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ThrombosisHypertensionWound HealingRadiation Countermeasures - Acute Radiation Syndrome (ARS)Parkinson’s DiseaseAutism Spectrum DisorderDepression
Neuroscience and Additional ModelsBioModels offers customized solutions by working with clients to develop novel models for disease areas that may not be readily or easily standardized in the field. Furthermore, models are sometimes necessary for areas in biological research that are a bit less mainstream, representing niche areas of inquiry. At BioModels, requests from clients for custom models have been translated into the development of tested and validated models including thrombosis and blood pressure monitoring.
Assess your novel therapeutics for efficacy and mechanism of action in BioModels’ established thrombosis models. Thrombosis, the formation of a clot inside a blood vessel, can have devastating consequences, including death. BioModels’ thrombosis models allow you to evaluate blood clot formation in blood vessels. The BioModels team is experienced with a venous and arterial thrombosis models which are available with diverse experimental endpoints, such as:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Assess your novel therapeutics for efficacy and mechanism of action in BioModels’ established hypertension models. Hypertension, or high blood pressure, affects approximately 25% of the adult population in the United States. Left untreated, hypertension can lead to a number of health problems, such as heart disease, heart attack, and stroke. BioModels’ hypertension models allow you to evaluate high blood pressure by monitoring systolic and diastolic pressures. The BioModels team is experienced with spontaneous and diet-induced hypertension models which are available with diverse experimental endpoints, such as:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Assess your novel therapeutics for efficacy in BioModels’ established wound healing models. Chronic nonhealing wounds are correlated with diseases such as diabetes, hypertension, chronic kidney disease and can have huge quality of life effects on patients. BioModels’ wound healing models allow you to evaluate the complex biological processes associated with healing and repair. The BioModels team is experienced with splinted wound healing model which is available with diverse experimental endpoints, such as:
At BioModels, you can assess your novel therapeutics for efficacy and mechanism of action in our established models of Acute Radiation Syndrome (ARS) to address unmet clinical needs for patients. ARS refers to an acute illness caused by exposure to a high dose of penetrating radiation to the body which can affect three distinct areas of the body, the bone marrow, the gastrointestinal tract (GI-ARS), and the cardiovascular/central nervous system (CNS). We offer well-established mouse models of both total body irradiation (TBI) and gastrointestinal tract-focused toxicity through shielding of the long bones to assess critical disease mechanisms and phenotypes. Our literature-validated experimental endpoints include:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Assess your experimental materials for efficacy and mechanism of action in BioModels’ established Parkinson’s Disease model. Parkinson’s disease is a neurodegenerative disorder that results in motor dysfunction. BioModels’ Parkinson’s Disease model captures a spectrum of disease phenotypes, including behavioral and histological endpoints. We offer diverse experimental endpoints, such as:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Assess your novel therapeutics for efficacy in BioModels’ established autism spectrum disorder model. Autism is characterized by impairments in social and communication skills and is diagnosed early in childhood development. BioModels’ autism model allows you to evaluate deficits in social behaviors including social approach, social interaction and abnormal ultrasonic vocalizations. The BioModels team is experienced with the BTBR autism model which is available with experimental endpoints, such as:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Assess your novel therapeutics for efficacy in BioModels’ established depression models. Major depression is a debilitating mental illness, symptoms can include listlessness, feeling hopeless, thoughts of death or suicide, and anhedonia. BioModels’ depression models allow you to screen potential antidepressant therapies. The BioModels team is experienced with the forced swim test and tail suspension test which are available with experimental endpoints, such as:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Study Models
The venous thrombosis model can be used to evaluate the impact of anti-coagulants and has been used to evaluate the potential for compounds to increase the propensity for clot formation. In rodents, thrombus is induced by the direct application of a solution of ferric chloride (FeCl3) to the adventitial surface of the femoral vein. Thrombus formation is measured using intravital video microscopy alone or in combination with a laser Doppler flow probe to monitor vessel occlusion. In addition to the primary endpoint of time to complete occlusion, other flow parameters, including a visual evaluation of blood flow using the Thrombolysis in Myocardial Infarction (TIMI) scoring scale, are assessed. In mice, test article responses can be compared to the effects of Lovenox (Enoxaparin sodium).
