Interaction of Burkholderia pseudomallei and Burkholderia thailandensis with human monocyte-derived dendritic cells

Horton, Rachel Elizabeth; Morrison, Nigel Alexander; Beacham, Ifor R.; Peak, Ian R.

doi:10.1099/jmm.0.038588-0

Cited by 9 publications

(7 citation statements)

References 42 publications

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“…Furthermore, B. pseudomallei replicated inside spleen DC in mice contradicting our in vitro studies whereby murine BMDC were capable of killing intracellular B. pseudomallei. Previous in vitro studies using human and murine DC have consistently shown that DC grown under in vitro culture conditions and protected by antibiotics are capable of killing intracellular B. pseudomallei (15,17). However, organ-specific differences in the ability of DC to kill intracellular B. pseudomallei were observed in vivo, in particular within the spleen, where DC were a site for B. pseudomallei persistence.…”

Section: Discussionmentioning

confidence: 76%

“…BMDC infected with B. pseudomallei in vitro developed a mature phenotype, indicated by increased expression of MHC-II and CD86, and elicited bactericidal activity against intracellular B. pseudomallei, as shown in previous studies (15,17). Migration of DC from the site of infection to secondary lymphoid organs requires upregulation of CCR7, enabling recognition of migratory cues by CC-chemokines, CCL19 and CCL21 (14,36).…”

Section: Discussionmentioning

confidence: 97%

“…DC maturation was triggered by B. pseudomallei, demonstrated by increased expression of molecules for antigen presentation and costimulation, along with increased cytokine production (15,17). Furthermore, host susceptibility to B. pseudomallei infection was associated with altered DC functional responses (15).…”

mentioning

confidence: 99%

“…Investigations of the functional responses of DC toward B. pseudomallei have shown internalization and killing of intracellular B. pseudomallei by DC occurs in vitro (15)(16)(17)(18)(19). DC maturation was triggered by B. pseudomallei, demonstrated by increased expression of molecules for antigen presentation and costimulation, along with increased cytokine production (15,17).…”

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confidence: 99%

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Migration of Dendritic Cells Facilitates Systemic Dissemination of Burkholderia pseudomallei

et al. 2014

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Burkholderia pseudomallei, the etiological agent for melioidosis, is an important cause of community-acquired sepsis in northern Australia and northeast Thailand. Due to the rapid dissemination of disease in acute melioidosis, we hypothesized that dendritic cells (DC) could act as a vehicle for dissemination of B. pseudomallei. Therefore, this study investigated the effect of B. pseudomallei infection on DC migration capacity and whether migration of DC enabled transportation of B. pseudomallei from the site of infection. B. pseudomallei stimulated significantly increased migration of bone marrow-derived DC (BMDC), both in vitro and in vivo, compared to uninfected BMDC. Furthermore, migration of BMDC enabled significantly increased in vitro trafficking of B. pseudomallei and in vivo dissemination of B. pseudomallei to secondary lymphoid organs and lungs of C57BL/6 mice. DC within the footpad infection site of C57BL/6 mice also internalized B. pseudomallei and facilitated dissemination. Although DC have previously been shown to kill intracellular B. pseudomallei in vitro, the findings of this study demonstrate that B. pseudomallei-infected DC facilitate the systemic spread of this pathogen.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Migration of Dendritic Cells Facilitates Systemic Dissemination of Burkholderia pseudomallei

et al. 2014

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“…B. pseudomallei is a facultative intracellular bacterium that enters and survives in nonphagocytic and phagocytic cells, including neutrophils (8)(9)(10)(11)(12)(13)(14). Following entry into the host cell, the bacteria escape from the endocytic vacuole into the cytosol, where they exhibit intracellular motility based on actin polymerization and flagella (15)(16)(17).…”

mentioning

confidence: 99%

Entry, Intracellular Survival, and Multinucleated-Giant-Cell-Forming Activity of Burkholderia pseudomallei in Human Primary Phagocytic and Nonphagocytic Cells

et al. 2017

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The human pathogen and the related species are facultative intracellular bacteria characterized by the ability to escape into the cytosol of the host cell and to stimulate the formation of multinucleated giant cells (MNGCs). MNGC formation is induced via an unknown mechanism by bacterial type VI secretion system 5 (T6SS-5), which is an essential virulence factor in both species. Despite the vital role of the intracellular life cycle in the pathogenesis of the bacteria, the range of host cell types permissive for initiation and completion of the intracellular cycle is poorly defined. In the present study, we used several different types of human primary cells to evaluate bacterial entry, intracellular survival, and MNGC formation. We report the capacity of to enter, efficiently replicate in, and mediate MNGC formation of vein endothelial and bronchial epithelial cells, indicating that the T6SS-5 is important in the host-pathogen interaction in these cells. Furthermore, we show that invades fibroblasts and keratinocytes and survives inside these cells as well as in monocyte-derived macrophages and neutrophils for at least 17 h postinfection; however, MNGC formation is not induced in these cells. In contrast, infection of mixed neutrophils and RAW264.7 macrophages with stimulated the formation of heterotypic MNGCs in a T6SS-5-dependent manner. In summary, the ability of the bacteria to enter and survive as well as induce MNGC formation in certain host cells may contribute to the pathogenesis observed in infection.

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LC3-associated phagocytosis in microbial pathogenesis

Schille

Crauwels

Bohn

et al. 2018

International Journal of Medical Microbiology

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Phagocytosis is essential for uptake and elimination of pathogenic microorganisms. Autophagy is a highly conserved mechanism for incorporation of cellular constituents to replenish nutrients by degradation. Recently, parts of the autophagy machinery - above all microtubule-associated protein 1 light chain 3 (LC3) - were found to be specifically recruited to phagosomal membranes resulting in phagosome-lysosome fusion and efficient degradation of internalized cargo in a process termed LC3-associated phagocytosis (LAP). Many pathogenic bacterial, fungal and parasitic microorganisms reside within LAP-targeted single-membrane phagosomes or vacuoles after infection of host cells. In this minireview we describe the state of knowledge on the interaction of pathogens with LAP or LAP-like pathways and report on various pathogens that have evolved strategies to circumvent degradation in LAP compartments.

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Interaction of Burkholderia pseudomallei and Burkholderia thailandensis with human monocyte-derived dendritic cells

Cited by 9 publications

References 42 publications

Migration of Dendritic Cells Facilitates Systemic Dissemination of Burkholderia pseudomallei

Migration of Dendritic Cells Facilitates Systemic Dissemination of Burkholderia pseudomallei

Entry, Intracellular Survival, and Multinucleated-Giant-Cell-Forming Activity of Burkholderia pseudomallei in Human Primary Phagocytic and Nonphagocytic Cells

LC3-associated phagocytosis in microbial pathogenesis

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