Salmonella enterica Serovar Typhi Plasmid Impairs Dendritic Cell Responses to Infection

Li, Wei; Wu, Shuyan; Li, Yuanyuan; Chu, Yuanyuan; Huang, Rui

doi:10.1007/s00284-012-0136-1

Cited by 7 publications

(7 citation statements)

References 23 publications

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“…Salmonella enterica serovar Typhimurium interferes with the migration of intestinal DCs and hinders antigen presentation via the ubiquitination and degradation of MHC class II molecules, which prevents bacterial killing [5], [6]. Helicobacter pylori replicates within autophagosomes and retains cytosolic MHC class II molecules; H. pylori also prevents interleukin (IL)-12 production and induces IL-10 secretion, thereby inhibiting the anti-microbial Th1 response [7], [8].…”

Section: Introductionmentioning

confidence: 99%

Intracellular Bacteria Interfere with Dendritic Cell Functions: Role of the Type I Interferon Pathway

Gorvel

Textoris

Banchereau³

et al. 2014

PLoS ONE

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Dendritic cells (DCs) orchestrate host defenses against microorganisms. In infectious diseases due to intracellular bacteria, the inefficiency of the immune system to eradicate microorganisms has been attributed to the hijacking of DC functions. In this study, we selected intracellular bacterial pathogens with distinct lifestyles and explored the responses of monocyte-derived DCs (moDCs). Using lipopolysaccharide as a control, we found that Orientia tsutsugamushi, the causative agent of scrub typhus that survives in the cytosol of target cells, induced moDC maturation, as assessed by decreased endocytosis activity, the ability to induce lymphocyte proliferation and the membrane expression of phenotypic markers. In contrast, Coxiella burnetii, the agent of Q fever, and Brucella abortus, the agent of brucellosis, both of which reside in vacuolar compartments, only partly induced the maturation of moDCs, as demonstrated by a phenotypic analysis. To analyze the mechanisms used by C. burnetii and B. abortus to alter moDC activation, we performed microarray and found that C. burnetii and B. abortus induced a specific signature consisting of TLR4, TLR3, STAT1 and interferon response genes. These genes were down-modulated in response to C. burnetii and B. abortus but up-modulated in moDCs activated by lipopolysaccharide and O. tsutsugamushi. This transcriptional alteration was associated with the defective interferon-β production. This study demonstrates that intracellular bacteria specifically affect moDC responses and emphasizes how C. burnetii and B. abortus interfere with moDC activation and the antimicrobial immune response. We believe that comparing infection by several bacterial species may be useful for defining new pathways and biomarkers and for developing new treatment strategies.

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Section: Introductionmentioning

confidence: 99%

Intracellular Bacteria Interfere with Dendritic Cell Functions: Role of the Type I Interferon Pathway

Gorvel

Textoris

Banchereau³

et al. 2014

PLoS ONE

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“…For Salmonella, the induction of macrophage apoptosis is a specific virulence mechanism promoting cell-to-cell spread in vivo. As reported previously, S. typhi harboring pR ST98 had the potential to enhance macrophage apoptosis rate and to restrain DCs autophagy (8,9). However, its exact effect on apoptosis and autophagy in infected macrophages remains elusive.…”

Section: Ntroductionmentioning

confidence: 78%

“…Here we utilized RAPA to study the effect of plasmid pR ST98 on the interaction between bacterial virulence and autophagy of macrophages J774A.1. Previous data demonstrated that pR ST98 was related with the apoptosis of macrophages through the (8,9), whether the plasmid affects macrophage autophagy is unknown. The inhibition of autophagy in S. typhi-WT infected macrophages was observed in this study; however, there remains the question as to what role pR ST98 plays in the relationship between autophagy and apoptosis.…”

