Strong inflammatory responses and apoptosis in the oviducts of egg-laying hens caused by genotype VIId Newcastle disease virus

Abstract

BackgroundNewcastle disease virus (NDV) can cause serious damage to the reproductive tracts of egg-laying hens and leads to egg production and quality reduction. However, the mechanism of severe pathological damage in the oviducts of egg-laying hens after NDV infection has not been fully elucidated. In this study, the correlation between the primary pathological lesions and viral load in the oviducts of egg-laying hens infected with the velogenic genotype VIId NDV strain was evaluated by pathological observation and virus detection. Subsequently, apoptosis, the expression of immune-related genes and lymphocyte infiltration into the infected oviducts were determined to explore the potential causes of the pathological changes.ResultsA higher viral load and severe tissue lesions and apoptotic bodies were observed in the oviduct of NDV-infected hens compared with the control. Immune-related genes, including TLR3/7/21, MDA5, IL-2/6/1β, IFN-β, CXCLi1/2, and CCR5, were significantly upregulated in the magnum and uterus. IL-2 presented the highest mRNA level change (137-fold) at 5 days post infection (dpi) in the magnum. Infection led to CD3+CD4+ and CD3+CD8α+ lymphocyte infiltration into the magnum of the oviduct. A higher viral load was found to be associated with pathological changes and the elevated expression of proinflammatory cytokines in the NDV-infected hens.ConclusionsOur results indicate that the severe lesions and apoptosis in the oviducts of egg-laying hens caused by genotype VIId NDV strains are associated with the excessive release of inflammatory cytokines, chemokines and lymphocyte infiltration, which contribute to the dysfunction of the oviducts and the decrease of egg production in hens.

Newcastle disease virus RNA-induced IL-1β expression via the NLRP3/caspase-1 inflammasome

“…IL-1β is the central mediator of the inflammatory response, and neutralizing IL-1β using a specific antibody has been shown to reduce the inflammatory response to influenza A virus [8]. Studies have shown that following infection with NDV virulent strains, various organs exhibited varying degrees of exudative inflammation and inflammatory factors, such as IL-1β, IL-6, IL-18 and IFNβ, which were released in large quantities, resulted in high animal mortality rates, and were also observed in Experiment 1 of this study [1,2,45]. Alternatively, infection with lentogenic strains resulted in only mild non-lifethreatening clinical symptoms, with all chickens eventually recovering.…”

“…Newcastle disease (ND) is a highly contagious disease of poultry that leads to acute fever and sepsis and is caused by the Newcastle disease virus (NDV). This virus consists of a negative-sense, single-stranded RNA genome of approximately 15 190 nucleotides that encodes the structural proteins NP, P, M, F, HN, and L and the non-structural proteins V and W. Infection with virulent strains of NDV causes a strong immune response, with different organs expressing varying degrees of exudative inflammation, resulting in the release of large quantities of inflammatory factors, such as IL-1β, IL-6, IL-18, and IFN-β [1,2]. Thus, exploring the mechanisms underlying the NDV-induced inflammatory response can aid in understanding the pathogenesis of Newcastle disease.…”

Newcastle disease virus induces testicular damage and disrupts steroidogenesis in specific pathogen free roosters

“…Infectious factors, such as avian leukosis virus [8], Marek's disease virus [9], and NDV [10], affect reproductive performance. Although, NDV replicates in the ovary and oviduct [11], causing severe inflammation and apoptosis, and result into decreased egg production [12][13][14] and fertility rates [15], the pathologic effects of NDV on the male reproductive system are yet to be characterized.…”

“…The innate immune response is the first line of defence against invading viruses and stimulates a specific mucosal and humoral immune response [18]. In NDV infection, after the detection of viruses by pattern recognition receptors (PRRs), complex host-pathogen interaction pathways direct an intense inflammatory response to inhibit viral replication [14,19] and elevate plasma glucocorticoids [20]. These pro-inflammatory cytokines and their crosstalk with hormones shape the immune system to control the potential harmful effects and the return of homeostasis after the clearance of a pathogen [21,22].…”

“…In poultry, studies of NDV pathogenesis have mainly focused on the intestines, lungs, trachea, brain, spleen and feathers [14,[24][25][26][27][28][29]. Studies on the effects of NDV infection on histological lesions, innate immune responses, and steroidogenesis in the testes are rare.…”