the airways of mice with AAD compared with controls. Recombinant relaxin treatment in a mouse model of AAD reversed collagen deposition and epithelial thickening, and significantly improved AHR (all P < 0.05 vs. vehicle control), but did not influence airway inflammation or goblet cell hyperplasia. Relaxin treatment was associated with increased matrix metalloproteinase-2 levels, suggesting a possible mechanism for its antifibrotic effects. Endogenous relaxin expression is decreased in murine AAD, whereas exogenous relaxin represents a novel treatment capable of reversing established airway remodeling and AHR.

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Saxon, Andrew, Andr^ ^eacute; E. Nel, and David Diaz-Sanchez. "DIESEL PARTICULATES IN ALLERGIC AIRWAYS DISEASE." Nihon Bika Gakkai Kaishi (Japanese Journal of Rhinology) 38, no. 1 (1999): 123–28. http://dx.doi.org/10.7248/jjrhi1982.38.1_123.

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Gordon, Geoffrey H., and Michael J. Bernstein. "PSYCHIATRIC MIMICS OF ALLERGIC AIRWAYS DISEASE." Immunology and Allergy Clinics of North America 16, no. 1 (February 1996): 199–214. http://dx.doi.org/10.1016/s0889-8561(05)70243-5.

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Persson, Carl, and Lena Uller. "Epithelial perviousness in allergic airways disease." Journal of Allergy and Clinical Immunology 140, no. 4 (October 2017): 1211. http://dx.doi.org/10.1016/j.jaci.2017.01.047.

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Rakhmatullina, N. M., Yu V. Pastushenko, O. R. Trofimova, N. A. Sibgatullina, D. G. Akhmedzyanova, and G. N. Zakirov. "Modern methods of allergen-specific immunotherapy in allergic rhinitis treatment." Kazan medical journal 97, no. 2 (April 15, 2016): 288–94. http://dx.doi.org/10.17750/kmj2016-288.

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The article presents the modern methods of allergen-specific immunotherapy in patients with allergic rhinitis. Allergen-specific immunotherapy - a method of treating allergic diseases, involves reducing the organism’s sensitivity to the allergen effects by repeated administration of allergen extract, starting with the minimum dose. Given the allergic rhinitis high prevalence, as well as its tendency to increase, strong interest in effective methods of its treatment is fully justified. Over the last 20 years, it has become clear that asthma and rhinitis are two types of manifestations of a single pathological process in the airways. It has been proven that allergic disease clinical features may change over time. In addition, patients with allergy are prone to multivalent sensitization. Currently none of the drugs used to relieve allergic rhinitis symptoms can not change the organism’s response to an allergen. Allergen-specific immunotherapy can reduce allergic disease symptoms severity, reduces the need in drugs use, decreases the chance of additional sensitization to other allergens, prevents the asthma development. This therapy has become one of the most widely used effective methods of atopic diseases treatment: seasonal and perennial rhinoconjunctivitis, atopic asthma. Allergen-specific immunotherapy can lead to a change in the immunological response to the relevant allergens in early stages, acting through regulatory cells. Current studies are aimed, on the one hand, at reducing the therapeutic allergovaccines ability to cause allergic reactions, on the other - to maintain or enhance their immunogenic properties. Achieving this goal is possible by changing the route of administration and delivery of therapeutic allergens (non-injection methods of allergen-specific immunotherapy), and using a variety of allergens modification techniques.

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Svensson, Christer, Morgan Andersson, Lennart Greiff, and Carl G. A. Persson. "Nasal Mucosal Endorgan Hyperresponsiveness." American Journal of Rhinology 12, no. 1 (January 1998): 37–44. http://dx.doi.org/10.2500/105065898782103016.

