Lung or pulmonary fibrosis is a progressive condition where chronic inflammation and abnormal wound healing lead to the excessive deposition of collagen and extracellular matrix, causing stiffening of the lungs and impairing oxygen transfer.
Aragen is renowned for its consistency and reproducibility in Induced Pulmonary Fibrosis (IPF) models, a reputation built over the past two decades. We offer the following in vivo models, essential for advancing lung fibrosis treatment options and improving patient outcomes.
- Bleomycin-induced pulmonary fibrosis (IPF) in C57BL/6 Mice
- Disease stage-based in vivo models (Acute and Chronic)
- Age-related in vivo models (Young and Old)
- Silica-induced lung fibrosis: For studying silicosis and other fibrotic lung diseases.
Bleomycin-Induced Pulmonary Fibrosis (IPF) Mice Model
The bleomycin-induced pulmonary fibrosis model is a widely used preclinical tool to study idiopathic pulmonary fibrosis (IPF), a chronic and progressive lung disease in humans. Bleomycin, a chemotherapeutic agent that causes DNA damage, is commonly used to generate pulmonary fibrosis. The model is useful for studying stages of IPF (acute and chronic) and comparing the disease progression in young and old mice, as aging can influence the severity and course of fibrosis. As the most widely used preclinical model for IPF, it helps evaluate drug efficacy and deepens our understanding of the disease pathophysiology.
Methodology
Study animals: C57BL/6
Fibrosis induction: Clinical grade bleomycin-instilled via oropharyngeal route or osmotic pump
Option of test article administration: PO, IP, IV, IM, SC, nebulization, and osmotic pumps
Treatment regimen: Therapeutic or Prophylactic
Study Parameters
Disease Stage-Based Acute and Chronic In Vivo Models
This pulmonary fibrosis in vivo model involves using bleomycin or other fibrosis-inducing agents at different time points to create acute or chronic fibrotic conditions in the lungs. The significance of having both acute and chronic models lies in their ability to mirror various stages of disease progression, allowing researchers to examine the temporal aspects of fibrosis, inflammation, and tissue remodeling. This provides a comprehensive approach to studying lung fibrosis and evaluating potential therapies that may target different stages of disease.
Acute Bleomycin-Induced Lung Fibrosis Mice Model
The acute bleomycin-induced pulmonary fibrosis model in mice involves a single high-dose bleomycin instillation, leading to rapid inflammation, epithelial injury, and early fibrosis. This model reflects the acute phase of lung injury and fibrosis, making it ideal for studying inflammatory responses and early fibrotic changes.
Induction of lung fibrosis
Bleomycin
(Oropharyngeal administration)
Treatment
(IP, IV, SC, IM, ID, intranasal, sublingual)
Daily observations/body weights
Functional readouts, Terminate study/harvest organs
Endpoint analysis
(BAL leukocyte counts, cytokine analysis, Sircol assay, Hydroxyproline, Gene expression, Histology)
Consistency and Reproducibility: Bleomycin-Induced Pulmonary Fibrosis In Vivo Models
Robust Data from Multiple Case Studies
The bleomycin-induced lung fibrosis models have been extensively used in numerous preclinical studies successfully performed at Aragen, demonstrating high reproducibility and consistency in inducing fibrosis in C57BL/6 mice model. This reliability is crucial for evaluating the therapeutic potential of new anti-fibrotic agents and understanding the pathophysiological mechanisms that drive fibrosis. Detailed case studies highlight the robustness of these models, making them a cornerstone of lung fibrosis research. The consistent fibrotic induction allows for rigorous evaluation of drug candidates, validated through traditional histopathology, and enhanced by digital pathology, providing precise, quantifiable insights into the disease progression.
Chronic Bleomycin-Induced Lung Fibrosis Mice Model
The chronic bleomycin-induced pulmonary fibrosis model in mice involves repeated bleomycin instillations, leading to progressive inflammation, fibrosis, and lung remodeling over the time. This model closely mimics human Idiopathic Pulmonary Fibrosis (IPF), with persistent fibrosis that worsens rather than resolving. It is ideal for studying the long-term progression of fibrosis, chronic inflammation, and potential therapeutic interventions for advanced disease.
Repetitive Bleomycin induction Day 0, week 2, week 4
(oropharyngeal administration)
Treatment
(options: IP, IV, SC, IM, ID, intranasal, sublingual)
Daily observations/body weights
Functional readouts, Terminate study/harvest organs
Endpoint analysis
(BAL leukocyte counts, cytokine analysis, Sircol assay, Hydroxyproline, Gene expression, Histology)
Age-based In Vivo Lung Fibrosis Mice Model
Aged mice models are used to study the development of lung fibrosis in the context of aging. As the body ages, the ability to repair lung tissue diminishes, and fibrosis may develop more rapidly. This model is important for understanding how aging accelerates the progression of lung fibrosis and can be used to explore age-specific therapies that target senescence, cellular repair mechanisms, and the inflammatory response in aging lungs.
Induction of lung fibrosis:
bleomycin administration (oropharyngeal route)
Treatment
(IP, IV, SC, IM, ID, Intranasal, Sublingual)
Daily observations/body weights
Functional readouts, Terminate study/harvest organs
Endpoint analysis
(BAL leukocyte counts, cytokine analysis, Sircol assay, Hydroxyproline, Gene expression, Histology)
Silica-Induced Lung Fibrosis Model
Aragen offers silica-induced pulmonary fibrosis model in mice, where silica instillation induces persistent inflammation in the alveoli, leading to progressive fibrotic processes that do not resolve over time. This model replicates non-resolving lung fibrosis, providing a reliable platform for assessing disease progression and evaluating antifibrotic therapies in preclinical studies. It closely mimics human interstitial lung diseases, such as silicosis, offering insights into the inflammatory and fibrotic processes involved, and is valuable for studying environmental and occupational causes of lung fibrosis and testing potential treatments.
Silica-Induced Lung Fibrosis Model
Aragen offers silica-induced pulmonary fibrosis model in mice, where silica instillation induces persistent inflammation in the alveoli, leading to progressive fibrotic processes that do not resolve over time. This model replicates non-resolving lung fibrosis, providing a reliable platform for assessing disease progression and evaluating antifibrotic therapies in preclinical studies. It closely mimics human interstitial lung diseases, such as silicosis, offering insights into the inflammatory and fibrotic processes involved, and is valuable for studying environmental and occupational causes of lung fibrosis and testing potential treatments.
Induction of lung fibrosis:
Silica administration (oropharyngeal route)
Treatment
(IP, IV, SC, IM, ID, Intranasal, Inhalation, Sublingual)
Daily observations/body weights
Terminate study/harvest organs, functional readouts
Endpoint analysis
(BAL leukocyte counts, cytokine analysis, Sircol assay, Hydroxyproline, Gene expression, Histology)
