The experimental models have been extensively used over the centuries as important tools to elucidate the inflammatory mechanisms enrolled in the physiopathology of different diseases. The more we understand the mechanisms enrolled in the disease development and progression, the closer we are to therapeutic targets and consequent new proposals for therapeutic management. In respiratory diseases, such as chronic obstructive pulmonary disease, animal models have been useful and resemble several features observed in the clinic of this disease. Cigarette smoke (CS)- and Elastase-induced models have been the most employed models of COPD and highlight different inflammatory signaling pathways that orchestrate the development and progression of COPD. Thus, many potential future therapeutics for COPD whose are currently in clinical development were identified as potential therapeutic targets in pre-clinical research notably using experimental models. In this context, the advances in cellular and molecular techniques have been essential for the success of the development of experimental models to allow a deeper investigation of molecular mechanisms and possible biomarkers orchestrating COPD.

Since COPD is a multifactorial disease, it is difficult to find an animal model that resembles all clinical features at once. However, there are many experimental approaches described in the literature. And depending on the interest area, researchers could choose among them, based on the advantages and disadvantages of each model. For example, the CS-induced models are recognized by better representing the etiology of this disease in humans, since smoking is a main risk factor for COPD development due to the chronic inflammatory process induction. However, the elastase-induced models have been extensively used to describe the remodeling process of the different extracellular matrix components of tissue lung after its destruction by the proteases. At this moment, the scientific community has been moving efforts to elucidate the molecular mechanisms that orchestrate these events described in this disease physiopathology.

In this Research Topic, we aim to present a collection of manuscripts describing the newest findings in the cellular and molecular mechanisms enrolled in the inflammatory process and tissue lung destruction and remodeling based on the animal models of COPD. We welcome studies as Original Research, Method, Mini Review, and Case Report articles, focusing on, but not limited to, the following subtopics:

--Immunological mechanisms in COPD models
--Inflammatory signaling pathways in COPD models
--Inflammasomes in COPD
--Regulation of immunity by miRNA in COPD
--Immunological mechanisms in animal models of COPD exacerbation

Please note that manuscripts without a strong immunological focus (not just inflammation) are out of scope for this Research Topic.

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Frontiers in Immunology

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