Proinflammatory Response of Human Trophoblastic Cells to Brucella abortus Infection and upon Interactions with Infected Phagocytes1

Fernández, Andrea G.; Ferrero, Mariana C.; Hielpos, M. Soledad; Fossati, Carlos A.; Baldi, Pablo C.

doi:10.1095/biolreprod.115.131706

Cited by 23 publications

(28 citation statements)

References 37 publications

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“…canis infection with the secretion of IL-8 and RANTES, which attract neutrophils and monocytes to the infection site, and these phagocytes upon contact with the bacterium produce factors that further increase the inflammatory response of trophoblasts. Similar interactions between human trophoblasts and phagocytes in the context of Brucella abortus infection have been recently described by us [ 33 ].…”

Section: Discussionsupporting

confidence: 77%

Proinflammatory response of canine trophoblasts to Brucella canis infection

et al. 2017

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Brucella canis infection is an important cause of late-term abortion in pregnant bitches. The pathophysiological mechanisms leading to B. canis–induced abortion are unknown, but heavily infected trophoblasts are consistently observed. As trophoblasts responses to other pathogens contribute to placental inflammation leading to abortion, the aim of the present study was to characterize the cytokine response of canine trophoblasts to B. canis infection. To achieve this, trophoblasts isolated from term placenta of healthy female dogs were infected with B. canis, culture supernatants were harvested for cytokine determinations, and the load of intracellular viable B. canis was determined at different times post-infection. Additionally, cytokine responses were assessed in non-infected trophoblasts stimulated with conditioned media (CM) from B. canis-infected canine monocytes and neutrophils. Finally, cytokine response and bacteria replication were assessed in canine placental explants infected ex vivo. B. canis successfully infected and replicated in primary canine trophoblasts, eliciting an increase in IL-8 and RANTES (CCL5) secretion. Moreover, the stimulation of trophoblasts with CM from B. canis-infected monocytes and neutrophils induced a significant increase in IL-8, IL-6 and RANTES secretion. B. canis replication was confirmed in infected placental explants and the infection elicited an increased secretion of TNF-α, IL-8, IL-6 and RANTES. This study shows that canine trophoblasts produce proinflammatory cytokines in response to B. canis infection and/or to stimulation with factors produced by infected monocytes and neutrophils. These cytokines may contribute to placental inflammation leading to abortion in B. canis-infected pregnant bitches.

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Section: Discussionsupporting

confidence: 77%

Proinflammatory response of canine trophoblasts to Brucella canis infection

et al. 2017

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“…Sw.71 is a well-characterized cell lineage that has been accepted as a study model for human trophoblast biology [54,57]. Studies have shown that Sw.71 secretes an array of cytokines when stimulated with different bacterial products [58,59]. In this study, major products secreted by Sw.71 upon contact with E. coli or the 2 Lactobacillus species were chemokines, a property of these trophoblast cells that has been previously reported [54,60].…”

Section: Resultssupporting

confidence: 61%

Differential Secretion of Inflammatory Cytokines by Human Trophoblasts in the Presence of Escherichia coli, Lactobacillus crispatus, and Lactobacillus jensenii

