Phagocytosis and Killing of Bacteria by Professional Phagocytes and Dendritic Cells

Nagl, Markus; Kacani, Laco; Müllauer, Brigitte; Lemberger, Eva-Maria; Stoiber, Heribert; Sprinzl, Georg Mathias; Schennach, Harald; Dierich, Manfred P.

doi:10.1128/cdli.9.6.1165-1168.2002

Cited by 75 publications

(79 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This infection rate is higher than that reported for other intracellular pathogens, such as Leishmania major, where amastigotes infect only 36% of fetal skin-derived DCs at 18 h after inoculation (45). Unlike professional phagocytes, the major function of DCs is not to clear pathogens but to present antigens to the immune system (37). Quantification of intracellular rickettsiae in BMDCs (Fig.…”

Section: Discussionmentioning

confidence: 52%

Differential Interaction of Dendritic Cells withRickettsia conorii: Impact on Host Susceptibility to Murine Spotted Fever Rickettsiosis

Fang¹,

Ismail²,

Soong

et al. 2007

Infect Immun

View full text Add to dashboard Cite

Spotted fever group rickettsioses are emerging and reemerging infectious diseases, some of which are life-threatening. In order to understand how dendritic cells (DCs) contribute to the host resistance or susceptibility to rickettsial diseases, we first characterized the in vitro interaction of rickettsiae with bone marrow-derived DCs (BMDCs) from resistant C57BL/6 (B6) and susceptible C3H/HeN (C3H) mice. In contrast to the exclusively cytosolic localization within endothelial cells, rickettsiae efficiently entered and localized in both phagosomes and cytosol of BMDCs from both mouse strains. Rickettsia conorii-infected BMDCs from resistant mice harbored higher bacterial loads compared to C3H mice. R. conorii infection induced maturation of BMDCs from both mouse strains as judged by upregulated expression of classical major histocompatibility complex (MHC) and costimulatory molecules. Compared to C3H counterparts, B6 BMDCs exhibited higher expression levels of MHC class II and higher interleukin-12 (IL-12) p40 production upon rickettsial infection and were more potent in priming naïve CD4؉ T cells to produce gamma interferon. In vitro DC infection and T-cell priming studies suggested a delayed CD4 ؉ T-cell activation and suppressed Th1/Th2 cell development in C3H mice. The suppressive CD4؉ T-cell responses seen in C3H mice were associated with a high frequency of Foxp3 ؉ T regulatory cells promoted by syngeneic R. conorii-infected BMDCs in the presence of IL-2. These data suggest that rickettsiae can target DCs to stimulate a protective type 1 response in resistant hosts but suppressive adaptive immunity in susceptible hosts.

show abstract

Section: Discussionmentioning

confidence: 52%

Differential Interaction of Dendritic Cells withRickettsia conorii: Impact on Host Susceptibility to Murine Spotted Fever Rickettsiosis

Fang¹,

Ismail²,

Soong

et al. 2007

Infect Immun

View full text Add to dashboard Cite

show abstract

“…In agreement with this finding, Aline et al (10) have demonstrated that the intracellular replication of Toxoplasma gondii in DC is inhibited by an oxygen-dependent mechanism. Thus, even if DC might have a reduced ability to kill pathogens when compared with professional phagocytes (60), these cells posses the ability to clear intracellular pathogens by an oxygen-dependent mechanism.…”

Section: Discussionmentioning

confidence: 99%

Toll Receptor-Mediated Regulation of NADPH Oxidase in Human Dendritic Cells

Vulcano

Dusi

Lissandrini

et al. 2004

The Journal of Immunology

122

108

View full text Add to dashboard Cite

Activation of NADPH oxidase represents an essential mechanism of defense against pathogens. Dendritic cells (DC) are phagocytic cells specialized in Ag presentation rather than in bacteria killing. Human monocyte-derived DC were found to express the NADPH oxidase components and to release superoxide anions in response to phorbol esters and phagocytic agonists. The NADPH oxidase components p47phox and gp91phox were down-regulated during monocyte differentiation to DC, and maturation of DC with pathogen-derived molecules, known to activate TLRs, increased p47phox and gp91phox expression and enhanced superoxide anions release. Similar results were obtained with plasmacytoid DC following maturation with influenza virus. In contrast, activation of DC by immune stimuli (CD40 ligand) did not regulate NADPH oxidase components or respiratory burst. NADPH oxidase-derived oxygen radicals did not play any role in DC differentiation, maturation, cytokine production, and induction of T cell proliferation, as based on the normal function of DC generated from chronic granulomatous disease patients and the use of an oxygen radical scavenger. However, NADPH oxidase activation was required for DC killing of intracellular Escherichia coli. It is likely that the selective regulation of oxygen radicals production by pathogen-activated DC may function to limit pathogen dissemination during DC trafficking to secondary lymphoid tissues.

