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Loss of the virulence plasmid by Shigella sonnei promotes its interactions with CD207 and CD209 receptors

Authors
 Bi-Cong Wu  ;  Njiri A Olivia  ;  John Mambwe Tembo  ;  Ying-Xia He  ;  Ying-Miao Zhang  ;  Ying Xue  ;  Cheng-Lin Ye  ;  Yin Lv  ;  Wen-Jin Li  ;  Ling-Yu Jiang  ;  Xi-Xiang Huo  ;  Zi-Yong Sun  ;  Zhong-Ju Chen  ;  Ji-Chao Qin  ;  An-Yi Li  ;  Chae Gyu Park  ;  John D Klena  ;  Hong-Hui Ding  ;  Tie Chen 
Citation
 JOURNAL OF MEDICAL MICROBIOLOGY, Vol.70(3) : 1297, 2021-03 
Journal Title
 JOURNAL OF MEDICAL MICROBIOLOGY 
ISSN
 0022-2615 
Issue Date
2021-03
Keywords
C-type lectins (CD207 and CD209) ; Shigella sonnei ; antigen presenting cells (APCs)
Abstract
Introduction. Shigella sonnei, the cause of bacillary dysentery, belongs to Gram-negative enteropathogenic bacteria. S. sonnei contains a 210 kb virulence plasmid that encodes an O-antigen gene cluster of LPSs. However, this virulence plasmid is frequently lost during replication. It is well-documented that after losing the O-antigen and becoming rough strains, the Gram-negative bacteria may express an LPS core on its surface. Previous studies have suggested that by using the LPS core, Gram-negative bacteria can interact with several C-type lectin receptors that are expressed on antigen-presenting cells (APCs).Hypothesis/Gap Statement. S. sonnei by losing the virulence plasmid may hijack APCs via the interactions of LPS-CD209/CD207.Aim. This study aimed to investigate if the S. sonnei rough strain, by losing the virulence plasmid, interacted with APCs that express C-type lectins of human CD207, human CD209a and mouse CD209b.Methodology. SDS-PAGE silver staining was used to examine the O-antigen expression of S. sonnei WT and its rough strain. Invasion assays and inhibition assays were used to examine the ability of S. sonnei WT and its rough strain to invade APCs and investigate whether CD209 and CD207 are receptors for phagocytosis of rough S. sonnei. Animal assays were used to observe the dissemination of S. sonnei.Results. S. sonnei did not express O-antigens after losing the virulence plasmid. The S. sonnei rough strain invades with APCs, including human dendritic cells (DCs) and mouse macrophages. CD209 and CD207 are receptors for phagocytosis of rough S. sonnei. Expression of the O-antigen reduces the ability of the S. sonnei rough strain to be disseminated to mesenteric lymph nodes and spleens.Conclusion. This work demonstrated that S. sonnei rough strains - by losing the virulence plasmid - invaded APCs through interactions with CD209 and CD207 receptors.
Full Text
https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.001297#tab2
DOI
10.1099/jmm.0.001297
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Park, Chae Gyu(박채규) ORCID logo https://orcid.org/0000-0003-1906-1308
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/182929
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