Alhousseini

Vadillo-Ortega

Palacios‐González

et al. 2020

Gynecol Obstet Invest

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Introduction: The existence of a placental microbiome would require a non-antagonistic relationship between potentially colonizing bacteria and trophoblasts. Objective: The immunologic response of trophoblasts to specific potentially invading bacteria needs further analysis. Methodology: Immortalized first trimester human trophoblasts Swan 71 (Sw.71) were coincubated with Escherichia coli, Lactobacillus jensenii, Lactobacillus crispatus, and incubated alone (i.e., control group; 4 conditions with n = 6 for each condition). Chemokines and cytokines were measured. ANOVA with post hoc pairwise analysis was used to compare cytokines/chemokines concentrations in the 4 culture media. Results: Sw.71 co-incubated with E. coli, L. jensenii or L. crispatus resulted in differential secretion of 11 of the 26 assayed cytokines/chemokines. Sw.71 co-incubated with any of the 3 bacteria responded with significant increased secretion of interleukin (IL)-8 and granulocyte macrophage colony-stimulating factor. All bacteria elicited the secretion of IL-6 and interferon (IFN) α2, 2 proinflammatory cytokines. In addition, Lactobacillus species resulted in increased secretion of IL-12p40 and IFNγ. While E. coli did not modify secretion of anti-inflammatory cytokines, Sw.71 cells responded to co-incubation with Lactobacillus species by secreting increased levels of IL-10 and IL-1ra. Both Lactobacillus species led to a decreased secretion of IL-4. Conclusion: All 3 bacterial species triggered significant release of chemokines and inflammatory cytokines, suggesting that a commensal relationship with trophoblasts may not be feasible.

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“…Infection of placental cells could alter this equilibrium by provoking a local inflammatory environment, contributing to pregnancy complications. In a recent report, Fernández, Ferrero, Hielpos, Fossati, and Baldi () observed increased IL‐6, IL‐8, and MCP‐1 secretion in the human cytotrophoblastic Swan‐71 cells infected with B . abortus .…”

Section: Discussionmentioning

confidence: 94%

“…Infection of placental cells could alter this equilibrium by provoking a local inflammatory environment, contributing to pregnancy complications. In a recent report, Fernández, Ferrero, Hielpos, Fossati, and Baldi (2016) This work is another step in understanding the physiopathology of Brucella infections in pregnant women. A plausible hypothesis is that bacteria would reach the placenta hidden inside maternal immune cells, known to be attracted to the implantation site and to infiltrate the maternal decidua during early pregnancy (Robbins & Bakardjiev, 2012).…”

Section: Consequences Of Brucella Infection On Trophoblast Functionsmentioning

confidence: 99%

Infection by Brucella melitensis or Brucella papionis modifies essential physiological functions of human trophoblasts

García‐Méndez

Hielpos

Soler-Lloréns

et al. 2019

Cellular Microbiology

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Brucellosis is a zoonosis caused by bacteria of the Brucella genus. In ruminants, brucellosis causes abortion, followed by chronic infection and secretion of bacteria in milk. In humans, it usually presents as flu‐like symptoms, with serious complications if untreated. Epidemiological studies have only recently established that brucellosis can also cause pregnancy complications in women, but the pathogenic mechanisms are unknown. Pioneering studies in ruminants showed that Brucella infect trophoblasts and then colonise the placenta where they grow to high density. A recent study showed that the main zoonotic Brucella species can infect human cytotrophoblasts (CTB) and extravillous trophoblasts (EVT). In this work, we show that Brucella papionis (associated with stillbirth in primates) also infects human trophoblasts. However, it replicates actively in CTB, whereas its replication is very restricted within EVT. We also observed alteration of several trophoblastic functions upon infection by B. papionis or Brucella melitensis (the most prevalent species in human brucellosis). Infection altered the production of hormones, the ability of CTB to form syncytiotrophoblasts, and the invasion capacity of EVT. We also found that infection can spread between different types of trophoblasts. These findings constitute a new step in understanding how Brucella infection causes adverse pregnancy outcomes.

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Proinflammatory Response of Human Trophoblastic Cells to Brucella abortus Infection and upon Interactions with Infected Phagocytes1

Cited by 23 publications

References 37 publications

Proinflammatory response of canine trophoblasts to Brucella canis infection

Proinflammatory response of canine trophoblasts to Brucella canis infection

Differential Secretion of Inflammatory Cytokines by Human Trophoblasts in the Presence of <b><i>Escherichia coli</i></b>, <b><i>Lactobacillus crispatus</i></b>, and <b><i>Lactobacillus jensenii</i></b>

Infection by Brucella melitensis or Brucella papionis modifies essential physiological functions of human trophoblasts

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