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Nonspecific hyperresponsiveness of the upper and lower airways is a well-known characteristic of different inflammatory airway diseases but the underlying mechanisms have not yet been satisfactorily explained. In attempts to elucidate the relation of hyperresponsiveness to disease pathophysiology we have particularly examined the possibility that different airway endorgans may alter their function in allergic airway disease. The nose, in contrast to the bronchi, is an accessible part of the airways where in vivo studies of airway mucosal processes can be carried out in humans under controlled conditions. Different endorgans can be defined in the airway mucosa: subepithelial microvessels, epithelium, glands, and sensory nerves. Techniques may be applied further in the nose to determine selectively the responses/function of these endorgans. Topical challenge with methacholine will induce a glandular secretory response, and topical capsaicin activates sensory c-fibers and induces nasal smart. Topical histamine induces extravasation of plasma from the subepithelial microvessels. The plasma exudate first floods the lamina propria and then moves up between epithelial cells into the airway lumen. This occurs without any changes in the ultrastructure or barrier function of the epithelium. We have therefore forwarded the view of mucosal exudation of bulk plasma as a physiological airway tissue response with primarily a defense function. Since the exudation is specific to inflammation, we have also suggested mucosal exudation as a major inflammatory response among airway endorgan functions. Using a “nasal pool” device for concomitant provocation with histamine and lavage of the nasal mucosa we have assessed exudative responses by analyzing the levels of plasma proteins (e.g., albumin, α2-macroglobulin) in the returned lavage fluids. A secretory hyperresponsiveness occurs in both experimental and seasonal allergic rhinitis. This type of nasal hyperreactivity may develop already 30 minutes after allergen challenge. It is attenuated by topical steroids and oral antihistamines. We have demonstrated that exudative hyperresponsiveness develops in both seasonal allergic rhinitis and common cold, indicating significant changes of this important microvascular response in these diseases. An attractive hypothesis to explain airway hyperresponsiveness has been increased mucosal absorption permeability due to epithelial damage, possibly secondary to the release of eosinophil products. However, neither nonspecific nor specific endorgan hyperresponsiveness in allergic airways may be explained by epithelial fragility or damage since nasal absorption permeability (measured with 51Cr-EDTA and dDAVP) was decreased or unchanged in our studies of allergic and virus-induced rhinitis, respectively. Thus, the absorption barrier of the airway mucosa may become functionally tighter in chronic eosinophilic inflammation.

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Al-Alawi, Alia, C. Frank Ryan, Julia D. Flint, and Nestor L. Müller. "Aspergillus-Related Lung Disease." Canadian Respiratory Journal 12, no. 7 (2005): 377–87. http://dx.doi.org/10.1155/2005/759070.

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Aspergillus is a ubiquitous dimorphic fungus that causes a variety of human diseases ranging in severity from trivial to life-threatening, depending on the host response. An intact host defence is important to prevent disease, but individuals with pre-existing structural lung disease, atopy, occupational exposure or impaired immunity are susceptible. Three distinctive patterns of aspergillus-related lung disease are recognized: saprophytic infestation of airways, cavities and necrotic tissue; allergic disease including extrinsic allergic alveolitis, asthma, allergic bronchopulmonary aspergillosis, bronchocentric granulomatosis and chronic eosinophilic pneumonia; and airway and tissue invasive disease -- pseudomembranous tracheobronchitis, acute bronchopneumonia, angioinvasive aspergillosis, chronic necrotizing aspergillosis and invasive pleural disease. A broad knowledge of these clinical presentations and a high index of suspicion are required to ensure timely diagnosis and treatment of the potentially lethal manifestations of aspergillus-related pulmonary disease. In the present report, the clinical, radiographic and pathological aspects of the various aspergillus-related lung diseases are briefly reviewed.

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Xiong, Yelin, Gunasegaran Karupiah, Simon P. Hogan, Paul S. Foster, and Alistair J. Ramsay. "Inhibition of Allergic Airway Inflammation in Mice Lacking Nitric Oxide Synthase 2." Journal of Immunology 162, no. 1 (January 1, 1999): 445–52. http://dx.doi.org/10.4049/jimmunol.162.1.445.