Laser Doppler flow monitor which utilizes non-invasive surface probes is used to measure femoral vein blood flow in thrombosis-induced animals.
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The arterial thrombosis model can be used to compare the anti-thrombogenic activities of novel therapeutics to provide a pre-clinical means of assessing the potential benefits of new drugs and drug combinations in reducing the risk of arterial thrombosis. In rodents, thrombus is induced by the direct application of a solution of ferric chloride (FeCl3) to the adventitial surface of the carotid artery. Thrombus formation is measured using intravital video microscopy alone or in combination with a laser Doppler flow probe to monitor vessel occlusion. In addition to the primary endpoint of time to complete occlusion, other flow parameters, including a visual evaluation of blood flow using the Thrombolysis in Myocardial Infarction (TIMI) scoring scale, are assessed.
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Study Models
The spontaneous hypertension model can be used to evaluate the potential benefits of novel therapeutics, and drug combinations in reducing high blood pressure. Spontaneous hypertension is modeled using rodents that have a genetic predisposition to developing hypertension. Non-invasive blood pressure monitoring is employed to evaluate systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate.
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The diet-induced hypertension model can also be used to evaluate the potential benefits of novel therapeutics, and drug combinations in reducing high blood pressure. Hypertension is induced in Dahl-Salt Sensitive rats by a high salt diet. High blood pressure is observed from approximately 1 week on high salt diet. Non-invasive blood pressure monitoring is employed to evaluate systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate.
Blood pressure is monitored twice a week in Dahl-Salt sensitive rats using a non-invasive blood pressure system to measure mean arterial blood pressure (top), systolic blood pressure (middle) and diastolic blood pressure (bottom).
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Study Models
Wound healing can be modeled using normal animals or diabetic animals that have a predisposition for impaired wound healing. After being anesthetized, animals have a full-thickness area of skin removed from the center of the back. Animals are evaluated daily for weight change and three times a week for wound healing progression. Wounds can either be splinted, which prevents wound closure by skin contraction and thus allowing wounds to heal through granulation and re-epithelialization, a process similar to that in humans, or be left to heal with contraction allowed to contribute to the wound healing process.
Animals are weighed daily, and body weight change as compared to Day 0 is calculated. The AUC is calculated to compare treatment groups and is shown in the inset. (**** p<0.0001; compared to db/db group)
Wound length and width is measured 3x/week from Day 0 until end of the study. The AUC is calculated to compare treatment groups and is shown in the inset. (*** p<0.001; compared to db/db group)
Blood glucose levels are measured on Day -1 and at sacrifice on Day 28. (**** p<0.0001; compared to db/db group)
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Study Models
There is a critical need to develop therapies to prevent radiation exposure related deaths resulting from gastrointestinal and bone marrow toxicities. Currently, only potassium iodide is recognized as a radio-protectant in this context, protecting only the thyroid from ingested radioactive iodine. At BioModels, evaluate your test compounds for efficacy in targeting the GI tract, the bone marrow, or both in our total body irradiation mouse model. Non-anesthetized animals are placed in a pie-shaped multi-chamber plastic restrainer and placed inside the radiation source. A single, precise dose of total body irradiation (x-ray) at varying levels is administered to groups of mice to generate a dose response curve. The radiation dose can be titrated to achieve the lethal dose appropriate for your study. The main endpoints of the model include survival and body weight change. Histological endpoints can also be examined to address the mechanism of action.
C57Bl/6 animals that receive TBI (x-ray) are weighed daily, and body weight change as compared to Day 0 are calculated and shown over the course of the study for each radiation (x-ray) dose level.
Survival of C57Bl/6 mice that receive TBI (x-ray) is tracked daily over the course of the study.
