Listeria monocytogenes induces mast cell extracellular traps

Campillo-Navarro, Marcia; Leyva-Paredes, Kahiry; Donis-Maturano, Luis; González-Jiménez, Marco Antonio; Paredes-Vivas, Yuriria; Cérbulo-Vázquez, Arturo; Serafín‐López, Jeanet; Garcı́a-Pérez, Blanca Estela; Ullrich, Stephen E.; Flores‐Romo, Leopoldo; Pérez‐Tapia, Sonia Mayra; Estrada‐Parra, Sergio; Estrada-Garcı́a, Iris; Chacón‐Salinas, Rommel

doi:10.1016/j.imbio.2016.08.006

Cited by 49 publications

(66 citation statements)

References 39 publications

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“…Beyond its role in allergic reactions, mast cells also play a crucial role in the innate immune response against virus, bacteria, fungi, protozoa, and helminths. Being some of the first cells to sense the presence of pathogens their activation leads to the induction of inflammation and triggering of microbicidal mechanisms that help to contain infection 2,39 . Whether this function is affected by VPA needs to be analyzed.…”

Section: Resultsmentioning

confidence: 99%

The histone deacetylase inhibitor valproic acid attenuates phospholipase Cγ2 and IgE-mediated mast cell activation

Rodríguez-López

Soria-Castro

Campillo-Navarro

et al. 2020

Journal of Leukocyte Biology

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Mast cell activation through the high‐affinity IgE receptor (FcεRI) plays a central role in allergic reactions. FcεRI‐mediated activation triggers multiple signaling pathways leading to degranulation and synthesis of different inflammatory mediators. IgE‐mediated mast cell activation can be modulated by different molecules, including several drugs. Herein, we investigated the immunomodulatory activity of the histone deacetylase inhibitor valproic acid (VPA) on IgE‐mediated mast cell activation. To this end, bone marrow‐derived mast cells (BMMC) were sensitized with IgE and treated with VPA followed by FcεRI cross‐linking. The results indicated that VPA reduced mast cell IgE‐dependent degranulation and cytokine release. VPA also induced a significant reduction in the cell surface expression of FcεRI and CD117, but not other mast cell surface molecules. Interestingly, VPA treatment inhibited the phosphorylation of PLCγ2, a key signaling molecule involved in IgE‐mediated degranulation and cytokine secretion. However, VPA did not affect the phosphorylation of other key components of the FcεRI signaling pathway, such as Syk, Akt, ERK1/2, or p38. Altogether, our data demonstrate that VPA affects PLCγ2 phosphorylation, which in turn decreases IgE‐mediated mast cell activation. These results suggest that VPA might be a key modulator of allergic reactions and might be a promising therapeutic candidate.

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Section: Resultsmentioning

confidence: 99%

The histone deacetylase inhibitor valproic acid attenuates phospholipase Cγ2 and IgE-mediated mast cell activation

Rodríguez-López

Soria-Castro

Campillo-Navarro

et al. 2020

Journal of Leukocyte Biology

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“…Bacterial insult can also lead to the release of enzymes and proteases stored in MCs granules. Beta‐hexosaminidase was found to inhibit Listeria monocytogenes growth in vitro and to protect against Staphylococcus epidermidis infections in vivo . Similarly, stimulation of murine peritoneal cavity‐derived MCs with Streptococci induced the release of a chymase as well as a novel enzyme, granzyme D .…”

Section: Mc–microbiota Interactions Promoting MC Activationmentioning

confidence: 98%

“…Finally, similar to neutrophils’ antibacterial strategies, stimulation of human MCs with L. monocytogenes induced the release of so‐called MCs extracellular traps (MCETs) through the production of ROS. These MCETs are extracellular structures composed of DNA, histones, tryptase, and antimicrobial peptides such as LL‐37, which are able to reduce bacterial growth .…”

