Journal
MICROORGANISMS
Volume 9, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/microorganisms9112407
Keywords
avian metapneumovirus; Mycoplasma gallisepticum; TOC; co-infection; innate immunity; interferon
Categories
Funding
- Deutsche Forschungsgemeinschaft
- University of Veterinary Medicine Hannover, Foundation
- R2N, Federal State of Lower Saxony
- Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [398066876/GRK 2485/1]
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This study investigated the impact of co-infections on pathogen invasion and host immune responses in respiratory diseases. Dual-inoculations resulted in more severe host reactions, while pre-infection with AMPV followed by M. gallispeticum showed prolonged viral replication and significant innate immune responses. AMPV as the secondary pathogen impaired bacterial attachment process and delayed M. gallispeticum replication.
Respiratory pathogens are a health threat for poultry. Co-infections lead to the exacerbation of clinical symptoms and lesions. Mycoplasma gallisepticum (M. gallispeticum) and Avian Metapneumovirus (AMPV) are two avian respiratory pathogens that co-circulate worldwide. The knowledge about the host-pathogen interaction of M. gallispeticum and AMPV in the chicken respiratory tract is limited. We aimed to investigate how co-infections affect the pathogenesis of the respiratory disease and whether the order of invading pathogens leads to changes in host-pathogen interaction. We used chicken tracheal organ cultures (TOC) to investigate pathogen invasion and replication, lesion development, and selected innate immune responses, such as interferon (IFN) alpha, inducible nitric oxide synthase (iNOS) and IFN lambda mRNA expression levels. We performed mono-inoculations (AMPV or M. gallispeticum) or dual-inoculations in two orders with a 24-h interval between the first and second pathogen. Dual-inoculations compared to mono-inoculations resulted in more severe host reactions. Pre-infection with AMPV followed by M. gallispeticum resulted in prolonged viral replication, more significant innate immune responses, and lesions (p < 0.05). AMPV as the secondary pathogen impaired the bacterial attachment process. Consequently, the M. gallispeticum replication was delayed, the innate immune response was less pronounced, and lesions appeared later. Our results suggest a competing process in co-infections and offer new insights in disease processes.
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