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Abstract We have used mice rendered deficient for nitric oxide synthase 2 (NOS2) production to study the role of inducible nitric oxide (NO) in the pathogenesis of allergic airways disease. Using a model with OVA as aeroallergen, we show that the manifestations of disease, including infiltration of inflammatory cells, particularly eosinophils, loss of structural integrity of the airway walls, microvascular leakage, pulmonary edema, and airway occlusion are markedly less severe in the NOS2 mutants than in wild-type animals. Indeed, NOS2-deficiency resulted in a 55–60% reduction in both circulatory and pulmonary eosinophil numbers following aeroallergen treatment, although eosinophil maturation or efflux from the bone marrow was not suppressed. There were no obvious differences in levels of airway hyperreactivity recorded in OVA-treated wild-type and NOS2-deficient mice. Interestingly, the suppression of allergic inflammation was accompanied by marked increases in T cell production of IFN-γ but not by any obvious reduction in the secretion of either IL-4 or IL-5, nor by major changes in the IgG1 and IgE OVA-specific serum Ig profiles in the mutants. The markedly enhanced production of IFN-γ in NOS2−/− mice was apparently responsible for the suppression of both eosinophilia and disease, as in vivo depletion of this factor restored allergic pathology in these animals. Our data indicate that NOS2 promotes allergic inflammation in airways via down-regulation of IFN-γ activity and suggest that inhibitors of this molecule may represent a worthwhile therapeutic strategy for allergic diseases including asthma.

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Sheih, Alyssa, and Steven F. Ziegler. "Airway epithelial cells promote allergic sensitization to cockroach allergen through GM-CSF production." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 192.20. http://dx.doi.org/10.4049/jimmunol.196.supp.192.20.

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Abstract Allergic asthma is an inflammatory disease of the airways driven by an overactive immune response against allergens. Allergen-specific TH2 cells are critical to the pathogenesis of asthma but factors controlling the initiation of TH2 responses are not well understood. The emerging picture is one that points to a role for airway epithelial cells (AECs) and epithelial-derived cytokines in promoting TH2 immunity to allergens. However, allergens are structurally diverse and can elicit different epithelial-derived cytokines. Thus, there are multiple pathways that lead to TH2 immunity and mechanisms of sensitization that are unique to individual allergens remain to be elucidated. Cockroach allergen (CRA) is an environmental allergen that is strongly associated with the incidence of allergic asthma. Despite its clinical importance, very little is known about the molecular and cellular pathways involved in allergic sensitization to CRA. To determine the mechanisms that regulate allergic sensitization to CRA, we intranasally sensitized and challenged mice with CRA to induce allergic airway inflammation with hallmark features of asthma. Using this model, we demonstrate that allergic sensitization to CRA requires activation of AECs. MyD88 deletion in AECs reduced allergic airway response to CRA as well as production of GM-CSF during sensitization. Using a neutralizing antibody against GM-CSF, we showed that GM-CSF is essential for TH2 priming and allergic sensitization to CRA, likely through activation of dendritic cells. When GM-CSF was intranasally delivered during sensitization, TH2-mediated eosinophilia was restored in the absence of MyD88. Thus, AECs promote allergic sensitization to CRA through production of GM-CSF.

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Hsu, Peter S., and Dianne E. Campbell. "A bug's view of allergic airways disease." Paediatric Respiratory Reviews 19 (June 2016): 69–74. http://dx.doi.org/10.1016/j.prrv.2016.02.002.

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Braunstahl, Gert-Jan, and Peter W. Hellings. "Nasobronchial interaction mechanisms in allergic airways disease." Current Opinion in Otolaryngology & Head and Neck Surgery 14, no. 3 (June 2006): 176–82. http://dx.doi.org/10.1097/01.moo.0000193186.15440.39.

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Pitchford, S. C. "Defining a role for platelets in allergic inflammation." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1104–8. http://dx.doi.org/10.1042/bst0351104.

