Dendritic cells and Brucella spp. interaction: the sentinel host and the stealthy pathogen

Ávila-Calderón, Eric Daniel; Flores‐Romo, Leopoldo; Witonsky, Sharon G.; Donis-Maturano, Luis; Becerril-García, Miguel A.; Arreola, Ma Guadalupe Aguilera; Arellano-Reynoso, Beatriz; Güemes, Francisco Suárez; Contreras-Rodríguez, Araceli

doi:10.1007/s12223-019-00691-6

Cited by 20 publications

(10 citation statements)

References 110 publications

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“…It is estimated that Shigella causes approximately 125 million diarrhea episodes and approximately 160,000 deaths every years, with a third are related to young children ( Baker and The, 2018 ). Shigella produces Shigella enterotoxin and serotype toxin 1 into the enteric cavity, which further invade and destroy the epithelium of the large intestine, eventually leading to aggressive watery or mucus-like/bloody diarrhea ( Nisa et al., 2020 ).…”

Section: Gut Microbiota-mediated Diarrhea and Its Mechanismmentioning

confidence: 99%

Gut Microbiota and Diarrhea: An Updated Review

Xia

Jiang

et al. 2021

Front. Cell. Infect. Microbiol.

113

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Diarrhea is a common problem to the whole world and the occurrence of diarrhea is highly associated with gut microbiota, such as bacteria, fungi, and viruses. Generally, diarrheal patients or animals are characterized by gut microbiota dysbiosis and pathogen infections may lead to diarrheal phenotypes. Of relevance, reprograming gut microbiota communities by dietary probiotics or fecal bacteria transplantation are widely introduced to treat or prevent diarrhea. In this review, we discussed the influence of the gut microbiota in the infection of diarrhea pathogens, and updated the research of reshaping the gut microbiota to prevent or treat diarrhea for the past few years. Together, gut microbiota manipulation is of great significance to the prevention and treatment of diarrhea, and further insight into the function of the gut microbiota will help to discover more anti-diarrhea probiotics.

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Section: Gut Microbiota-mediated Diarrhea and Its Mechanismmentioning

confidence: 99%

Gut Microbiota and Diarrhea: An Updated Review

Xia

Jiang

et al. 2021

Front. Cell. Infect. Microbiol.

113

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“…Dendritic cells (DCs) that display a higher susceptibility than macrophages to Brucella infection (Billard, Cazevieille, Dornand, & Gross, 2005) are essential for the induction of innate and adaptive immune responses against this pathogen (Avila- Calderon et al, 2019;Papadopoulos & Gorvel, 2015). DCs control bacterial growth through secretion of pro-inflammatory cytokines such as interleukin-12 or enzyme like NOS2 (Copin, De Baetselier, Carlier, Letesson, & Muraille, 2007;Macedo et al, 2008).…”

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confidence: 99%

Omp25‐dependent engagement of SLAMF1 byBrucella abortusin dendritic cells limits acute inflammation and favours bacterial persistence in vivo

Degos

Hysenaj

González-Espinoza

et al. 2020

Cellular Microbiology

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The strategies by which intracellular pathogenic bacteria manipulate innate immunity to establish chronicity are poorly understood. Here, we show that Brucella abortus outer membrane protein Omp25 specifically binds the immune cell receptor SLAMF1 in vitro. The Omp25‐dependent engagement of SLAMF1 by B. abortus limits NF‐κB translocation in dendritic cells (DCs) with no impact on Brucella intracellular trafficking and replication. This in turn decreases pro‐inflammatory cytokine secretion and impairs DC activation. The Omp25‐SLAMF1 axis also dampens the immune response without affecting bacterial replication in vivo during the acute phase of Brucella infection in a mouse model. In contrast, at the chronic stage of infection, the Omp25/SLAMF1 engagement is essential for Brucella persistence. Interaction of a specific bacterial protein with an immune cell receptor expressed on the DC surface at the acute stage of infection is thus a powerful mechanism to support microbe settling in its replicative niche and progression to chronicity.

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“…IFN-γ mediated Th1 immune response is essential for Brucella clearance [ 52 ]. Brucella can affect the maturation of DC by blocking the TLR2 receptor pathway, and interfere with the establishment of type Th1 immune response by reducing the secretion of IL-12 and preventing the activation of T-lymphocyte by DC [ 53 ].…”

Section: Brucella Evades Killing Of Host Immunementioning

confidence: 99%

The Mechanism of Facultative Intracellular Parasitism of Brucella

Zhou

et al. 2021

IJMS

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Brucellosis is a highly prevalent zoonotic disease characterized by abortion and reproductive dysfunction in pregnant animals. Although the mortality rate of Brucellosis is low, it is harmful to human health, and also seriously affects the development of animal husbandry, tourism and international trade. Brucellosis is caused by Brucella, which is a facultative intracellular parasitic bacteria. It mainly forms Brucella-containing vacuoles (BCV) in the host cell to avoid the combination with lysosome (Lys), so as to avoid the elimination of it by the host immune system. Brucella not only has the ability to resist the phagocytic bactericidal effect, but also can make the host cells form a microenvironment which is conducive to its survival, reproduction and replication, and survive in the host cells for a long time, which eventually leads to the formation of chronic persistent infection. Brucella can proliferate and replicate in cells, evade host immune response and induce persistent infection, which are difficult problems in the treatment and prevention of Brucellosis. Therefore, the paper provides a preliminary overview of the facultative intracellular parasitic and immune escape mechanisms of Brucella, which provides a theoretical basis for the later study on the pathogenesis of Brucella.

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Dendritic cells and Brucella spp. interaction: the sentinel host and the stealthy pathogen

Cited by 20 publications

References 110 publications

Gut Microbiota and Diarrhea: An Updated Review

Gut Microbiota and Diarrhea: An Updated Review

Omp25‐dependent engagement of SLAMF1 byBrucella abortusin dendritic cells limits acute inflammation and favours bacterial persistence in vivo

The Mechanism of Facultative Intracellular Parasitism of Brucella

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