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Exposure to high levels of ionizing radiation results in toxicities of the gastrointestinal (GI) tract that often lead to death. There is a critical need to develop therapies that treat the damaged GI tract to reduce or prevent exposure-related deaths. At BioModels, evaluate your test compounds for efficacy in targeting the GI tract in our validated GI-directed acute radiation syndrome mouse model. In this model, one hind limb of an anesthetized animal is protected using a lead shield while a single, precise dose of total body irradiation (x-ray) is delivered. The main endpoints of the model include survival and body weight change. Histological endpoints can also be examined to address the mechanism of action.
C57Bl/6 animals that receive TBI with long bone protection are weighed daily, and body weight change as compared to Day 0 are calculated and shown over the course of the study for each radiation (x-ray) dose level.
Survival of C57Bl/6 mice that receive TBI (x-ray) with long bone protection is tracked daily over the course of the study.
C57Bl/6 mice receive TBI (x-ray) with long bone protection. Representative images show the epithelial architecture of the villi and crypts of normal jejunum (A) and damaged jejunum (B) 4 days after exposure to radiation.
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Study Models
The MPTP model of Parkinson’s Disease is among the most widely used in the indication. Pathologically, it presents with dopaminergic neuron loss in the substantia nigra with associated depletion of striatal neuron terminals/dopamine levels. Additionally, the model may present with some behavioral deficits. Rotarod trials are employed to evaluate motor dysfunction; diseased animals demonstrate reduced latencies to fall from the rod.
Animals are evaluated for motor dysfunction via rotarod assessment.
Samples are assessed for dopaminergic neuron loss by tyrosine hydroxylase staining of the substantia nigra.
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Study Models
BioModels offers a BTBR autism model. Autism spectrum disorder is modeled using BTBR mice which display several symptoms of autism including reduced social interactions, and abnormal vocalizations. These unique behavioral phenotypes of the BTBR mouse represent possible analogs to social and communication deficits presented in the human condition. BioModels has validated an index of sociability in BTBR mice using the three chambered social approach test. This model is well-published and translatable to social and communication deficits presented in the human condition.
Mice are free to explore 3 chambers: one with a confined mouse (stranger), one with a novel object (center), and one empty, as a measure of social preference. (** p<0.01, **** p<0.0001; compared to stranger)
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Study Models
The forced swim test, also known as the Porsolt test, is a well-published and widely used method for screening antidepressant compounds. In this model, rodents are placed in a cylindrical tank filled with water and the time spent immobile versus struggling is measured. Immobility is thought to be an index of a depressive-like state which can be reduced by antidepressant treatment.
Mice or rats are placed in an inescapable chamber filled with water and time spent immobile is measured. (**p<0.01; compared to saline)
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The tail suspension test is similar to the forced swim test, but instead of using water, rodents are hung by their tails. The time spent immobile is measured as an index of a depressive-like state which can be reduced by antidepressant treatment.
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Pulmonary FibrosisSpecific Disease: Allergic AsthmaSpecific Disease: Acute Lung Injury, ARDS, and COPD
Pulmonary DiseaseBioModels has extensive experience with a variety of animal models that capture critical mechanisms of pulmonary disease. Work with our team to:
For more information or to set up an introductory call, please email info@biomodels.com.
Assess your experimental materials for efficacy and mechanism of action in BioModels’ established pulmonary fibrosis models. Pulmonary fibrosis is a chronic/progressive lung disease that presents with difficulty breathing due to thickened and scarred lung tissue. BioModels’ pulmonary fibrosis models capture a spectrum of disease mechanisms, allowing you to select the model most relevant for your hypothesis. The BioModels team is experienced with numerous preclinical pulmonary models, including bleomycin- and radiation-induced in vivo models and an in vitro model of fibrosis. Experimental endpoints for these models include:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Assess your experimental materials for efficacy and mechanism of action in BioModels’ established allergic asthma models. Asthma is a condition in which inflammation of the airways results in difficulty breathing, shortness of breath and wheezing. BioModels’ asthma models capture a spectrum of disease mechanisms, allowing you to select the model most relevant for your hypothesis. The BioModels team is experienced with numerous preclinical rodent allergic asthma models, including acute and chronic models that utilize various common allergens, and diverse experimental endpoints, such as:
Assess your experimental materials for efficacy and mechanism of action in BioModels’ established acute lung injury models. Acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and chronic obstructive pulmonary disease (COPD) are diseases characterized by neutrophilic inflammation of the lung and marked decreases in lung compliance in ALI or ARDS. In COPD however, there is increased lung compliance associated with progressive lung destruction. BioModels’ ALI models capture a spectrum of disease mechanisms, allowing you to select the model most relevant for your hypothesis. The BioModels team is experienced with numerous preclinical ALI models, including lipopolysaccharide (LPS) – and hydrochloric acid (HCl) -induced in vivo models. Experimental endpoints for these models include:
Don’t see what you’re looking for? We’re happy to discuss a customized option and/or establish a new model to fit your study needs.