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There is now considerable evidence suggesting a role for platelets as inflammatory cells. These actions are distinct from their classically known actions performed during thrombosis and haemostasis, and include the expression of adhesion molecules and contact-dependent activation of leucocytes, the release of a plethora of inflammatory mediators, activation in cells of the adaptive immune response and the ability to migrate and undergo chemotaxis. Chronic asthma is a disease characterized by a mixed inflammatory cell pulmonary infiltrate, AHR (airways hyper-responsiveness) and tissue remodelling. Clinical data from patients suffering from asthma, allergic rhinitis and allergic dermatitis reveal changes in platelet behaviour and function during or after allergen exposure. Furthermore, mouse models of allergic inflammation demonstrate a role for intact platelets in eosinophil and lymphocyte recruitment to the lungs, a mechanism that is P-selectin (platelet selectin)-dependent. Models of chronic inflammation also reveal the participation of platelets in tissue remodelling events whereby platelet depletion was found to be more effective in suppressing airway remodelling processes than the administration of a glucocorticosteroid. This process of destruction and repair to the architecture of airway tissue is therefore perhaps enhanced by platelet activation. Recent evidence demonstrates that platelets can undergo chemotaxis and indicates an ability to migrate through inflamed tissue, where they localize to specific tissue sites. Indeed, platelets have been shown to become activated and recruited to various body compartments in direct response to allergen via IgE and this is suggestive of a link between the innate and adaptive immune responses. Thus these actions may lead to pathophysiological events that alter disease progression, since platelet depletion suppresses AHR in allergic rabbits. Further investigations into the role of platelets in inflammation may be beneficial in the search for future therapeutic targets in the treatment of asthma and allergy.

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Arora, Meenakshi, Stephanie Poe, Timothy Oriss, Nandini Krishnamorthy, Manohar Yarlagadda, Timothy Billiar, Anuradha Ray, and Prabir Ray. "TLR4/MyD88-induced non-migratory myeloid cells suppress Th2 effector function in the lung (91.15)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 91.15. http://dx.doi.org/10.4049/jimmunol.184.supp.91.15.

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Abstract Bacterial lipopolysaccharide (LPS) is immunostimulatory at a low dose but immunosuppressive at a high dose in the respiratory tract as observed in animal studies. Relevant to LPS-mediated immunosuppression in the lungs of animals is the protective effect of high doses of LPS in allergic diseases such as asthma in humans. Our study investigated the impact of a high dose of LPS on cells of the innate immune system in the lung to elucidate the basis of LPS-mediated immunosuppression. A high LPS dose blunted house dust mite-induced airway eosinophilia and Th2 cytokines production. Conversely, adoptively transferred Th2 cells were unable to mount allergic airway inflammation in LPS-treated lungs. The high LPS dose promoted the development of a lung-resident myeloid cell type in a TLR4- and MyD88-dependent fashion that suppressed lung DC-mediated reactivation of primed Th2 cells. Adoptive transfer of these myeloid cells suppressed allergen-induced airway inflammation. These data suggest that LPS-induced non-migratory myeloid cells might contribute to the protective effects of LPS in allergic airways disease by dampening Th2 effector functions in the lung. RO1 HL060207 (P.R.), RO1 HL077430 (A.R.), RO1 HL084932 (A.R. and P.R.) and AHA 0865379D (M.A.)

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Samarasinghe, Amali, Kim LeMessurier, Amy Iverson, Stacie Woolard, and Jonathan McCullers. "Acute inflammatory asthma protects influenza infected mice from bacterial superinfection (P3065)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 187.8. http://dx.doi.org/10.4049/jimmunol.190.supp.187.8.

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Abstract The Centers of Disease Control identified asthmatics to suffer more severe morbidity from influenza during the 2009 pandemic. However, our data indicate that pre-existing allergic inflammation during viral infection is protective against influenza associated disease in mice. Since bacterial super-infections during influenza increase morbidity and mortality, we hypothesized that acute inflammatory asthma promotes bacterial colonization of the lungs after influenza infection thereby leading to a more severe outcome. We created a triple variant model system by infecting Aspergillus fumigatus sensitized and challenged mice with 1000 TCID50/ml of A/CA/4/2009 virus a week after the last fungal challenge. Mice were co-infected with 600 cfu of Streptococcus pneumoniae strain A66.1 a week later and monitored for six days. Mice with allergic asthma lost less weight after co-infection, had less airway resistance after methacholine challenge, and had at least a 50% reduction in mortality compared to non-asthmatic controls. Fewer inflammatory cells were recruited into the airways of allergic mice after co-infection. Allergic asthma delayed S. pneumoniae colonization in the airways and lungs but not blood compared to co-infection alone. Mice in the asthma and co-infection model had less normal flora outgrowth in the airways, lungs, and blood compared to those in the co-infection model. Allergic asthma protects against, or delays, bacterial super-infection after influenza challenge.

