Pulmonary Infection Model
Pulmonary Infection Model - Related Videos
02:55
Aerosol Delivery of Mycobacterium tuberculosis for Pulmonary Infection in a Mouse Model
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2026
Source: Mueller, A., et al. An Experimental Model to Study Tuberculosis-Malaria Coinfection upon Natural Transmission of Mycobacterium tuberculosis and Plasmodium berghei. J. Vis. Exp. (2014)This video demonstrates the aerosol delivery of Mycobacterium tuberculosis (Mtb) to mice using a nebulizer-based chamber system to induce pulmonary infection, providing a controlled and reproducible model for studying airborne tuberculosis transmission and host-pathogen interactions in vivo.
03:14
Obtaining Cytotoxic Amyloids Following Bacterial Infection of Rat Pulmonary Endothelial Cells
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2025
Source: Balczon, R., et al. Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa. J. Vis. Exp. (2018)This video demonstrates the procedure for generating cytotoxic supernatant from pulmonary endothelial cells following infection with Pseudomonas aeruginosa. It outlines how bacterial effector proteins disrupt host cell structure and induce the release of cytotoxic amyloid oligomers into the supernatant.
09:40
Hemodynamic Characterization of Rodent Models of Pulmonary Arterial Hypertension
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Cited by 35 •
2016
Pulmonary arterial hypertension (PAH) is a disease of pulmonary arterioles that leads to their obliteration and the development of right ventricular failure. Rodent models of PAH are critical in understanding the pathophysiology of PAH. Here we demonstrate hemodynamic characterization, with right heart catheterization and echocardiography, in the mouse and rat.
10:56
Transplantation of Pulmonary Valve Using a Mouse Model of Heterotopic Heart Transplantation
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Cited by 7 •
2014
In order to understand the cellular and molecular mechanisms underlying neotissue formation and stenosis development in tissue engineered heart valves, a murine model of heterotopic heart valve transplantation was developed. A pulmonary heart valve was transplanted to recipient using the heterotopic heart transplantation technique.
03:16
Processing of Infected Tissues for Bacterial Enumeration in a Mouse Co-Infection Model
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2026
Source: Lenhard, A., et al. A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness. J. Vis. Exp. (2022)This video demonstrates the processing of lungs from a mouse co-infected with a pathogenic bacterium and a virus. Mincing, homogenizing, and plating the lung tissue allows quantification of bacterial load, indicating bacterial spread to the lungs and disease severity.
FAQs
The experimental system brings pathogen exposure into contact with lung-related cells or tissues while host responses are observed under controlled conditions. This makes it possible to examine pathogen growth alongside changes in epithelial integrity, immune signaling, and inflammation. Comparing these responses helps researchers connect microbial behavior with tissue damage and host defense rather than studying either side in isolation.
Epithelial injury indicates how infection affects the cells forming the respiratory barrier, whereas immune signaling shows how the host detects and responds to the pathogen. Evaluating both processes helps distinguish direct tissue damage from inflammation associated with host defense. Together, these measurements provide a broader picture of disease mechanisms and help identify clinically relevant outcomes.
These systems provide different levels of biological context for studying infection. Cultured cells offer a controlled setting for examining interactions with individual lung cell types, while tissues and organoids can represent more complex respiratory structures. Animal hosts add whole-organism responses. Selecting among them allows researchers to balance experimental control with the complexity needed for a particular question.
Researchers can compare how different host systems respond to the same respiratory pathogen by monitoring pathogen growth, epithelial injury, immune signaling, and inflammation. Differences in these outcomes can indicate variation in susceptibility or defense. This approach links observable responses to disease mechanisms and supports biological investigations of why infection produces different effects in different hosts.
A typical workflow introduces a respiratory pathogen into a selected cultured cell system, tissue, organoid, or animal host. Researchers then monitor pathogen growth and assess effects on lung cells, including epithelial injury, immune signaling, and inflammatory responses. The chosen system and measurements should match the biological question, whether it concerns disease mechanisms, susceptibility, or treatment effects.
After infection is established in the experimental system, researchers can examine whether an antimicrobial or anti-inflammatory treatment changes the measured outcomes. Pathogen growth provides information relevant to antimicrobial activity, while epithelial injury and inflammatory responses help assess effects on host tissue and signaling. These comparisons support evaluation of treatment performance under controlled biological conditions.
Beyond investigating infection mechanisms, these models support comparisons of host susceptibility and assessment of vaccines, antimicrobial treatments, and anti-inflammatory treatments. Results can also connect experimental observations with clinically relevant outcomes related to prevention, diagnosis, and treatment of lung infections. Their value comes from integrating pathogen behavior, lung-cell responses, and host defense within a controlled study.