Abstract
Background: Neospora caninum, is the etiological agent of neosporosis, an infection that causes abortions in cattle and nervous system dysfunction in dogs. Invasion and egress are the key steps of the pathogenesis of N. caninum infection. Microneme proteins (MICs) play important roles in the recognition, adhesion, and invasion of host cells in other apicomplexan parasites. However, some MICs and their functions in N. caninum infection have rarely been reported. Methods: The homologous recombination strategy was used to investigate the function of MIC6 in N. caninum infection. Results: ΔNcMIC6 showed a smaller plaque size and weakened capacities of invasion and egress than Nc1. Transcription levels of the egress-related genes CDPK1, PLP1, and AMA1 of ΔNcMIC6 were downregulated. Due to the lack of NcMIC6, virulence of the pathogen in the infected mouse was weakened. The subcellular localization of NcMIC1 and NcMIC4 in ΔNcMIC6, however, did not change. Nevertheless, the transcription levels of MIC1 and MIC4 in ΔNcMIC6 were downregulated, and the expression and secretion of MIC1 and MIC4 in ΔNcMIC6 were reduced compared with that in Nc1. Furthermore, the absence of NcMIC6 weakened the virulence in mice and lower parasite load detected in mice brains. Conclusions: NcMIC6 is involved in host cell invasion and egress in N. caninum and may work synergistically with other MICs to regulate the virulence of the pathogen. These data lay a foundation for further research into the function and application of NcMIC6.
Highlights
Neospora caninum is an apicomplexan parasite that causes neuromuscular disease in dogs and reproductive disorders in cattle, impacting the global livestock industry greatly [1]
The absence of NcMIC6 weakened the virulence in mice and lower parasite load detected in mice brains
NcMIC6 is involved in host cell invasion and egress in N. caninum and may work synergistically with other Microneme proteins (MICs) to regulate the virulence of the pathogen
Summary
Neospora caninum is an apicomplexan parasite that causes neuromuscular disease in dogs and reproductive disorders in cattle, impacting the global livestock industry greatly [1]. As an obligate intracellular parasite, N. caninum actively invades the host cells and resides and replicates safely within vacuoles, which are surrounded by the parasitophorous vacuole membrane (PVM) [2]. This apicomplexan parasite shares a unique mode of substrate-dependent motility, which is crucial for invasion and egress. Conclusions: NcMIC6 is involved in host cell invasion and egress in N. caninum and may work synergistically with other MICs to regulate the virulence of the pathogen. These data lay a foundation for further research into the function and application of NcMIC6
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