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Bonanno, Anna, Sebastiano Gangemi, Stefania La Grutta, Velia Malizia, Loredana Riccobono, Paolo Colombo, Fabio Cibella, and Mirella Profita. "25-Hydroxyvitamin D, IL-31, and IL-33 in Children with Allergic Disease of the Airways." Mediators of Inflammation 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/520241.

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Low vitamin D is involved in allergic asthma and rhinitis. IL-31 and IL-33 correlate with Th2-associated cytokines in allergic disease. We investigated whether low vitamin D is linked with circulating IL-31 and IL-33 in children with allergic disease of the airways. 25-Hydroxyvitamin D [25(OH) Vit D], IL-31, and IL-33 plasma levels were measured in 28 controls (HC), 11 allergic rhinitis (AR) patients, and 35 allergic asthma with rhinitis (AAR) patients. We found significant lower levels of 25(OH) Vit D in AR and in AAR than in HC. IL-31 and IL-33 plasma levels significantly increased in AAR than HC. IL-31 and IL-33 positively correlated in AR and AAR. 25(OH) Vit D deficient AAR had higher levels of blood eosinophils, exacerbations, disease duration, and total IgE than patients with insufficient or sufficient 25(OH) Vit D. In AAR 25(OH) Vit D levels inversely correlated with total allergen sIgE score and total atopy index. IL-31 and IL-33 did not correlate with 25(OH) Vit D in AR and AAR. In conclusion, low levels of 25(OH) Vit D might represent a risk factor for the development of concomitant asthma and rhinitis in children with allergic disease of the airways independently of IL-31/IL-33 Th2 activity.

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Berdnikovs, Sergejs, Robert Schleimer, Paul Bryce, and Hiam Abdala-Valencia. "Transcriptomic signatures convergent across multiple studies of upper and lower airway allergic disease support the unified airway hypothesis (HUM7P.321)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 184.30. http://dx.doi.org/10.4049/jimmunol.192.supp.184.30.

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Abstract Asthma is frequently associated with co-morbid diseases of the upper airways, including chronic rhinosinusitis (CRS). This has led to a hypothesis that the upper and lower airway may be immunologically linked, functioning as a continuous mucosal epithelial barrier interacting with the environment. Despite a growing number of transcriptomics studies, the differences and similarities between upper and lower airways in allergic disease are still poorly understood. We analyzed raw microarray data from three independent studies of CRS and four studies of asthma, and conducted a secondary multivariate and pathway analysis to identify genes commonly altered in both diseases. Despite regional differences, close to 20% of genes found to be differentially expressed in CRS were also found to be differentially expressed in the lower airways of asthmatics. Notable examples are IL6R, IL13RA2, MSMB, MUC5B, POSTN, SERPINB2, TFF2, WIF1 and WNT5A. Pathway analysis revealed that key processes represented by these shared genes are developmental pathway signaling, epithelial-mesenchymal transition and innate immune response, suggesting co-existence of epithelial remodeling and persistence of innate immune signals. Interestingly, many of the genes altered in CRS that we identified in the upper airways are also asthma susceptible genes previously identified through GWAS studies (e.g., IL1RL1, ORMDL3), indicating a common role for these genes in the pathogenesis of respiratory allergic diseases.

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Royce, Simon G., Clarice Lim, Ruth C. Muljadi, Chrishan S. Samuel, Katherine Ververis, Tom C. Karagiannis, Andrew S. Giraud, and Mimi L. K. Tang. "Trefoil Factor–2 Reverses Airway Remodeling Changes in Allergic Airways Disease." American Journal of Respiratory Cell and Molecular Biology 48, no. 1 (January 2013): 135–44. http://dx.doi.org/10.1165/rcmb.2011-0320oc.

