Pathogenic Mechanisms
Pathogenic Mechanisms - Related Videos
10:39
Single Cell Measurements of Vacuolar Rupture Caused by Intracellular Pathogens
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Cited by 22 •
2013
We describe a method for tracking the endomembrane rupture elicited by the intracellular bacteria Shigella flexneri and Mycobacterium tuberculosis upon host cell invasion. Our assay makes use of CCF4, a host cytoplasmic FRET probe in live or fixed cells. This reporter is degraded by an enzyme activity present on the bacterial surface.
11:36
Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms
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Cited by 6 •
2020
We describe an in vivo immunization, translational hepatitis model in BALB/c mice that can be utilized to study the pathogenesis of drug-induced autoimmune hepatitis including sex differences seen in this disease. We will describe how this model demonstrates reproducible analyses using in vivo and in vitro experimental techniques.
12:54
Detection of Foodborne Bacterial Pathogens from Individual Filth Flies
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Cited by 20 •
2015
A PCR-based protocol was adapted to detect Cronobacter spp., Salmonella enterica, and Listeria monocytogenes from body surfaces and alimentary canals of individual wild-caught flies. The goal of this protocol is to detect and isolate bacterial pathogens from individual insects collected as part of an environmental sampling program during foodborne outbreak investigations.
05:08
A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease
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Cited by 5 •
2022
The present protocol describes the development of a Crohn's-like colitis model in rodents. Transmural inflammation leads to stenosis at the TNBS instillation site, and mechanical enlargement is observed in the segment proximal to the stenosis. These changes allow studying mechanical stress in colitis.
12:45
Mechanical Stimulation of Chondrocyte-agarose Hydrogels
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Cited by 29 •
2012
The biosynthesis of cartilaginous extracellular matrix by chondrocytes can be affected by application of mechanical stimuli. This method describes the technique of applying dynamic compressive strains to chondrocytes encapsulated in 3D constructs and the evaluation of induced changes in chondrocyte metabolism.
FAQs
Disease progression can reflect a sequence of linked events rather than a single microbial action. An infectious agent may first adhere to host cells, invade tissues, replicate, and produce toxins, while the host response may limit or intensify damage. Examining these stages helps explain why infection can advance from initial colonization to tissue injury and clinical complications.
Clinical outcomes depend on the interaction between microbial capabilities and the condition of the host. Virulence factors can increase an agent’s ability to adhere, invade, replicate, or damage tissues, whereas host susceptibility influences how effectively infection is controlled. This interaction helps explain why the same infectious agent may produce different levels of disease in different individuals.
Inflammation can become a source of pathology when the host response itself contributes to tissue injury. Consequently, disease severity may reflect both microbial activity and the extent of inflammatory damage. Distinguishing direct injury from harmful host responses gives medical researchers a broader basis for interpreting disease progression and considering treatments aimed at infection or its complications.
Mechanistic analysis connects a disease feature with the biological event that produces it. If adhesion, invasion, replication, toxin production, immune evasion, or inflammation is central to progression, that process can inform diagnostic investigation or therapeutic development. This approach helps move beyond describing symptoms by linking measurable disease findings to microbial behavior and host responses.
Prevention strategies can be designed around the stages that allow infection to establish or spread. Understanding how an agent interacts with host cells, tissues, and immune defenses helps identify points where vaccination or infection control may interrupt disease development. Mechanistic knowledge therefore supports prevention by focusing attention on vulnerable parts of the infectious process rather than only its later consequences.
Understanding disease mechanisms can support antimicrobial development by revealing biologically important processes involved in infection, including replication, toxin production, and interactions with host defenses. The same knowledge also supports personalized management because host susceptibility influences outcomes. Considering both microbial virulence and individual host factors can help frame treatment and complication management more precisely.