Study Models
The intratracheal (IT) bleomycin-induced pulmonary fibrosis model is the standard model of human lung fibrosis. After being anesthetized, animals have a cannula inserted into the trachea and down into the lungs and then bleomycin is slowly infused into the lungs. Animals are evaluated daily for body weight and respiratory status. After animals are sacrificed, lung weight, collagen content and fibrosis scores are determined.
C57Bl/6 mice are administered Bleomycin once on Day 0 by intratracheal route. Endpoints are assessed on Day 21.
Pathology assessment of Day 21 lungs from IT-Bleomycin administered animals. Ashcroft score was determined in H&E-stained tissue using a modified Ashcroft Scale graded from 0-8. Fibrosis score was determined in Masson’s Trichrome-stained tissue using a 0-5 semi-quantitative scoring scale of area staining positive for collagen. Infiltrate score was determined in H&E-stained tissue using a 0-5 semi-quantitative scoring scale based on severity of mononuclear cell infiltration. Images are from animals receiving saline or 3.0 U/kg Bleomycin. Histopathology, immunohistochemistry, and analysis were performed by Dallas Tissue Research. (*p<0.05 compared to the saline-control)
Alpha smooth muscle actin (αSMA) and Collagen I + III Immunohistochemistry in Day 21 lungs from IT-Bleomycin administered animals. Whole slide images were used for global and regional αSMA quantification using a deep learning algorithm. Images are from animals administered either saline or 3.0 U/kg Bleomycin. Histopathology, immunohistochemistry, and analysis were performed by Dallas Tissue Research.
Wet lung weight and wet lung weight normalized to Day 21 body weight of Day 21 lungs from IT-Bleomycin administered animals.
IT-Bleomycin administered animals are weighed daily, and body weight compared to Day 0 is calculated. The AUC is calculated to compare treatment arms and is shown in the inset. (*p<0.05 compared to the saline-control)
IT-Bleomycin administered animals have lung mechanics measured on Day 21 using a flexiVent mechanical ventilator. Improved lung function is observed in mice administered intratracheal bleomycin when treated with either pirfenidone or anti-TGFβ neutralizing antibody. (**p<0.01 compared to the naïve group)
Lungs from IT-Bleomycin administered animals were collected on Day 21, processed for histopathology, and a modified Ashcroft score was assigned by a board-certified veterinary pathologist. Fixed tissue was also assessed for percent area of fibrotic lung tissue. Pulverized lung samples were assessed hydroxyproline. Lower levels of fibrosis are observed in mice administered intratracheal bleomycin when treated with either pirfenidone or anti-TGFβ neutralizing antibody. (*p<0.05; **p<0.01; ***p<0.001 compared to the naïve group)
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The systemic (SC osmotic pump) bleomycin-induced pulmonary fibrosis model induced by subcutaneously (SC) administering bleomycin over the course of 28 days. To induce disease, an osmotic pump containing bleomycin is subcutaneously implanted in the backs of anesthetized mice. Animals are evaluated daily for body weight and respiratory status. Following planned euthanasia, lung weight, collagen content and fibrosis scores are determined.
C57Bl/6 mice are administered Bleomycin for 28 days through a SC implanted osmotic pump and Day 28 lungs are processed for histopathology. H&E-stained lungs from animals administered saline or 50 mg/kg, 100 mg/kg, or 150 mg/kg Bleomycin.