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Гогунська, І., Д. Заболотна, С. Зайков, И. Кайдашев, Т. Уманець, В. Чоп’як, Л. Яшина, et al. "ПРОЕКТ “ARIA”: ШЛЯХИ НАДАННЯ МЕДИЧНОЇ ДОПОМОГИ ПРИ АЛЕРГІЧНОМУ РИНІТІ (2019 РІК) – УКРАЇНА." Medical and Ecological Problems 23, no. 5-6 (December 16, 2019): 3–14. http://dx.doi.org/10.31718/mep.2019.23.5-6.01.

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In all societies, the burden and cost of allergic diseases are increasing rapidly, and change management strategies are needed to support the transformation of the health care system for integrated care. A meeting was held in Paris, December 3, 2018 for chronic disease care. It was organised by MASK (Mobile Airways Sentinel NetworK) and POLLAR (Impact of Air Pollution on Asthma and Rhinitis, EIT Health), in collaboration with professional and patient organizations in the field of allergy and airway diseases. The evaluation of real-life Integrated Care Pathways (ICPs) was recommended fordigitally-enabled, integrated, person-centred care for rhinitis and asthma multimorbidity embedding environmental exposure. ICPs are structured multi-disciplinary care plans detailing key steps of patient care. They promote the translation of guideline recommendations into local protocols and their application to clinical practice. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology explicitly considers all types of study designs but guideline developers often prefer to restrict guidelines to RCTs. GRADE also considers evidence about values and preferences, acceptability and feasibility or directness of findings. There is an increasing trend to use real-world evidence (RWE) to inform clinical practice. AIRWAYS ICPs (Integrated care pathways for airway diseases) were the first steps towards the development of ICPs for rhinitis and asthma multimorbidity. During the Paris meeting, next-generation guidelines for the pharmacologic treatment of AR were developed using existing GRADE-based guidelines for AR tested using RWE provided by mobile technology and chamber studies. These recommendations were used to refine the MASK algorithm for AR treatment proposed by a consensus group. In allergic rhinitis (AR), there is an urgent need to develop next-generation guidelines for pharmacotherapy and ICPs for allergen immunotherapy (AIT). Two separate documents were produced following the Paris meeting. This paper clarifies the ways of implementing this direction in Ukraine.

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Fokkens, W. J., and P. W. Hellings. "Rhinology in the forefront of European political attention." Rhinology journal 53, no. 4 (December 1, 2015): 289. http://dx.doi.org/10.4193/rhin.53e4.

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On Oct. 14, 2015, a symposium on Precision Medicine in Allergy and Airways Diseases took place in the European Parliament in Brussels. The burden of disease in patients with rhinitis and rhinosinusitis was brought to the attention of European policy makers and different stakeholders involved in patient care, highlighting the high prevalence of allergic rhinitis and rhinosinusitis reaching epidemic proportions, the major socio-economic consequences and the impact uncontrolled disease despite evidence-based treatment. The Commissioner of Health and Food Safety of Europa, Vytenis Andriukaitis, as well as the presidents of large European Academies and Associations agreed upon the fact that a joint action plan is needed to arrest the epidemic of allergy and chronic airways diseases in Europe via joining forces between patient organizations, health care professionals and researchers.

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Horvat, Jay C., Malcolm R. Starkey, Richard Y. Kim, Kenneth W. Beagley, Julie A. Preston, Peter G. Gibson, Paul S. Foster, and Philip M. Hansbro. "Chlamydial Respiratory Infection during Allergen Sensitization Drives Neutrophilic Allergic Airways Disease." Journal of Immunology 184, no. 8 (March 12, 2010): 4159–69. http://dx.doi.org/10.4049/jimmunol.0902287.

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Steelant, B., S. F. Seys, G. Boeckxstaens, C. A. Akdis, J. L. Ceuppens, and P. W. Hellings. "Restoring airway epithelial barrier dysfunction: a new therapeutic challenge in allergic airway disease." Rhinology journal 54, no. 3 (September 1, 2016): 195–205. http://dx.doi.org/10.4193/rhino15.376.

