Different Bacterial Pathogens, Different Strategies, Yet the Aim Is the Same: Evasion of Intestinal Dendritic Cell Recognition

Bedoui, Sammy; Kupz, Andreas; Wijburg, Odilia L. C.; Walduck, Anna; Rescigno, María; Strugnell, Richard A.

doi:10.4049/jimmunol.0902871

Cited by 40 publications

(39 citation statements)

References 75 publications

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“…Instead, the Salmonella bacteria interfere with the induction of adaptive immune responses and with the trafficking of dendritic cells to draining lymph nodes and the bloodstream. Residing sheltered from immune attack inside dendritic cells, S. Typhimurium exploits the migrating properties of dendritic cells to reach into deeper tissues and organs (35). Interestingly, our data showed reduced dissemination of Salmonella from the gastrointestinal tract into systemic organs in the absence of PECAM-1.…”

Section: Discussionsupporting

confidence: 46%

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Absence of Platelet Endothelial Cell Adhesion Molecule 1, PECAM-1/CD31,In VivoIncreases Resistance to Salmonella enterica Serovar Typhimurium in Mice

et al. 2013

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Section: Discussionsupporting

confidence: 46%

“…Various biological roles for PECAM-1 in thrombosis, inflammation, and the immune system have been identified (35). The role of PECAM-1 in the inflammatory process seems to depend on the stimulus and tissues involved and the genetic background when murine studies are concerned (reviewed in references 35, 36 and 37).…”

Section: Discussionmentioning

confidence: 99%

Absence of Platelet Endothelial Cell Adhesion Molecule 1, PECAM-1/CD31,In VivoIncreases Resistance to Salmonella enterica Serovar Typhimurium in Mice

et al. 2013

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“…3), perhaps as a result of notable differences in their respective sizes and morphologies. In fact, interactions of the host cytoskeleton with different microbes vary significantly based on the characteristics of the microbes involved (45). Although Wnt5a does not have any direct effect on the L. donovani parasite (Supplemental Fig.…”

Section: Discussionmentioning

confidence: 99%

Wnt5a Signaling Promotes Host Defense againstLeishmania donovaniInfection

Chakraborty

Kurati

Mahata

et al. 2017

The Journal of Immunology

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Leishmania donovani infects macrophages, disrupting immune homeostasis. The underlying mechanism that sustains infection remains unresolved. In view of the potential of Wnt5a signaling to support immune homeostasis, we evaluated the interrelationship of Wnt5a signaling and Leishmania donovani infection. Upon infecting macrophages separately with antimony drug–sensitive and –resistant L. donovani, we noted disruption in the steady-state level of Wnt5a. Moreover, inhibition of Wnt5a signaling by small interfering RNA transfection in vitro or by use of inhibitor of Wnt production in vivo led to an increase in cellular parasite load. In contrast, treatment of macrophages with recombinant Wnt5a caused a decrease in the load of antimony-sensitive and -resistant parasites, thus confirming that Wnt5a signaling antagonizes L. donovani infection. Using inhibitors of the Wnt5a signaling intermediates Rac1 and Rho kinase, we demonstrated that Wnt5a-mediated inhibition of parasite infection in macrophages is Rac1/Rho dependent. Furthermore, phalloidin staining and reactive oxygen species estimation of Wnt5a-treated macrophages suggested that a Wnt5a-Rac/Rho–mediated decrease in parasite load is associated with an increase in F- actin assembly and NADPH oxidase activity. Moreover, live microscopy of L. donovani–infected macrophages treated with Wnt5a demonstrated increased endosomal/lysosomal fusions with parasite-containing vacuoles (parasitophorous vacuoles [PV]). An increase in PV–endosomal/lysosomal fusion accompanied by augmented PV degradation in Wnt5a-treated macrophages was also apparent from transmission electron microscopy of infected cells. Our results suggest that, although L. donovani evades host immune response, at least in part through inhibition of Wnt5a signaling, revamping Wnt5a signaling can inhibit L. donovani infection, irrespective of drug sensitivity or resistance.

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“…Nonetheless, several pathogens have developed strategies to suppress DC maturation so that they can thrive in hostile conditions (28). The stimulation of TLRs in DCs by pathogen-associated microbial patterns leads to the activation of various inflammatory signaling pathways and antimicrobial mechanisms (29).…”

mentioning

confidence: 99%

Recruitment of Dendritic Cells Is Responsible for Intestinal Epithelial Damage in the Pathogenesis of Necrotizing Enterocolitis by Cronobacter sakazakii

Emami

Mittal

Wang

et al. 2011

The Journal of Immunology

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Cronobacter sakazakii is a Gram-negative pathogen associated with the cases of necrotizing enterocolitis (NEC) that result from formula contamination. In a mouse model of NEC, we demonstrate that C. sakazakii infection results in epithelial damage by recruiting greater numbers of dendritic cells (DCs) than macrophages and neutrophils in the gut and suppresses DC maturation, which requires outer membrane protein A (OmpA) expression in C. sakazakii. Pretreatment of intestinal epithelial cell monolayers with supernatant from OmpA+ C. sakazakii/DC culture markedly enhanced membrane permeability and enterocyte apoptosis, whereas OmpA− C. sakazakii/DC culture supernatant had no effect. Analysis of OmpA+ C. sakazakii/DC coculture supernatant revealed significantly greater TGF-β production compared with the levels produced by OmpA− C. sakazakii infection. TGF-β levels were elevated in the intestinal tissue of mice infected with OmpA+ C. sakazakii. Cocultures of CaCo-2 cells and DCs in a “double-layer” model followed by infection with OmpA+ C. sakazakii significantly enhanced monolayer leakage by increasing TGF-β production. Elevated levels of inducible NO synthase (iNOS) were also observed in the double-layer infection model, and abrogation of iNOS expression prevented the C. sakazakii-induced CaCo-2 cell monolayer permeability despite the presence of DCs or OmpA+ C. sakazakii/DC supernatant. Blocking TGF-β activity using a neutralizing Ab suppressed iNOS production and prevented apoptosis and monolayer leakage. Depletion of DCs in newborn mice protected against C. sakazakii-induced NEC, whereas adoptive transfer of DCs rendered the animals susceptible to infection. Therefore, C. sakazakii interaction with DCs in intestine enhances the destruction of the intestinal epithelium and the onset of NEC due to increased TGF-β production.

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Different Bacterial Pathogens, Different Strategies, Yet the Aim Is the Same: Evasion of Intestinal Dendritic Cell Recognition

Cited by 40 publications

References 75 publications

Absence of Platelet Endothelial Cell Adhesion Molecule 1, PECAM-1/CD31,In VivoIncreases Resistance to Salmonella enterica Serovar Typhimurium in Mice

Absence of Platelet Endothelial Cell Adhesion Molecule 1, PECAM-1/CD31,In VivoIncreases Resistance to Salmonella enterica Serovar Typhimurium in Mice

Wnt5a Signaling Promotes Host Defense againstLeishmania donovaniInfection

Recruitment of Dendritic Cells Is Responsible for Intestinal Epithelial Damage in the Pathogenesis of Necrotizing Enterocolitis by Cronobacter sakazakii

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