Related Experiment Video
Updated: Jun 5, 2026

Evaluation of Host-Pathogen Responses and Vaccine Efficacy in Mice
Published on: February 22, 2019
Pertussis: a matter of immune modulation
Daan de Gouw1, Dimitri A Diavatopoulos, Hester J Bootsma
1Laboratory of Pediatric Infectious Diseases, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Abstract:
Pertussis, or whooping cough, is a highly contagious, acute respiratory disease of humans that is caused by the Gram-negative bacterial pathogen Bordetella pertussis. In the face of extensive global vaccination, this extremely monomorphic pathogen has persisted and re-emerged, causing approximately 300,000 deaths each year. In this review, we discuss the interaction of B. pertussis with the host mucosal epithelium and immune system. Using a large number of virulence factors, B. pertussis is able to create a niche for colonization in the human respiratory tract. The successful persistence of this pathogen is mainly due to its ability to interfere with almost every aspect of the immune system, from the inhibition of complement- and phagocyte-mediated killing to the suppression of T- and B-cell responses. Based on these insights, we delineate ideas for the rational design of improved vaccines that can target the 'weak spots' in the pathogenesis of this highly successful pathogen.
Insights
Pertussis (whooping cough) is a contagious respiratory illness caused by Bordetella pertussis. This review explores how the bacteria overcome host defenses and suggests strategies for developing better vaccines.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Pertussis, caused by Bordetella pertussis, remains a significant global health threat despite vaccination efforts.
- The pathogen causes approximately 300,000 deaths annually, highlighting its persistence and re-emergence.
- Understanding host-pathogen interactions is crucial for controlling this disease.
Purpose of the Study:
- To review the intricate interactions between Bordetella pertussis and the host's mucosal epithelium and immune system.
- To elucidate the mechanisms by which B. pertussis establishes colonization and evades immune responses.
- To identify potential targets for improved vaccine development based on pathogen "weak spots".
Main Methods:
- This review synthesizes existing research on Bordetella pertussis pathogenesis.
- It analyzes the role of bacterial virulence factors in host colonization.
- It examines the pathogen's strategies for subverting innate and adaptive immunity.
Main Results:
- B. pertussis employs numerous virulence factors to colonize the respiratory tract.
- The pathogen effectively disrupts host immune functions, including complement-mediated killing, phagocytosis, and T- and B-cell responses.
- These immune evasion mechanisms contribute to the pathogen's successful persistence.
Conclusions:
- Bordetella pertussis possesses sophisticated mechanisms to overcome host defenses.
- Targeting key virulence factors and immune evasion strategies could lead to more effective pertussis vaccines.
- Further research into these interactions will inform the rational design of next-generation vaccines.
More Related Videos
07:17Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
16:56Sublingual Immunotherapy as an Alternative to Induce Protection Against Acute Respiratory Infections
Published on: August 30, 2014
Related Concept Videos
Regulation of Bacterial Virulence
Vaccinations
Development of Immunocompetence
The initial cells that migrate from the fetal thymus settle within the skin and epithelial tissues lining the mouth, digestive tract, and in females, the uterus and vagina. These cells, including skin-based dendritic cells, serve as antigen-presenting cells, playing a key role in T cell activation.
Subsequent T...
Immunological Memory
What is Immunological Memory?
Immunological memory is an integral function of the immune system that allows it to recognize and react more rapidly and effectively to pathogens previously encountered. This feature is...
Pneumonia II: Pathophysiology
Diphtheria