Browsing by Author "Tembo, John Mambwe"

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Distinct Patterns of Host Adherence by Neisseria gonorrhoeae Isolated from Experimental Gonorrhea
(Canadian Journal of Infectious Diseases and Medical Microbiology, 2021-05-15) Yingxia, He; Zhang, Song; Zhang, Yingmiao; Bicong, Wu; Xue, Ying; Chenglin, Ye; Qiao, Li; Adhiambo, Njiri Olivia; Tembo, John Mambwe; Hongxiang, Chen; Huahua, Cai; Tie, Chen
Neisseria gonorrhoeae (N. gonorrhoeae, gonococci, or GC), the etiologic agent of gonorrhea, is a human-obligate bacterial pathogen. -e GC surface contains pili that mediate the adherence to host cells. Studies have shown that GC pili, coded by pilin genes, undergo remarkable changes during human experimental gonorrhea, possibly generated by DNA phase variation during infection. -e question that arises is whether the changes in pilins can alter the adherence capacity of N. gonorrhoeae to host cells. In this study, six variants initially isolated from male volunteers infected with one single clone of GC were examined for their adherence patterns with human Chang conjunctiva cells. In this study, we showed that the variants showed distinct adherence patterns to this cell line under light microscopy and scanning electron microscopy. Moreover, two reisolates showed higher adherence capacities than that of the input strain. -e results provide an additional example as to how the pilus variation may play a role in the pathogenesis of N. gonorrhoeae.
Loss of the virulence plasmid by Shigella sonnei promotes its interactions with CD207 and CD209 receptors
(Journal of Medical Microbiology, 2021) Wu, Bi-cong; Olivia, Njiri A.; Tembo, John Mambwe; He, Ying-xia; Zhang, Ying-miao; Xue, Ying; Ye, Cheng-lin; Lv, Yin; Li, Wen-jin; Jiang, Ling-Yu; Huo, Xi-xiang; Sun, Zi-yong; Chen, Zhong-ju; Qin, Ji-chao; Li, An-yi; Park, Chae Gyu; Klena, John D.; Ding, Hong-hui; Chen, Tie
Introduction. Shigella sonnei, the cause of bacillary dysentery, belongs to Gram-negative enteropathogenic bacteria. S. sonnei contains a 210kb 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 Gramnegative 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.