Animal models are crucial in advancing our knowledge and understanding of pulmonary diseases. Using alternatives models, such as computer simulations, is simply not advanced enough to elucidate all the biological mechanisms inside a living creature.
Animal modelling in respiratory research must present translational pathologic characteristics to enable researchers to understand complex diseases including pulmonary fibrosis, asthma, and COPD (Chronic Obstructive Pulmonary Disorder). Mice are the primary choice for many research studies, with three main strains of mice typically used in respiratory research, A/J1, BALB/c2, and C57B/63. It is important to note that certain strains are better suited for some applications than others.
Asthma is a respiratory disease with a complex history. Guinea pigs were the most popular models in the past, as they have natural airway hyperresponsiveness and are easily sensitized.4 However, the murine models rapidly became the most commonly used model in the early 1990s.5 Mice are ideal for asthma studies as they are low cost, convenient, and various transgenic models are available. A/J mice have airways that are spontaneously hyperresponsive to bronchoconstricting agents, however BALB/c mice are typically used in immunological studies as they exhibit the TH2-biased immune response and produce monoclonal antibodies to a ovalbumin (OVA) and house dust mite (HDM) allergen.
Pulmonary fibrosis can be caused by various factors, including diseases, injury, aging, environmental exposures, drug administration, and idiopathic origins. In this application, C57BL/6 mice are the most common strain due to their fully known genome and transgenic possibilities. When developing the model, bleomycin is often used, however the method of bleomycin delivery can alter the pathogenesis. Endotracheal delivery may result in patchy distribution and heterogeneity, while ventilator-assisted drug delivery offers homogeneous distribution with lower doses. 6
COPD is an inherently heterogeneous disease, with both emphysema and chronic bronchitis components, controlled by susceptibility factors like environmental exposures and host genetics. The two most common COPD models include elastase delivery and cigarette-smoke exposures. While elastase is useful for simple exposures with rapid and significant lung injury development, it does not replicate the slow progression of COPD development. The gold standard for COPD models is the cigarette-exposure model, as it mimics human exposure more accurately, and A/J mice develop cigarette-smoke-induced emphysema more quickly than other strains.7
Welcome to SCIREQ’s knowledge center. You can find everything from software registration to document downloads to complete list of SCIREQ publications in this section. Everything you need to get the most out of your SCIREQ system.
