Mechanisms of asthma and allergic inflammationAllergy and asthma
Section snippets
Eosinophil biology
If the years 2002 and 2003 signaled the death of the eosinophil in asthma, then 2004 was a comeback year. The exact role of the eosinophil in asthma and other allergic diseases remains somewhat controversial, but numerous articles in the JACI and elsewhere continue to provide interesting information on eosinophil biology and its potential relevance to diseases such as asthma.
Given the selective expression of the chemokine receptor CCR3 on eosinophils, Radinger et al,1 using the BALB/c ovalbumin
Mast cells and basophils
Since its US Food and Drug Administration approval and introduction to the market in September 2003, omalizumab (Xolair; Novartis, Genentech Pharmaceuticals) provides the latest option for management of moderate-to-severe persistent asthma. In addition to its direct ability to block IgE attachment to FcεRI, studies uncovered a remarkable ability of IgE to regulate surface expression of its own receptor.10 This initial report suggested the effect on circulating basophils was rapid and complete
Contribution of smooth muscle cells to airway inflammation in asthma
A model of the contribution of smooth muscle cells to airway inflammation in asthma is shown in Fig 1. Airway inflammation is a characteristic feature of asthma and likely contributes to both airway obstruction and airway hyperresponsiveness. Although many factors contribute to airway inflammation, studies to date have largely focused on the effect of cells recruited to the airway and their activation and release of inflammatory mediators to cause pulmonary dysfunction. During the past year,
Cysteinyl leukotrienes
A model of the role of cysteinyl leukotrienes in the generation of allergic inflammation is shown in Fig 2. To further understand the complexity and contribution of cysteinyl leukotrienes to processes of airway inflammation in asthma, Parameswaran et al27 at McMaster University evaluated the effect of the leukotriene receptor antagonist pranlukast on allergen-induced changes in circulating dendritic cells in patients with mild asthma. Blood samples were obtained before and 3 and 24 hours after
Nitric oxide
Nitric oxide (NO) generation is associated with ongoing airway inflammation. Measurements of exhaled nitric oxide (eNO) have begun to serve as a biomarker for the presence of airway inflammation, and a reduced eNO level is an indicator of positive responses to anti-inflammatory medications, such as corticosteroids. Mahut et al29 evaluated levels of eNO in 28 children with refractory asthma, which they defined as persistent airflow limitation, or exacerbations, despite the use of high-dose
T cells in asthma
Using a rodent model, Isogai et al31 evaluated the hypothesis that T cells might migrate from the airways to the bone marrow to stimulate cells at this location and thus perpetuate the inflammatory response. Using the Brown Norway rat, the investigators introduced purified fluorescein-labeled CD4+ T cells into the trachea of naive or sensitized animals. Eighteen hours later, the rats were challenged with antigen, and cells were then harvested from the bone marrow, BAL fluid, lungs, lung blood
Genetics
The association of genes and their polymorphisms with features of asthma has been an important advance over the past decade. Last year saw a number of studies that evaluated the associations of various genes with features of asthma. As noted in a number of these articles, replication of earlier reports is essential to confirm these genetic associations. From these studies, it has also become apparent that different populations of patients might have different asthma characteristics, and the
Conclusions
Our understanding and appreciation of allergic cellular events and their integration into diseases like asthma continues to expand. Although these processes appear complex and sometimes independent when presented as single articles, their contribution to the overall theme of allergic diseases becomes more apparent when looked at over a longer time period, such as the past year. The JACI has been pleased to provide its readers with new and key observations that help to fit the puzzle together
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Cited by (139)
Immunomodulatory and anti-inflammatory effects of Aerva lanata in ovalbumin induced allergic asthmatic mice
2022, Journal of EthnopharmacologyCitation Excerpt :Allergic asthma is a prolonged lungs inflammation due to infiltration of eosinophils, neutrophils and leukocytes into the bronco-alveolar fluid (BALF). As, inflammation is regarded the initial and lasting characteristic of asthma, treatment of asthma focuses on long-term inflammation management (Bochner and Busse, 2005; Yang et al., 2010). It has been found that infiltrating eosinophils in the lungs induce T-helper 2 (Th2) type immune reactions primarily by exposing antigens (Kool et al., 2011).
Morin ameliorates ovalbumin-induced allergic rhinitis via inhibition of STAT6/SOCS1 and GATA3/T-bet signaling pathway in BALB/c mice
2019, Journal of Functional FoodsCitation Excerpt :Infiltration of inflammatory cells like eosinophils is a characteristic feature of inflammatory immune disorders including asthma, AR, atopic dermatitis, etc. (Bochner & Busse, 2005). Efflux of eosinophils in the environment of the nasal mucosa is the hallmark of nasal hypersensitivity with a non-specific allergen which occurs in AR patients (Bochner & Busse, 2005). It is thought that eosinophils play an important role in carrying out histopathologic and physiologic impairment in nasal mucosa via the release of eosinophil-derived cytotoxic proteins including eosinophils cationic protein, major basic protein, and eosinophil peroxidase (EPO).
Cohabitation with a sick partner increases allergic lung inflammatory response in mice
2014, Brain, Behavior, and Immunity
Disclosure of potential conflict of interest: B. Bochner is a paid consultant for Amgen, Aventis, and GlaxoSmithKline and a codiscoverer with GlaxoSmithKline of Siglec-8, for which they share a patent; he is on the Speakers' Bureau for Merck, Genentech, and Novartis; and he is on advisory boards for Pfizer and Glycomimetics, Inc. W. W. Busse has consultant arrangements with Bristol-Meyers Squibb, Dynavax, Hoffman Laroche, and Fujisawa; has received grants–research support from GlaxoSmithKline, Fujisawa, Aventis, Hoffman Laroche, and Pfizer; is on the speakers' bureau for Merck, GlaxoSmithKline, and Aventis; and is on advisory boards for GlaxoSmithKline, Aventis, Pfizer, and AstraZeneca.