Title |
Incomplete autophagy promotes the replication of Mycoplasma hyopneumoniae |
Author |
Zhaodi Wang†, Yukang Wen†, Bingqian Zhou, Yaqin Tian, Yaru Ning, and Honglei Ding* |
Address |
Laboratory of Veterinary Mycoplasmology, College of Veterinary Medicine, Southwest University, Chongqing 400715, P. R. China |
Bibliography |
Journal of Microbiology, 59(8),782–792, 2021,
|
DOI |
10.1007/s12275-021-1232-3
|
Key Words |
autophagy, Mycoplasma hyopneumoniae, LC3, p62,
replication |
Abstract |
Autophagy is an important cellular homeostatic mechanism
for recycling of degradative proteins and damaged organelles.
Autophagy has been shown to play an important role in cellular
responses to bacteria and bacterial replication. However,
the role of autophagy in Mycoplasma hyopneumoniae infection
and the pathogenic mechanism is not well characterized.
In this study, we showed that M. hyopneumoniae infection
significantly increases the number of autophagic vacuoles in
host cells. Further, we found significantly enhanced expressions
of autophagy marker proteins (LC3-II, ATG5, and
Beclin 1) in M. hyopneumoniae-infected cells. Moreover, immunofluorescence
analysis showed colocalization of P97 protein
with LC3 during M. hyopneumoniae infection. Interestingly,
autophagic flux marker, p62, accumulated with the induction
of infection. Conversely, the levels of p62 and LC3-II
were decreased after treatment with 3-MA, inhibiting the
formation of autophagosomes, during infection. In addition,
accumulation of autophagosomes promoted the expression
of P97 protein and the survival of M. hyopneumoniae in PK-
15 cells, as the replication of M. hyopneumoniae was downregulated
by adding 3-MA. Collectively, these findings provide
strong evidence that M. hyopneumoniae induces incomplete
autophagy, which in turn enhances its reproduction in
host cells. These findings provide novel insights into the interaction
of M. hyopneumoniae and host. |