C57Bl/6 mice are administered Bleomycin for 28 days through a SC implanted osmotic pump. Pathology assessment of Day 28 lungs from SC Osmotic Pump-Bleomycin administered animals. Ashcroft score is determined in H&E-stained tissue using a modified Ashcroft Scale graded from 0-8. Fibrosis score is determined in Masson’s Trichrome-stained tissue using a 0-5 semi-quantitative scoring scale of area staining positive for collagen. (*p<0.05 compared to the saline-control).
C57Bl/6 mice are administered Bleomycin for 28 days through a SC implanted osmotic pump. Animals are weighed daily, and body weight compared to Day 0 is calculated. The AUC is calculated to compare treatment arms and is shown in the inset. Wet lung weight normalized to Day 28 body weight of Day 28 lungs from SC Osmotic Pump-Bleomycin administered animals. (*p<0.05; ***p<0.001 compared to the saline-control).
C57Bl/6 mice are administered Bleomycin for 28 days through a SC implanted osmotic pump and BAL fluid is assessed at 28 days for total cells and total neutrophils following administration of either 50 mg/kg, 100 mg/kg, or 150 mg/kg Bleomycin. (*p<0.05; **p<0.01 compared to the saline-control).
C57Bl/6 mice are administered Bleomycin for 28 days through a SC implanted osmotic pump and lung mechanics are assessed at 28 days following administration of either 50 mg/kg, 100 mg/kg, or 150 mg/kg Bleomycin. (*p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 compared to the saline-control).
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The radiation-induced pulmonary fibrosis model is induced by targeting a dose of radiation specifically to the thorax of a mouse, developing disease over the course of 4-6 months. While fibrosis is slow to develop in this model, changes in lung function can be detected as early as 8 weeks post-irradiation. After being anesthetized, a single dose of radiation is targeted to the thorax, while the remainder of the body is protected with a lead shield. Animals are evaluated daily for body weight and respiratory status. After animals are sacrificed, lung weight, collagen content and fibrosis scores are determined.
Lung mechanics are measured at either 4, 8, 12, or 16 weeks following administration of 20 Gy of radiation targeted to the thorax using a flexiVent mechanical ventilator. After 16 weeks, lung elastance (Ers) and tissue elastance (H) are increased in animals that received targeted radiation to the thorax.
Total cells and neutrophils recovered in broncho-alveolar lavage fluid at week 16 of a radiation-induced pulmonary fibrosis model.
Animals are singly housed with a running wheel following administration of 20 Gy of radiation targeted to the thorax on Day 0. Daily distance traveled on the running wheel is recorded.
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At BioModels, we utilize a human in vitro model of TGF-β-induced fibrosis to screen potential therapeutics. TGFβ is added to confluent normal human lung fibroblasts (NHLF) for 48 hours. Supernatants and cell lysates are collected for endpoint analysis. Protein levels of Procollagen type 1-C peptide (PIP) and Plasminogen activator Inhibitor-1 (PAI-1) are determined to evaluate progression of fibrosis. Additionally, alpha smooth muscle actin (αSMA) is measured to indicate myofibroblast formation.
Confluent NHLFs are incubated for 48 hours with TGFβ. Levels of PIP and PAI-1 are assessed in cell culture supernatant and αSMA is measured in the cell lysate. (**p<0.01; ****p<0.0001 compared to the saline-control).
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Study Models
BioModels offers a mouse model of ovalbumin (OVA) induced allergic asthma. In the acute model, mice are sensitized with an intraperitoneal (IP) injection of OVA and adjuvant and then challenged with intranasal delivery of OVA followed by collections on day 16. Chronic versions of this model run from 4-12 weeks. The OVA model recapitulates many of the hallmarks of allergic asthma in humans, including elevated IgE and Th2 related cytokines, mucus hypersecretion, airway inflammation, goblet cell hyperplasia, epithelial hypertrophy, and airway hyperreactivity. Endpoints in this model include total and differential cell counts and inflammatory mediator content in the broncho-alveolar lavage fluid, airway hyperreactivity and detailed lung mechanics, as well as histopathology and immunohistochemistry.
