Mouse models of allergic diseases.
ABSTRACT The increasing prevalence of allergic diseases worldwide is posing significant socio-economic challenges. The pathogenesis of these diseases reflects a complex interaction of genetic and environmental factors. The heterogeneity of disease phenotypes challenges the concept of single mechanisms of disease. As human experimentation is limited, animal models have been developed to provide insights into pathogenesis and potential for discovery of novel therapeutics. Mice have served in models of many of the allergic diseases including asthma, allergic rhinitis, food allergy, atopic dermatitis (AD), and allergic conjunctivitis. Although much has been learned from these investigations, there are limitations when these models are translated to the human diseases.
- SourceAvailable from: PubMed Central[Show abstract] [Hide abstract]
ABSTRACT: Asthma is a complex, inflammatory disorder characterized by airflow obstruction of variable degrees, bronchial hyper-responsiveness, and airway inflammation. Asthma is caused by environmental factors and a combination of genetic and environmental stimuli. Genetic studies have revealed that multiple loci are involved in the etiology of asthma. Recent cellular, molecular, and animal-model studies have revealed several cellular events that are involved in the progression of asthma, including: increased Th2 cytokines leading to the recruitment of inflammatory cells to the airway, and an increase in the production of reactive oxygen species and mitochondrial dysfunction in the activated inflammatory cells, leading to tissue injury in the bronchial epithelium. Further, aging and animal model studies have revealed that mitochondrial dysfunction and oxidative stress are involved and play a large role in asthma. Recent studies using experimental allergic asthmatic mouse models and peripheral cells and tissues from asthmatic humans have revealed antioxidants as promising treatments for people with asthma. This article summarizes the latest research findings on the involvement of inflammatory changes, and mitochondrial dysfunction/oxidative stress in the development and progression of asthma. This article also addresses the relationship between aging and age-related immunity in triggering asthma, the antioxidant therapeutic strategies in treating people with asthma.Pharmaceuticals 02/2011; 4(3):429-456. DOI:10.3390/ph4030429
- [Show abstract] [Hide abstract]
ABSTRACT: Respiratory syncytial virus (RSV) is a common cause of severe lower respiratory tract diseases (bronchiolitis and pneumonia) during infancy and early childhood. There is increasing evidence which indicates that severe pulmonary disease caused by RSV infection in infancy is associated with recurrent wheezing and development of asthma later in childhood. However, the underlying mechanisms linking RSV infection to persistent airway hyperresponsiveness and dysfunction are not fully defined. To study these processes in ways which are not available in humans, animal models have been established and have provided valuable insight into the pathophysiology of RSV-induced disease. In this paper, we discuss experimental models of RSV infection in mice and highlight a new investigative approach in which mice are initially infected as neonates and then reinfected later in life. The findings shed light on the mechanisms underlying the association between early severe RSV infection and development of asthma later in childhood.07/2011; 2011:748038. DOI:10.1155/2011/748038
- [Show abstract] [Hide abstract]
ABSTRACT: Schizandra chinensis Baillon (SC) is traditionally used as a medicinal plant in the Orient. Recently, SC has become recognized as an adaptogen by the mainstream medical community. Phytoadaptogens influence respiratory, cardiovascular, uterus myotonic, and immune activities. Atopic dermatitis (AD) is an allergic inflammatory skin disease caused by aberrant and over-reactive immune responses. This study assessed the suppressive effect of SC extract (SCE) on 1-chloro-2,4-dinitrobenzene (DNCB)-induced AD in a NC/Nga mouse model. AD was induced by topically applying 0.2% DNCB to the hairless-back of NC/Nga mice for 4 weeks. Treated mice received SCE or dexamethasone after AD induction. SCE markedly suppressed DNCB-induced dermatitis, as determined by a count of scratching frequency; measurement of IgE, IgM, and histamine levels in serum; and histological observation of epidermal hyperplasia and mast-cell infiltration. Additionally, SCE lessened DNCB-induced histamine receptor mRNA expression in skin tissue and the splenic expressions of interleukin (IL)-4, IL-5, and high-affinity IgE receptor B protein. SCE appears useful for suppression of AD, even though the active pathway(s) remain unknown.Immunopharmacology and Immunotoxicology 08/2011; 34(2):292-8. DOI:10.3109/08923973.2011.602689 · 1.11 Impact Factor