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Asthma is a heterogeneous disease characterized by numerous phenotypes relating to age of onset, triggers, comorbidities, severity (assessed by multiple exacerbations, lung function pattern) and finally the inflammatory cells involved in the pathophysiologic pathway. These phenotypes can vary over time in relation to changes in the principal triggers involved in the aetiology of the disease. Nevertheless, in a patient with multiple allergies and early-onset disease (defined as multiple sensitizations and allergic comorbidities), the prognosis of asthma is poor with a high risk of persistence and severity of the disease during childhood. Future research will focus on classifying phenotypes into groups based on pathophysiologic mechanisms (endotypes) and the biomarkers attached to these endotypes, which could predict prognosis and lead to targeted therapy. Currently, these biomarkers are related to inflammatory cells associated with the asthma endotype, essentially eosinophils and neutrophils (and related cytokines) attached to Th-2 and non Th-1 pathways, respectively. The most severe asthma (refractory asthma) is linked to neutrophil-derived inflammation (frequently associated with female sex, obesity and possibly disorganized airway microbiota) encountered in very young children or teenagers. Severe asthma is also linked to or a marked eosinophil inflammatory process (frequently associated with multiple atopy and, more rarely, with non-atopic hypereosinophilic asthma in children) and frequently encountered in teenagers. Severe phenotypes of asthma could also play a role in the origin of chronic obstructive pulmonary disease in adult life. [ABSTRACT FROM AUTHOR]

Adherence in asthma is an important cause for concern. Although nearly 50% of asthma patients are considered poorly adherent to therapeutic advices, adherence is still difficult to assess, understand and improve despite major medical consequences. In this review, we revisited the literature of the last 10 years related to adherence in severe asthma. The concepts have changed and 'compliance' is usually replaced by 'adherence'. Assessment of adherence is addressing ethical issues, but provides important insight into difficult-to-treat asthma. Different tools have been used but none is routinely recommended. Health-related outcomes (poor control, exacerbations, hospitalizations, lung function decline), which are clearly associated with severe asthma, are often worsened by non-adherence with consequences also on patient related outcomes (quality of life). The potential behaviour associated with non-adherence and all other related factors including easy-to-recognize psychological traits can help for patient's future management. Therapeutic educational interventions have been recognized with a scientifically proven efficiency even though evolution and improvements are needed. A multidisciplinary approach is required in severe asthma. Therapeutic adherence for a given patient is always a prerequisite to any other aspects when addressing severe asthma phenotypes. Severe asthma should be considered only in those who still experienced poor asthma outcomes despite optimal adherence. At a glance, poor adherence and severe asthma should be considered antinomic. Better understanding of the causes and customised management are potential future directions. [ABSTRACT FROM AUTHOR]

Allergy to rodents in the workplace is an important occupational health problem affecting research, pharmaceutical and toxicological sectors and can have a serious impact on employees working in this area. Despite measures to reduce aeroallergen exposures to rodents in the workplace, there are few signs that this occupational health problem is declining. Rodent allergens are well characterized and exposure-response relationships have been demonstrated to be complex. More recently, the importance of rodent allergens outside of the workplace has been demonstrated in several studies of individuals with asthma. This review focuses on rodent allergy both in the workplace and in the home and examines the complex exposure-response relationships between allergen exposure and sensitization and asthma. Risk factors for rodent allergy and mechanisms of tolerance to rodent allergens are discussed. Cite this as: H. Jeal and M. Jones, Clinical & Experimental Allergy, 2010 (40) 1593-1601. [ABSTRACT FROM AUTHOR]

Background The role in allergic asthma development of the immune response against fungi with concomitant exposure to other common aeroallergens has yet to be determined. In particular, there is little understanding of how inhaled fungi affect the host response to mite allergens. Objective To characterize the in vitro and in vivo effects of concurrent exposure of Aspergillus fumigatus ( Af) and Dermatophagoides farinae ( Derf) on dendritic cells (DCs) in the development of allergic asthma. Methods Murine bone marrow-derived DCs were pulsed with Derf and/or live or heat-inactivated Af. Cytokine production and the expression of pathogen recognition receptors (PRRs) were determined in vitro. Subsequently, these DCs were inoculated into the airway of naïve mice to assess the development of allergic airway inflammation in vivo. The effect of antibodies against PRRs was also evaluated. Results Live Af significantly enhanced IL-10 production and the expression of Toll-like receptor (TLR) 2 and Dectin-1 in Derf-pulsed DCs. Live Af infection significantly attenuated Derf-pulsed DC-induced allergic airway inflammation in vivo. Antibodies against either TLR2 or Dectin-1 significantly reversed the inhibitory effects of live Af in the development of Derf-pulsed DC-induced allergic airway inflammation. Conclusion Concurrent exposure of DCs to fungal antigens has profound influences on the subsequent mite allergen-induced allergic airway inflammation. Live Af could regulate the functions of airway DCs in the development of mite allergen-induced allergic airway inflammation via regulation of their PRRs. Our results suggest that concurrent exposure to pathogens such as fungi and mite allergens has profound influences on the subsequent allergen-induced allergic airway inflammation. Furthermore, modulating PRR signalling could provide a therapeutic regimen for the development of asthma. Cite this as: S. Fukahori, H. Matsuse, T. Tsuchida, T. Kawano, S. Tomari, C. Fukushima and S. Kohno, Clinical & Experimental Allergy, 2010 (40) 1507–1515. [ABSTRACT FROM AUTHOR]

The author reflects on the study conducted by C. D. Thomson and colleagues regarding asthma in children. The author states that there had been no evidence in the relationship of dietary selenium levels with asthma which was tackled in the study and the effect of nutritional antioxidants to the development of asthma in children. An overview of the occurrence of allergic asthma in children is presented.