BALB/c mice are sensitized with an IP injection of OVA with adjuvant on days 0 and 7. Mice are then challenged with OVA intranasally on days 13, 14, and 15 and endpoints are assessed on day 16. Reference treatment animals receive 3 mg/kg dexamethasone 1 hour prior to the challenges.
Total cells and eosinophils recover in broncho-alveolar lavage fluid on day 16 of an OVA-induced acute allergic asthma model. Mice demonstrate a dose responsive increase in total cells and eosinophils. Dexamethasone lower total inflammatory cell counts and eosinophils in the BAL fluid.
Lung Resistance and Elastance is measured on day 16 of an OVA-induced acute allergic asthma model, following exposure to increasing doses of methacholine. Animals that are sensitized and challenged with OVA displayed increased lung resistance and elastance parameters in comparison to Naïve animals. 3 mg/kg Dexamethasone treatment reduced airway hyperreactivity in diseased animals.
H&E-stained lung sections from naïve mice and mice from an OVA-induced acute allergic asthma model with and without 3 mg/kg dexamethasone treatment. The infiltration of mixed inflammatory cells observed in diseased animals is decreased in animals treated with 3 mg/kg dexamethasone.
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BioModels offers house dust mite (HDM) models of allergic asthma. An example of the acute HDM regimen would include sensitization on days 0 and 7 via the respiratory tract, challenge on day 14 with endpoints on day 15. Similar to the OVA model, the HDM models recapitulate many of the chronic asthma hallmarks seen in humans, however the HDM models utilize more clinically relevant allergens, as well as a more relevant route of sensitization, the respiratory tract.
BALB/c mice are sensitized with an intranasal (IN) administration of HDM on days 0 and 7. Mice are then challenged with HDM intranasally on Day 14 and endpoints are assessed on day 15. Reference treatment animals receive 3 mg/kg dexamethasone 1 hour prior to the challenge.
Total cells, eosinophils, and neutrophils recovered in broncho-alveolar lavage fluid on day 15 of an HDM-induced acute allergic asthma model. Sensitized and challenged mice demonstrate an increase in total cells, eosinophils, and neutrophils. 3 mg/kg dexamethasone treatment lowered total cells, eosinophils, and neutrophils in the BAL fluid.
Lung Resistance is measured on day 15 of an HDM-induced acute allergic asthma model, following exposure to increasing doses of methacholine. Animals that are sensitized and challenged with HDM display increased lung resistance in comparison to Naïve animals. 3 mg/kg Dexamethasone or 1 mg/kg Fluticasone Propionate (FP) treatments reduced airway hyperreactivity in diseased animals.
H&E- and PAS-stained lung sections from naïve mice and mice from an HDM-induced acute allergic asthma model on day 15. Infiltration of mixed inflammatory cells are observed in diseased animals in comparison to Naïve animals. Increases in multifocal inflammation within alveolar spaces (black arrow) and surrounding vessels (red arrows) are observed in lungs of diseased animals. Larger bronchioles lined with moderate numbers of PAS-positive goblet cells (green arrows) can be seen in lungs of diseased animals whereas saline control lungs had PAS-negative cells (black arrows).
Significant increases in Th2 inflammatory mediators (IL-4, IL-5, and IL-6) are observed in BAL fluid of diseased animals, though changes in IL-1β, a Th1 cytokine are not observed. Levels of IL-4, IL-5, and IL-6 in BAL fluid are significantly lower in animals treated with either 3 mg/kg Dexamethasone (Dex) or 1 mg/kg Fluticasone Propionate (FP). (*p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 compared to the vehicle-control)
BALB/c mice are sensitized with a subcutaneous (SC) administration of 50 µg HDM in CFA on day 0. Mice are then challenged with 50 µg HDM intranasally on Day 14 and endpoints are assessed on day 16. Reference compound and test article treatments are generally administered on or around days 13-16.
