Bordetella Pertussis
Bordetella Pertussis - Related Videos
08:18
Evaluation of Vaccine-Induced Immunity Against Bacterial Infection in a Mouse Model
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2025
In this video, we describe a protocol to test the efficacy of an acellular pertussis vaccine against Bordetella pertussis infection in mice. Post-vaccination, the mice were subjected to infection, and their tissue homogenate was cultured to analyze the bacterial colonies as a readout of the vaccine-induced protective immunity.
01:56
Inducing Paralysis in a Mouse Model via Transfer of Aquaporin-4-Specific Th17 Cells
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2025
This video demonstrates the procedure of inducing paralysis by transferring activated Th17 cells targeting aquaporin-4 into a mouse model. In the central nervous system, the activated Th17 cells interact with aquaporin-4-expressing astrocytes, triggering an immune response that leads to tail and limb paralysis in the mouse.
08:03
Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
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Cited by 169 •
2014
Experimental autoimmune encephalomyelitis (EAE) is an established animal model of multiple sclerosis. C57BL/6 mice are immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 (MOG35-55), resulting in an ascending flaccid paralysis caused by autoreactive immune cells in the central nervous system. Protocols for disease induction and monitoring will be discussed.
04:18
Assessing Motor Function in an Experimental Autoimmune Neuritis Mouse Model
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2025
This video demonstrates the process of assessing motor dysfunction in a mouse model through the administration of Pertussis toxin and an inoculum containing myelin-mimicking peptides and adjuvants, followed by treadmill tests to assess motor function and evaluate the resulting nerve damage due to immune activation and demyelination.
03:16
Generation of Experimental Autoimmune Encephalomyelitis in a Mouse Model
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2025
This video demonstrates the method of inducing experimental autoimmune encephalomyelitis (EAE) by injecting myelin-derived peptides with an adjuvant to activate autoreactive T cells, which migrate to the brain. Pertussis toxin is administered to increase blood-brain barrier permeability, allowing these T cells and other immune cells to enter the brain. These immune cells cause demyelination, leading to impaired nerve transmission and development of EAE.
FAQs
Adhesins help determine where Bordetella pertussis establishes itself by promoting attachment to ciliated airway epithelial cells. This attachment positions the bacterium at the surface where host-pathogen interactions and toxin activity can affect airway defenses. In immunology and infection research, examining adhesion helps connect bacterial colonization with later respiratory symptoms and impaired clearance.
Pertussis toxin and tracheal cytotoxin connect bacterial presence with changes in the airway and host response. Their described effects include disrupted immune signaling, impaired mucociliary clearance, and prolonged coughing. Studying these toxins helps researchers analyze how bacterial virulence contributes to inflammation, alters airway defenses, and produces consequences that extend beyond initial colonization.
When mucociliary clearance is disrupted, the airway's ability to remove material from its surface is compromised. In pertussis, this effect helps explain why coughing can persist rather than representing only a brief response to colonization. Studying this process connects toxin-associated airway dysfunction with symptom duration and the persistence of infection-related irritation.
Virulence factors influence more than local airway function: they also shape inflammation and immune signaling during infection. This makes B. pertussis useful for studying how a pathogen's products affect protective immunity. Researchers can relate these factors to host responses, helping explain why immune protection and disease severity are important linked but distinct outcomes.
An investigation can track the sequence from airway colonization to adhesin-mediated attachment, toxin-associated disruption of immune signaling or mucociliary clearance, and resulting respiratory effects. Researchers can then interpret these findings alongside inflammation and protective immunity. This workflow keeps bacterial virulence, host response, and clinical consequences connected rather than treating symptoms or immunity as isolated outcomes.
By identifying adhesins and toxins that influence colonization, immune signaling, and airway dysfunction, researchers can define bacterial features relevant to protective immunity. These host-pathogen studies provide a basis for evaluating whether immune responses address important stages of infection. The work supports vaccine development while also clarifying why preventing severe disease and controlling transmission are related goals.
Research linking airway colonization, toxin-associated effects, and respiratory manifestations provides context for diagnostic strategies. These relationships help investigators consider which features of infection are biologically meaningful when studying detection. Diagnostic work complements vaccine research by addressing recognition of infection, while virulence studies explain the processes and host responses that detection efforts seek to identify.
Waning immunity matters because protection against Bordetella pertussis is not treated as a permanently fixed outcome in infection research. Studying it helps explain how immune protection may relate to renewed transmission or severe disease over time. This perspective connects laboratory analysis of protective immunity with broader efforts to control spread and reduce serious consequences.