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An intact functional mucosal barrier is considered to be crucial for the maintenance of airway homeostasis as it protects the host immune system from exposure to allergens and noxious environmental triggers. Recent data provided evidence for the contribution of barrier dysfunction to the development of inflammatory diseases in the airways, skin and gut. A defective barrier has been documented in chronic rhinosinusitis, allergic rhinitis, asthma, atopic dermatitis and inflammatory bowel diseases. However, it remains to be elucidated to what extent primary (genetic) versus secondary (inflammatory) mechanisms drive barrier dysfunction. The precise pathogenesis of barrier dysfunction in patients with chronic mucosal inflammation and its implications on tissue inflammation and systemic absorption of exogenous particles are only partly understood. Since epithelial barrier defects are linked with chronicity and severity of airway inflammation, restoring the barrier integrity may become a useful approach in the treatment of allergic diseases. We here provide a state-of-the-art review on epithelial barrier dysfunction in upper and lower airways as well as in the intestine and the skin and on how barrier dysfunction can be restored from a therapeutic perspective.

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Chicoine, Martin B., Bruce D. Mazer, Qutayba A. Hamid, and Christine T. McCusker. "Kinetics of allergic inflammation and airways hyperresponsiveness in a murine model of allergic rhinitis: The upper airway in lower airways disease." Journal of Allergy and Clinical Immunology 109, no. 1 (January 2002): S295. http://dx.doi.org/10.1016/s0091-6749(02)82038-3.

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Shapiro, Gail G. "Childhood Asthma: Update." Pediatrics In Review 13, no. 11 (November 1, 1992): 403–12. http://dx.doi.org/10.1542/pir.13.11.403.

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Definition and Pathophysiology Asthma is a reversible airways disease characterized by both smooth muscle hyperreactivity and airway inflammation. During the 1970s and early 1980s the focus was on smooth muscle constriction, and it was believed that better bronchodilators would greatly diminish our difficulties in controlling this condition. This, unfortunately, was not the case. The emphasis of therapy today has turned to airway inflammation. Lung biopsies from patients who have asthma show destruction of respiratory epithelium, basement membrane thickening, and inflammatory cellular infiltrate. Among the infiltrating cells are eosinophils, macrophages, and neutrophils that are called to the site of inflammation by the chemotactic products released by activated mast cells. Upon their arrival, these cells release their own products of inflammation, which amplify this immunologic response. A variety of neuropeptides also play a role, some serving to stabilize and others to destabilize the airway. One result of this airway inflammation is airways reactivity, also known as bronchial hyperresponsiveness. A common example of this scenario is the child who has allergic asthma and encounters a problematic allergen. This child has immunoglobulin E (IgE) to this allergen bound to mast cells in his or her airway. Upon exposure to the allergen, the binding of IgE and antigen triggers mast cell mediator release within minutes.

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Xu, Hui, Timothy B. Oriss, Barbro N. Melgert, Adam C. Henry, Li Chen, Andrew L. Mellor, David H. Munn, Charles G. Irvin, Prabir Ray, and Anuradha Ray. "Indoleamine 2,3-Dioxygenase is not required for tolerance induction in the airways but is important for allergic airway disease (39.8)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S26. http://dx.doi.org/10.4049/jimmunol.178.supp.39.8.

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Abstract Indoleamine 2,3 dioxgenase (IDO) has emerged as an important negative regulator of immune responses. However, the role of IDO in Th2 cell-mediated diseases is not completely clear. We investigated the role of IDO in the induction of inflammation or tolerance in the airways in response to ovalbumin (OVA). The results of these experiments show that IDO−/− mice are susceptible to tolerance induction. However, IDO−/− mice displayed significantly lower airway hyperresponsiveness (AHR), lower serum OVA-specific IgE and lower Th2 type cytokines (IL-5 and IL-13) in comparison to wt mice. In an OVA-induced chronic airway inflammation model, the IDO−/− mice also showed lower AHR and Th2 type cytokines in the lung and less infiltration of inflammatory cells in the airways. To dissect the mechanism underlying IDO-mediated promotion of allergic airway disease, we stimulated lung DC by allergens in vitro. The expression of important co-stimulatory molecules and MHC-II was lower in DCs from IDO−/− mice in comparison to those in DCs from wt control mice suggesting that the reduced airway Th2 type immune response in IDO−/− mice may be due, at least in part, to less effective co-stimulation between DCs and T cells. In summary, our data suggest that IDO is not required for the induction of airway tolerance, but may play a role in promoting Th2-induced allergic airway disease. Supported by NIH grants HL 77430 (to A.R) and HL60207 (to P.R.)