Total cells, eosinophils, and neutrophils recovered in broncho-alveolar lavage fluid on day 16 of an HDM-induced severe asthma model. Sensitized and challenged mice demonstrate a significant increase in total inflammatory cells, eosinophils, and neutrophils in BAL fluid. (*p<0.05; ****p<0.0001 compared to the vehicle-control)
Images from control (saline) and severe asthma model (50µg/50µg HDM) BAL fluid. Macrophages (M), Lymphocytes (L), Neutrophils (N), and Eosinophils (E) can all be observed in the BAL fluid from mice in the severe asthma model.
Lung Resistance is measured on day 16 of an HDM-induced severe asthma model, following exposure to increasing doses of methacholine. Animals that are sensitized and challenged with HDM display increased lung resistance in comparison to Naïve animals.
H&E- and PAS-stained lung sections from naïve mice and mice from an HDM-induced severe asthma model on day 16. An increased presence of perivascular and peribronchiolar inflammation (red arrows) is observed in diseased animals. Larger bronchioles of diseased animals are lined with moderate numbers of PAS-positive goblet cells (green arrows) whereas saline control lungs had PAS-negative cells (black arrows).
A mixed Th1/Th2 cytokine inflammatory profile in BAL fluid of diseased animals is observed in a severe asthma phenotype.
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Study Models
BioModels offers an LPS-induced acute lung injury (ALI) model. In the LPS-ALI model, mice are anesthetized and then administered LPS by the intranasal route. Animals are evaluated daily for body weight and respiratory status. Endpoints in the model are most often measured between 4-96 hours following LPS administration, with peak disease typically observed around 48 hours. Endpoints in this model include total and differential cell counts and inflammatory mediator content in the broncho-alveolar lavage fluid, detailed lung mechanics, as well as histopathology and immunohistochemistry.
BALB/c mice are administered LPS on Day 0 and BAL fluid is assessed at 24 hours.
BALB/c mice are administered LPS on Day 0 and BAL fluid is assessed at 24 hours for total cells and total neutrophils following administration of either 1 µg or 10 µg of LPS.
BALB/c mice are administered LPS on Day 0 and lung tissue is collected at 24 hours following administration of either 1 µg or 10 µg of LPS.
BALB/c mice are administered LPS on Day 0 and BAL fluid is assessed at 48 or 96 hours for total cells, total neutrophils, total protein, and cytokines following administration 10 µg of LPS. (*p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 compared to the naïve control).
BALB/c mice are administered LPS on Day 0 and plasma is assessed at 48 or 96 hours for cytokines following administration 10 µg of LPS. (*p<0.05; **p<0.01; ***p<0.001 compared to the naïve control).
BALB/c mice are administered LPS on Day 0 and weight change is assessed. Animals are weighed daily, and body weight change as compared to Day 0 is calculated. The AUC is calculated to compare treatment arms and is shown in the inset.
BALB/c mice are administered LPS on Day 0 and lung tissue is collected at 48 hours following administration of either 10 µg of LPS or 10 µg of LPS with Dexamethasone treatment.
BALB/c mice are administered LPS on Day 0 and lung mechanics are assessed at 48 hours following administration of either 10 µg of LPS or 10 µg of LPS with Dexamethasone treatment.
BALB/c mice are administered LPS on Day 0 and lung elastance and BAL fluid total cells, total neutrophils, and cytokines are assessed at 48 hours following administration 10 µg of LPS.
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BioModels offers a hydrochloric acid (HCl)-induced acute lung injury (ALI) mouse model. In the HCl-ALI model, mice are anesthetized and then administered HCl by the intratracheal route. Animals are evaluated daily for body weight and respiratory status. Endpoints in the model are most often measured 24 hours following HCl administration. Endpoints in this model include total and differential cell counts and inflammatory mediator content in the broncho-alveolar lavage fluid, detailed lung mechanics, as well as histopathology and immunohistochemistry.
BALB/c mice are administered HCl on Day 0 and BAL fluid is assessed at 24 hours for total neutrophils and total protein content following administration of either 50 µL, 62.5 µL, or 75 µL of HCl.
BALB/c mice are administered HCl on Day 0 and lung mechanics are assessed at 24 hours following administration of either 50 µL, 62.5 µL, or 75 µL of HCl.
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