TY - JOUR
T1 - Invasiveness of the Yersinia pestis ail protein contributes to host dissemination in pneumonic and oral plague
AU - Zhang, Yingmiao
AU - Ying, Xiaoling
AU - He, Yingxia
AU - Jiang, Lingyu
AU - Zhang, Song
AU - Bartra, Sara Schesser
AU - Plano, Gregory V.
AU - Klena, John D.
AU - Skurnik, Mikael
AU - Chen, Hongxiang
AU - Cai, Huahua
AU - Chen, Tie
N1 - Funding Information:
This study was supported by grants from the National Natural Science Foundation of China (NSFC 81271780 and 81471915) and by two local grants from Tongji Hospital, Tongji Medical College to Tie Chen.We would like to greatly thank Dr. Joseph Hinnebusch at the Rocky Mountain Laboratories, NIH, USA, for his long-term support and help to initiate the project of host-Yersinia spp. interactions. We thank Dr. Ruifu Yang for providing the luminescence-generated plasmid.
Funding Information:
This study was supported by grants from the National Natural Science Foundation of China (NSFC 81271780 and 81471915 ) and by two local grants from Tongji Hospital, Tongji Medical College to Tie Chen.
Publisher Copyright:
© 2020 Elsevier Ltd
Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2020/4
Y1 - 2020/4
N2 - Yersinia pestis, a Gram-negative bacterium, is the etiologic agent of plague. A hallmark of Y. pestis infection is the organism's ability to rapidly disseminate through an animal host. Y. pestis expresses the outer membrane protein, Ail (Attachment invasion locus), which is associated with host invasion and serum resistance. However, whether Ail plays a role in host dissemination remains unclear. In this study, C57BL/6J mice were challenged with a defined Y. pestis strain, KimD27, or an isogenic ail-deleted mutant derived from KimD27 via metacarpal paw pad inoculation, nasal drops, orogastric infection, or tail vein injection to mimic bubonic, pneumonic, oral, or septicemic plague, respectively. Our results showed that ail-deleted Y. pestis KimD27 lost the ability to invade host cells, leading to failed host dissemination in the pneumonic and oral plague models but not in the bubonic or septicemic plague models, which do not require invasiveness. Therefore, this study demonstrated that whether Ail plays a role in Y. pestis pathogenesis depends on the infection route.
AB - Yersinia pestis, a Gram-negative bacterium, is the etiologic agent of plague. A hallmark of Y. pestis infection is the organism's ability to rapidly disseminate through an animal host. Y. pestis expresses the outer membrane protein, Ail (Attachment invasion locus), which is associated with host invasion and serum resistance. However, whether Ail plays a role in host dissemination remains unclear. In this study, C57BL/6J mice were challenged with a defined Y. pestis strain, KimD27, or an isogenic ail-deleted mutant derived from KimD27 via metacarpal paw pad inoculation, nasal drops, orogastric infection, or tail vein injection to mimic bubonic, pneumonic, oral, or septicemic plague, respectively. Our results showed that ail-deleted Y. pestis KimD27 lost the ability to invade host cells, leading to failed host dissemination in the pneumonic and oral plague models but not in the bubonic or septicemic plague models, which do not require invasiveness. Therefore, this study demonstrated that whether Ail plays a role in Y. pestis pathogenesis depends on the infection route.
KW - Ail protein
KW - Host dissemination
KW - Invasion
KW - Oral plague
KW - Pneumonic plague
KW - Yersinia pestis
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U2 - 10.1016/j.micpath.2020.103993
DO - 10.1016/j.micpath.2020.103993
M3 - Article
C2 - 31988008
AN - SCOPUS:85078734188
VL - 141
JO - Microbial Pathogenesis
JF - Microbial Pathogenesis
SN - 0882-4010
M1 - 103993
ER -