show abstract

“…at the onset of infection in the two types of cells. Phagocytic activities of macrophages and immature DCs have not often been compared; moreover, conflicting conclusions have been reported (17,22,31). Macrophages and DCs were infected with B. suis; in parallel, the phagocytosis of 1 m latex beads or B. suis manB was analyzed as a control.…”

mentioning

confidence: 99%

High Susceptibility of Human Dendritic Cells to Invasion by the Intracellular PathogensBrucella suis, B. abortus, andB. melitensis

Billard

Cazevieille²,

Dornand

et al. 2005

Infect Immun

View full text Add to dashboard Cite

Bacteria from the Brucella genus are able to survive and proliferate within macrophages. Because they are phylogenetically closely related to macrophages, myeloid dendritic cells (DCs) constitute potential targets for Brucella bacteria. Here we report that DCs display a great susceptibility to Brucella infection. Therefore, DCs might serve as a reservoir and be important for the development of Brucella bacteria within their host.Brucella are facultative intracellular bacteria that induce chronic infections in a wide range of mammals, including domestic animals and humans. Brucella bacteria are responsible for brucellosis and Mediterranean fever, also known as Malta fever. After invasion of the lymphoid system, the bacteria develop within mononuclear phagocytes, and the infected cells play a crucial role in the dissemination of the bacteria in specific locations of the body (spleen, brain, heart, and bones). Of intramacrophagic pathogens, Brucella bacteria are among the most powerful and are able to multiply intracellularly up to several thousandfold. The common ontogeny of macrophages and myeloid dendritic cells (DCs) and the discovery of a primordial role for DCs in immunity have raised the question of a relationship between DCs and intramacrophagic pathogens. Therefore, we have investigated the possible interaction between Brucella bacteria and DCs.Macrophages and immature DCs were prepared from peripheral blood circulating monocytes obtained by centrifugation on Ficoll-Hypaque (Sigma, Lyon, France) of buffy coat from healthy donors. Monocytes were purified on a magnetic column using anti-CD14-antibody-conjugated microbeads (Miltenyi-Biotec, Paris, France) and differentiated for 5 days in complete medium (RPMI 1640-10% fetal calf serum) supplemented with 50 M ␤-mercaptoethanol, 500 U/ml of interleukin-4, and 1,000 U/ml of granulocyte-macrophage colony-stimulating factor (Immunotools, Friesoythe, Germany) for DCs or with 10 Ϫ7 M vitamin D3 (Hoffman-Laroche, Bale, Switzerland) for syngeneic macrophages. Immature DCs were CD14 null (100%), CD83 null (Ͼ95%), DC-SIGN positive (100%), and CD1a positive (100%) and CMH-II low (100%). Macrophages were 100% CD14 positive, CD54 low, CD80 low, and CD86 low. After their differentiation, the cells were infected for 1 h at a multiplicity of infection (MOI) of 50 with the green fluorescent protein (GFP)-expressing strains of three Brucella species, B. suis, B. abortus, and B. melitensis, or with different B. suis attenuated mutants (Table 1). They were then washed with phosphate-buffered saline (PBS) and reincubated in fresh medium supplemented with 30 g/ml gentamicin to kill remaining extracellular bacteria. Figure 1A shows the observation by fluorescence microscopy of cells infected with the GFPexpressing Brucella spp. (11) at 48 h postinfection (p.i.).As frequently described, whatever the species considered, Brucella bacteria have strongly proliferated inside macrophages. Strikingly, the cytoplasm of DCs was completely invaded, some cells containing several hundred Brucell...

show abstract

Phagocytosis and Killing of Bacteria by Professional Phagocytes and Dendritic Cells

Cited by 75 publications

References 20 publications

Differential Interaction of Dendritic Cells withRickettsia conorii: Impact on Host Susceptibility to Murine Spotted Fever Rickettsiosis

Differential Interaction of Dendritic Cells withRickettsia conorii: Impact on Host Susceptibility to Murine Spotted Fever Rickettsiosis

Toll Receptor-Mediated Regulation of NADPH Oxidase in Human Dendritic Cells

High Susceptibility of Human Dendritic Cells to Invasion by the Intracellular PathogensBrucella suis, B. abortus, andB. melitensis

Contact Info

Product

Resources

About