猪肺炎支原体
微生物学
生物
免疫系统
体液免疫
病菌
细胞外
抗血清
病毒学
抗体
抗菌剂
体外
细胞内
免疫
支原体科
肺炎
传输(电信)
细胞内寄生虫
中和
免疫学
软体动物
呼吸道
军团菌
支原体
先天免疫系统
作者
Yunchong Ma,Jiacui Lai,Xiuwu Lian,Yilin Li,Yue Wu,Honglei Ding
标识
DOI:10.1016/j.jinf.2026.106757
摘要
Several studies in this journal have reported that viruses can induce migrasome formation, which facilitates viral transmission and confers resistance to drug treatment [1,2,3].Mycoplasma hyopneumoniae is the etiological agent of mycoplasmal pneumonia of swine [4].Commercial vaccines can induce a humoral immune response post-immunization; however, they fail to prevent M. hyopneumoniae colonization and transmission [4,5].Previous studies indicated no correlation between humoral immunity and protective efficacy against the disease [5].Nevertheless, antiserum has been shown to inhibit M. hyopneumoniae growth in vitro [6].Furthermore, although various antimicrobials exhibit low in vitro minimal inhibitory concentrations against M. hyopneumoniae, they are ineffective at preventing infection or eradicating the bacterium from the respiratory tract [6].These findings suggest that M. hyopneumoniae employs uncharacterized mechanisms to evade clearance by antisera or antimicrobials in vivo.In this study, we aimed to clarify whether migrasomes act as vehicles to support the extracellular release and intercellular transmission of M. hyopneumoniae, thereby protecting this pathogen from neutralization by M. hyopneumoniae-specific antibodies and elimination by antimicrobials in the extracellular milieu.
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