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Stemmy, Erik, and Stephanie Constant. "The role of cyclophilins in regulating leukocyte recruitment in chronic allergic asthma. (35.14)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 35.14. http://dx.doi.org/10.4049/jimmunol.184.supp.35.14.

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Abstract Chronic allergic asthma is an airway disease characterized by persistent inflammation. Elevated numbers of eosinophils, activated lymphocytes, and mast cells, as well as increased levels of IL-5, are detectable in the airways and lung tissues of asthmatic patients even in the absence of allergen challenge. The factors regulating this persistent inflammation are not known. While classical chemokines such as eotaxins 1-3, RANTES, MIP-1α, and MCP-1 are highly elevated after acute allergen challenge, they return to baseline levels by 24h after exposure. Although better known as intracellular chaperone proteins or as the target of the immunosuppressive drug cyclosporine A, extracellular cyclophilins are also potent chemoattractants that are elevated during lung inflammation. We propose that extracellular cyclophilins could function as important chemoattractants regulating the leukocyte recruitment and persistence observed during the chronic phase of allergic asthma. To test this possibility, we made use of a mouse model of chronic asthma and inhibited the function of cyclophilins during the chronic phase of the disease using the drug NIM811, a non-immunosuppressive analog of cyclosporine A (provided by Novartis). Mice treated with NIM811 demonstrated a significant reduction (~50%) in airway and tissue inflammation upon acute allergen challenge. These findings suggest a potential role for cyclophilins in maintaining inflammation in chronic asthma.

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Larché, Mark. "Mechanisms of Peptide Immunotherapy in Allergic Airways Disease." Annals of the American Thoracic Society 11, Supplement 5 (December 2014): S292—S296. http://dx.doi.org/10.1513/annalsats.201402-090aw.

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Holgate, S. T., J. Corne, P. Jardieu, R. B. Fick, and C. H. Heusser. "Treatment of allergic airways disease with anti-IgE." Allergy 53 (September 1998): 83–88. http://dx.doi.org/10.1111/j.1398-9995.1998.tb04946.x.

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Bousquet, Jean, William Jacquot, A. Maurizio Vignola, Claus Bachert, and Paul Van Cauwenberge. "Allergic rhinitis☆A disease remodeling the upper airways?" Journal of Allergy and Clinical Immunology 113, no. 1 (January 2004): 43–49. http://dx.doi.org/10.1016/j.jaci.2003.09.047.

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48

Trivedi, S. G., and C. M. Lloyd. "Eosinophils in the pathogenesis of allergic airways disease." Cellular and Molecular Life Sciences 64, no. 10 (March 15, 2007): 1269–89. http://dx.doi.org/10.1007/s00018-007-6527-y.

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Daabis, Rasha. "Allergic Rhinitis and Asthma: The United Airways Disease." Pulmonary Research and Respiratory Medicine - Open Journal 3, no. 2 (September 9, 2016): e3-e4. http://dx.doi.org/10.17140/prrmoj-3-e005.

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Gorman, Shelley, Jacqueline P. McGlade, Misty J. M. Lambert, Deborah H. Strickland, Jennifer A. Thomas, and Prue H. Hart. "UV exposure and protection against allergic airways disease." Photochemical & Photobiological Sciences 9, no. 4 (2010): 571. http://dx.doi.org/10.1039/b9pp00136k.

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Journal articles on the topic 'Allergic Airways Disease'

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