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Updated: May 3, 2026

Influenza Virus Propagation in Embryonated Chicken Eggs
Published on: March 19, 2015
Nephropathogenic infectious bronchitis virus can induce duodenum inflammation and barrier defect in Hy-Line brown
Chenlu Feng1, Bingqing Zhang1, Cheng Huang1
1Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, China.
Abstract:
Nephropathogenic infectious bronchitis virus (NIBV) is a common virus in the poultry breeding industry. NIBV infection can cause damage to the kidneys, respiratory tract, and intestines of chickens, leading to clinical signs such as coughing, loose stool, and spotted kidneys in poultry. The intestine is the largest immune organ in the body, and there are few research that reports an intestinal damage caused by NIBV. This study aimed to show the effect of NIBV infection on duodenal intestinal barrier function. Hy-Line brown chickens were randomly divided into a control group and a disease group. At 28 days of age, the pullets in the disease group were inoculated with NIBV SX9 10-5/0.2 mL. SIgA (Secretory Immunoglobulin A) is the main effector molecule of the mucosal immune system. It serves as the first biological barrier for the body's intestinal tract to resist pathogen invasion and plays a crucial role in intestinal immunity. Our results showed that NIBV infection led bleeding spots in the duodenum and increase the duodenal SIgA contents. Histopathological observation and analysis found that villus height (VH) decreased, crypt depth (CD) increased, and the ratio of villus height to crypt depth (VH/CD) decreased significantly. Meanwhile, the number of goblet cells decreased. NIBV infections downregulated the expression of physical barrier-associated cytokines (ZO-1, Occludin, Claudin-1) and chemical barrier-associated cytokines (MUC2, TFF3) and upregulated the expression of immune barrier-associated cytokines (IL-2, IL-4, IL-17, TGF-β, TNF-α, and CCR7). In summary, NIBV replicated in the duodenum, causing an inflammatory reaction in the duodenum, damaging its physical, chemical, and immune barriers, and affecting normal duodenal function.
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