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Altered pro-inflammatory cytokine mRNA levels in chickens infected with infectious bronchitis virus
Hyesun Jang1, Bon-Sang Koo, Eun-Ok Jeon
1Preventive Veterinary Medicine, College of Veterinary Medicine, Chungbuk National University 12, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, Republic of Korea.
Abstract:
Infectious bronchitis virus (IBV) replicates primarily in the respiratory tract and grows in various organs in chickens, with or without pathological effects. The diversity of this virus has been verified by sequence analysis of the S1 glycoprotein gene, but this method must be supplemented with further analysis for characterization of the agent. To increase our understanding of the pathogenesis of the disease caused by this virus, we investigated the response of chickens to 2 IBV with different genotypes, KIIa and ChVI. The clinical signs induced by the viruses were observed. In addition, the mRNA levels of the pro-inflammatory cytokines, IL-6, IL-1β, and lipopolysaccharide-induced tumor necrosis factor-α factor and the serum levels of α1-acid glycoprotein, which is a major acute phase protein, were measured. The KIIa genotype (Kr/ADL110002/2011) induced clinical signs accompanied by the excessive production of pro-inflammatory cytokines and a higher viral load. In chickens infected with this isolate, simultaneous peaks in the viral copy number and cytokine production were observed at 7 dpi in the trachea and 9 d postinoculation in the kidney. On the other hand, the chickens infected with the ChVI genotype (Kr/ADL120003/2012) did not show a response other than a mild upregulation of cytokines at 1 d postinoculation, which appears to indicate the invasion of the virus. In summary, we confirmed a differential innate response following infection with distinct IBV. We hypothesize that an excessive innate response contributes to the scale of the pathophysiologic effect in chickens.
Insights
Distinct infectious bronchitis virus (IBV) genotypes trigger different innate immune responses in chickens. An excessive inflammatory response correlates with increased disease severity, highlighting genotype-specific pathogenesis.
Area of Science:
- Veterinary Virology
- Immunology
- Poultry Diseases
Background:
- Infectious Bronchitis Virus (IBV) causes significant economic losses in the poultry industry.
- IBV exhibits genetic diversity, necessitating further characterization beyond S1 glycoprotein gene sequencing.
- Understanding IBV pathogenesis requires investigating host-pathogen interactions and immune responses.
Purpose of the Study:
- To investigate and compare the pathogenesis and innate immune responses of chickens to two distinct IBV genotypes (KIIa and ChVI).
- To analyze clinical signs, viral load, pro-inflammatory cytokine mRNA levels, and acute phase protein serum levels following IBV infection.
Main Methods:
- Chickens were infected with IBV KIIa (Kr/ADL110002/2011) and ChVI (Kr/ADL120003/2012) genotypes.
- Clinical signs were monitored, and viral loads were quantified.
- mRNA levels of cytokines (IL-6, IL-1β, TNF-α) and serum levels of α1-acid glycoprotein were measured.
Main Results:
- The KIIa genotype induced severe clinical signs, high viral loads, and excessive pro-inflammatory cytokine production, peaking at 7 days post-inoculation (dpi) in the trachea and 9 dpi in the kidney.
- The ChVI genotype caused mild cytokine upregulation at 1 dpi, suggesting initial viral invasion without a strong inflammatory response.
- A differential innate immune response was observed between the two IBV genotypes.
Conclusions:
- Distinct IBV genotypes elicit significantly different innate immune responses in chickens.
- Excessive innate immune responses may contribute to the severity of pathological effects caused by certain IBV strains.
- Genotype-specific pathogenesis is a critical factor in IBV disease progression.
