Oxidative stress in allergic respiratory diseases

There is ample evidence that allergic disorders, such as asthma, rhinitis, and atopic dermatitis, are mediated by oxidative stress. Excessive exposure to reactive oxygen and nitrogen species is the hallmark of oxidative stress and leads to damage of proteins, lipids, and DNA. Oxidative stress occurs not only as a result of inflammation but also from environmental exposure to air pollution and cigarette smoke. The specific localization of antioxidant enzymes in the lung and the rapid reaction of nitric oxide with reactive oxygen species, such as superoxide, suggest that antioxidant enzymes might also function as cell-signaling agents or regulators of cell signaling. Therapeutic interventions that decrease exposure to environmental reactive oxygen species or augment endogenous antioxidant defenses might be beneficial as adjunctive therapies for allergic respiratory disorders.     

Asthma and allergic diseases: Cross talk of immune system and environmental factors

Air pollution and immune-related diseases including allergy and asthma are constantly on the rise worldwide. Thus, a comprehensive investigation of environmentally induced immune regulation is required for a deeper understanding of disease pathogenesis, progression as well as prevention. Here, we summarize the current knowledge on environmental factors such as microbiome or geographical locations with harmful or protective effects for human health and their different routes of exposure. This review comprises a brief outline regarding the latest findings on the interaction of environmental factors with innate and adaptive regulation of the immune system, exemplarily for one protective and one harmful environmental factor, respectively.     

Fungi and allergic lower respiratory tract diseases

Asthma is a common disorder that in 2009 afflicted 8.2% of adults and children, 24.6 million persons, in the United States. In patients with moderate and severe persistent asthma, there is significantly increased morbidity, use of health care support, and health care costs. Epidemiologic studies in the United States and Europe have associated mold sensitivity, particularly to Alternaria alternata and Cladosporium herbarum, with the development, persistence, and severity of asthma. In addition, sensitivity to Aspergillus fumigatus has been associated with severe persistent asthma in adults. Allergic bronchopulmonary aspergillosis (ABPA) is caused by A fumigatus and is characterized by exacerbations of asthma, recurrent transient chest radiographic infiltrates, coughing up thick mucus plugs, peripheral and pulmonary eosinophilia, and increased total serum IgE and fungus-specific IgE levels, especially during exacerbation. The airways appear to be chronically or intermittently colonized by A fumigatus in patients with ABPA. ABPA is the most common form of allergic bronchopulmonary mycosis (ABPM); other fungi, including Candida, Penicillium, and Curvularia species, are implicated. The characteristics of ABPM include severe asthma, eosinophilia, markedly increased total IgE and specific IgE levels, bronchiectasis, and mold colonization of the airways. The term severe asthma associated with fungal sensitization (SAFS) has been coined to illustrate the high rate of fungal sensitivity in patients with persistent severe asthma and improvement with antifungal treatment. The immunopathology of ABPA, ABPM, and SAFS is incompletely understood. Genetic risks identified in patients with ABPA include HLA association and certain T(H)2-prominent and cystic fibrosis variants, but these have not been studied in patients with ABPM and SAFS. Oral corticosteroid and antifungal therapies appear to be partially successful in patients with ABPA. However, the role of antifungal and immunomodulating therapies in patients with ABPA, ABPM, and SAFS requires additional larger studies.     

Immunology, climate change and vector-borne diseases

Global climate change might expand the distribution of vector-borne pathogens in both time and space, thereby exposing host populations to longer transmission seasons, and immunologically naive populations to newly introduced pathogens. In the African highlands, where cool temperatures limit malaria parasite development, increases in temperature might enhance malaria transmission. St Louis encephalitis viral replication and the length of the transmission season depend upon ambient temperature. Warming temperatures in the American southwest might place at risk migratory, non-immune elderly persons that arrive in early fall to spend the winter. Warm temperatures might intensify or extend the transmission season for dengue fever. Immunologists should examine this interplay between human immunocompetence and vector-borne disease risks in a warmer world.     

Precipitating factors in respiratory allergic disease in Indonesian children

Skin test results and IgE antibody levels measured by RAST indicate that hyper-sensitivity to house dust mite (D. pteronyssinus) is a major feature of asthma and allergic rhinitis in Indonesian children. Total serum IgE levels were higher in the allergic than in control children. 60% (twenty-one out of thirty-five) of the asthmatic children and 56% (five out of nine) of the children with allergic rhinitis had IgE antibodies to the helminth Ascaris lumbricoides compared with none out of four control children. A tendency was found for high IgE antibody levels to D. pteronyssinus to occur in association with low IgE antibody levels to A. lumbricoides and vice versa.     

Environmental urban factors (air pollution and allergens) and the rising trends in allergic respiratory diseases

Respiratory allergic diseases such as rhinitis and bronchial asthma appear to be increasing worldwide, affecting in particular subjects living in urban areas, and the reasons for this increase are still largely unknown. Although the role played by air pollution has yet to be clarified, a body of evidence suggests that urbanization, with its high levels of vehicle emissions and a westernised lifestyle are linked to the rising frequency of these diseases observed in most industrialized countries. Laboratory studies confirm the epidemiological evidence that inhalation of some pollutants, either individually or in combination, adversely affect lung function in asthmatics. Air pollutants may not only increase the frequency and intensity of symptoms in already allergic patients but may promote airway sensitization to airborne allergens in predisposed subjects. By attaching to the surface of pollen grains and of plant-derived paucimicronic particles, pollutants can modify the morphology of these antigen-carrying agents and alter their allergenic potential. In addition, by inducing airway inflammation, pollutants may overcome the mucosal barrier and so 'prime' allergen-induced responses. In other words airway mucosal damage and impaired mucociliary clearance induced by air pollution may facilitate the access of inhaled allergens to the cells of the immune system.