IMR Press / FBL / Volume 19 / Issue 3 / DOI: 10.2741/4220

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Inhibition of macrophage autophagy induced by Salmonella enterica serovar typhi plasmid

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1 Medical College of Soochow University, No. 199, Ren Ai Road, Suzhou, Jiangsu 215123, P. R. China
Academic Editor:Jianrong Wang
Front. Biosci. (Landmark Ed) 2014, 19(3), 490–503;
Published: 1 January 2014
(This article belongs to the Special Issue Autophagy: biology and disease)

pRST98, a chimeric plasmid isolated from Salmonella enterica serovar typhi (S. typhi), is involved in bacterial multidrug-resistance and virulence, however, its exact contributions to bacterial pathogenesis are still not fully understood. To investigate whether pRST98 exhibits potential to mediate macrophage autophagy and apoptosis, murine macrophage-like cell line (J774A.1) was infected with wild type strain (S. typhi-WT), mutant strain (S. typhi-DeltapRST98) and complement of S. typhi-DeltapRST98 (S. typhi-c-pRST98). Results revealed that S. typhi harboring pRST98 decreased the number of autophagy vacuoles of macrophages as well as the expression of Beclin 1 and LC3-II at the early stage of infection; apoptosis rate of macrophages infected with S. typhi-DeltapRST98 was lower than that infected with S. typhi-WT or S. typhi-c-pRST98. The survival rate of intracellular bacteria carrying pRST98 was much higher than that of plasmid free strain. After intervention with autophagy agonist rapamycin, apoptosis rate of the cells infected with S. typhi containing pRST98 and intracellular bacterial growth decreased. Our study suggested that pRST98 could inhibit autophagy and induce cell apoptosis for the host bacterial survival and proliferation.

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