Section: Mc–microbiota Interactions Promoting MC Activationmentioning

confidence: 99%

Mast cells at the crossroads of microbiota and IBD

2018

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The human gut harbors a wide range of microorganisms that play a fundamental role in the well-being of their host. A dysregulation of the microbial composition can lead to the development or exacerbation of gastrointestinal (GI) disorders. Emerging evidence supports the hypothesis that mast cells (MCs) play a role in host-microbiota communication, modulating the mutual influence between the host and its microbiota through changes in their activation state. The ability of some bacteria to specifically affect MC functions and activation has been extensively studied, with different and sometimes conflicting results, while only little is known about MC-fungi interactions. In this review, the most recent advances in the field of MC-bacteria and MC-fungi interactions will be discussed, with a particular focus on the role of these interactions in the onset of GI disorders such as inflammatory bowel diseases (IBD). Moreover, the connection between some MC-targeting drugs and IBD was discussed, suggesting probiotics as reasonable and promising therapy in the management of IBD patients. Keywords: Inflammatory bowel disease (IBD) r Intestine r Mast cells r Microbiota r Neurons Additional supporting information may be found online in the Supporting Information section at the end of the article. of the high affinity receptor for IgE on the surface of the cell and of the proteases-containing granules in the cytosol, under the influence of tissue-specific molecules (including SCF, IL-3, and IL-9) and bacterial-derived molecules (LPS and peptidoglycan) present in the local microenvironment [1]. Intestinal homing of MCs progenitors is mainly mediated by the interaction of α4β7 integrin expressed by MCs with ICAM-1, V-CAM, or MAdCAM-1 expressed by endothelial cells and it is influenced by CXCR2 ligation [2, 3].MCs possess a great number of costimulatory molecules, including members of the B7 family (ICOSL, PD-L1, and PD-L2,) and of the TNF/TNFR families (OX40L, CD153, Fas, 4-1BB, and glucocorticoid-induced TNFR), which allow them to interact with different partners both from immune and nonimmune cells populations as well as with bacteria and fungi through the expression of different pattern-recognition receptors (PRRs) [4]. Moreover, MCs harbor a high number of cytoplasmic granules that contain preformed immunomodulatory compounds such as proteases, histamine, heparin, and TNF-α. Given the wide pattern Eur.

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“…It has also been demonstrated that, whereas Streptococcus faecium and E. coli are phagocytosed by mast cells (Arock et al, 1998), Listeria monocytogenes is not (Dietrich et al, 2010). Finally, there are indications that mast cells can produce extracellular traps as a means of combating inter alia bacterial pathogens such as Streptococcus pyogenes (von Kockritz-Blickwede et al, 2008) or L. monocytogenes (Campillo-Navarro et al, 2017). Finally, there are indications that mast cells can produce extracellular traps as a means of combating inter alia bacterial pathogens such as Streptococcus pyogenes (von Kockritz-Blickwede et al, 2008) or L. monocytogenes (Campillo-Navarro et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Further, Sutherland et al demonstrated that mast cells induce killing of intracellular Klebsiella pneumoniae (Sutherland, Olsen, McKinstry, Villalta, & Wolters, 2008). Finally, there are indications that mast cells can produce extracellular traps as a means of combating inter alia bacterial pathogens such as Streptococcus pyogenes (von Kockritz-Blickwede et al, 2008) or L. monocytogenes (Campillo-Navarro et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

StreptococcalsagAactivates a proinflammatory response in mast cells by a sublytic mechanism

Beek

Waern

Eriksson

et al. 2019

Cellular Microbiology

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Mast cells are implicated in the innate proinflammatory immune defence against bacterial insult, but the mechanisms through which mast cells respond to bacterial encounter are poorly defined. Here, we addressed this issue and show that mast cells respond vividly to wild type Streptococcus equi by up‐regulating a panel of proinflammatory genes and by secreting proinflammatory cytokines. However, this response was completely abrogated when the bacteria lacked expression of sagA, whereas the lack of a range of other potential virulence genes (seeH, seeI, seeL, seeM, hasA, seM, aroB, pyrC, and recA) had no effect on the amplitude of the mast cell responses. The sagA gene encodes streptolysin S, a lytic toxin, and we next showed that the wild type strain but not a sagA‐deficient mutant induced lysis of mast cells. To investigate whether host cell membrane perturbation per se could play a role in the activation of the proinflammatory response, we evaluated the effects of detergent‐ and pneumolysin‐dependent lysis on mast cells. Indeed, exposure of mast cells to sublytic concentrations of all these agents resulted in cytokine responses of similar amplitudes as those caused by wild type streptococci. This suggests that sublytic membrane perturbation is sufficient to trigger full‐blown proinflammatory signalling in mast cells. Subsequent analysis showed that the p38 and Erk1/2 signalling pathways had central roles in the proinflammatory response of mast cells challenged by either sagA‐expressing streptococci or detergent. Altogether, these findings suggest that sagA‐dependent mast cell membrane perturbation is a mechanism capable of activating the innate immune response upon bacterial challenge.

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Listeria monocytogenes induces mast cell extracellular traps

Cited by 49 publications

References 39 publications

The histone deacetylase inhibitor valproic acid attenuates phospholipase Cγ2 and IgE-mediated mast cell activation

The histone deacetylase inhibitor valproic acid attenuates phospholipase Cγ2 and IgE-mediated mast cell activation

Mast cells at the crossroads of microbiota and IBD

StreptococcalsagAactivates a proinflammatory response in mast cells by a sublytic mechanism

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