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Intranasal Immunization and Milk Collection in Studies of Maternal Immunization in New Zealand White Rabbits Oryctolagus cuniculus
Published on: July 31, 2021
Pathogenicity, colonization, and innate immune response to Pasteurella multocida in rabbits
Wenhao Yang1, Mingtao Li1, Chengcheng Zhang1
1Jiangsu Co-Innovation Center for Prevention of Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, China.
Pasteurella multocida rapidly replicates in rabbits, causing severe respiratory disease and high mortality. Infection activates Toll-like receptor (TLR) pathways, increasing inflammatory cytokines and leading to septicemia.
Area of Science:
- Veterinary Pathology
- Infectious Diseases
- Immunology
Background:
- Pasteurella multocida (P. multocida) is a significant rabbit pathogen causing economic losses.
- Understanding P. multocida pathogenesis and immune response is crucial for disease management.
Purpose of the Study:
- To elucidate the pathogenic mechanisms of P. multocida in rabbits.
- To investigate the innate immune response following P. multocida infection.
Main Methods:
- Rabbit infection model with P. multocida.
- Clinical observation, pathological, and histopathological analysis.
- Bacterial load quantification in tissues and analysis of Toll-like receptor (TLR) and cytokine expression.
Main Results:
- P. multocida infection caused severe dyspnea, high mortality (60%), and significant lung pathology (consolidation, abscesses).
- Rapid bacterial replication occurred in multiple tissues, peaking at 2 days post-infection (dpi), with sustained high levels in lungs and thymus at 3 dpi.
- TLR2 and TLR4 signaling pathways were activated, leading to increased expression of pro-inflammatory cytokines (Il1β, Il6, Il8, Tnf-α), correlating with bacterial colonization.
Conclusions:
- P. multocida rapidly replicates in rabbits, leading to bacteremia and significant respiratory inflammation.
- Activation of TLR signaling pathways and subsequent cytokine induction are key contributors to the observed respiratory inflammation and septicemia.
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