Section: Discussionmentioning

confidence: 98%

“…As described previously, we made the first report that Salmonella plasmid virulence (spv) homologous genes also existed on pR ST98 . The spv genes were identified as a highly conserved region of 8 kb with five genes, named spvR, A, B, C and D. Further research indicated that pRST98 was associated with the increased virulence in mice, such as lethality, infection of spleen, liver and mesenteric lymph nodes, and serum resistance (8)(9)(10). We conclude that pRST98 is a chimeric plasmid both mediating bacterial multidrug resistance and increasing bacterial virulence.…”

Section: Ntroductionmentioning

confidence: 88%

“…In the late 1980s and early 1990s, a pandemic of multidrug resistant S. typhi occurred in P. R. China. Five hundreds and ninety one strains of S. typhi were isolated from the blood of patients by our laboratory in Suzhou, and more than 80% of these isolates were multidrug resistant (8,9). Plasmid profile analysis by our lab indicated that all those multidrug resistant strains carried a 98.6 mDa plasmid designated as pR ST98 , which mediates bacterial multidrug resistance to ampicillin (Amp), chloramphenicol (Cm), streptomycin (Sm), trimethoprim (TMP), sulfonamide (Su), gentamicin (Gm), neomycin (Nm), kanamycin (Kn), cephalosporin (Cp), carbenicillin (Cb), and tetracycline (Tc).…”

Section: Ntroductionmentioning

confidence: 99%

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Inhibition of macrophage autophagy induced by Salmonella enterica serovar typhi plasmid

Chu

Yang

et al. 2014

Front Biosci

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pR(ST98), 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 pR(ST98) 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-DeltapR(ST98)) and complement of S. typhi-DeltapR(ST98) (S. typhi-c-pR(ST98)). Results revealed that S. typhi harboring pR(ST98) 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-DeltapR(ST98) was lower than that infected with S. typhi-WT or S. typhi-c-pR(ST98). The survival rate of intracellular bacteria carrying pR(ST98) 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 pR(ST98) and intracellular bacterial growth decreased. Our study suggested that pR(ST98) could inhibit autophagy and induce cell apoptosis for the host bacterial survival and proliferation.

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Pathogen Manipulation of cIL-10 Signaling Pathways: Opportunities for Vaccine Development?

Eberhardt

Barry

2014

Current Topics in Microbiology and Immunology

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Interleukin-10 (IL-10) is a tightly regulated, pleiotropic cytokine that has profound effects on all facets of the immune system, eliciting cell-type-specific responses within cells expressing the IL-10 receptor (IL-10R). It is considered a master immune regulator, and imbalances in IL-10 expression, resulting from either inherent or infectious etiologies, have far reaching clinical ramifications. Regarding infectious diseases, there has been accumulating recognition that many pathogens, particularly those that establish lifelong persistence, share a commonality of their natural histories: manipulation of IL-10-mediated signaling pathways. Multiple viral, bacterial, protozoal, and fungal pathogens appear to have evolved mechanisms to co-opt normal immune functions, including those involving IL-10R-mediated signaling, and immune effector pathways away from immune-mediated protection toward environments of immune evasion, suppression, and tolerance. As a result, pathogens can persist for the life of the infected host, many of whom possess otherwise competent immune systems. Because of pathogenic avoidance of immune clearance, persistent infections can exact incalculable physical and financial costs, and represent some of the most vexing challenges for improvements in human health. Enormous benefits could be gained by the development of efficient prevention and/or therapeutic strategies that block primary infection, or clear the infection. There are now precedents that indicate that modalities focusing on pathogen-mediated manipulation of IL-10 signaling may have clinical benefit.

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Salmonella enterica Serovar Typhi Plasmid Impairs Dendritic Cell Responses to Infection

Cited by 7 publications

References 23 publications

Intracellular Bacteria Interfere with Dendritic Cell Functions: Role of the Type I Interferon Pathway

Intracellular Bacteria Interfere with Dendritic Cell Functions: Role of the Type I Interferon Pathway

Inhibition of macrophage autophagy induced by Salmonella enterica serovar typhi plasmid

Pathogen Manipulation of cIL-10 Signaling Pathways: Opportunities for Vaccine Development?

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