Participation of dectin-1 receptor on NETs release against Paracoccidioides brasiliensis: Role on extracellular killing

Bachiega, Tatiana Fernanda; Dias-Melício, Luciane Alarcão; Fernandes, Reginaldo Keller; Balderramas, Helanderson de Almeida; Rodrigues, Daniela Ramos; Ximenes, Valdecir Farias; Soares, Ângela Maria Victoriano de Campos

doi:10.1016/j.imbio.2015.09.003

Cited by 35 publications

(31 citation statements)

References 63 publications

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“…[59][60][61][62] In addition, PMN effector and modulator new mechanisms have been shown to participate in the response to this fungus, demonstrating the importance of this cytokine in PMN recruitment, activation and survival. 31,32,35,63,64 Thus, it has been shown a cross-talk between PI3-Kinase and NF-Kappa B pathways in TNF-alpha-stimulated PMN, resulting in NF-Kappa B ⁄ ERK1 ⁄ 2-dependent IL-8 production that acts in an autocrine manner, evidencing other pathways in the induction of IL-8. 65 In relation to IL-12, we noted that monocytes activation with IFNγ was able to keep IL-12 production in response to the fungus, even when Dectin-1 receptor was blocked, showing an IFNγ participation in IL-12 production.…”

Section: Discussionmentioning

confidence: 99%

“…22,23 Because of the high specificity of Dectin-1 receptor molecule to β-Glucans, there is a variety of fungi species that can be recognized, such as Cryptococcus neoformans, 24 Pneumocystis carinii, 25 Aspergillus fumigatus, 26 Saccharomyces cerevisiae, 18 Coccidioides posadasii, 27 Candida albicans 28,29 and, Paracoccidioides brasiliensis (P. brasiliensis). [30][31][32][33][34][35] Dectin-1 role in PCM is not yet fully understood. For instance Bonfin et al 30 reported that monocytes challenged with P. brasiliensis increases the expression of mRNA for TLR2 and Dectin-1.…”

Section: Introductionmentioning

confidence: 99%

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Role of Dectin‐1 receptor on cytokine production by human monocytes challenged with Paracoccidioides brasiliensis

Romagnolo

Silva

Coletta

et al. 2018

Mycoses

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Fungal recognition by Dectin-1 receptor triggers a series of cellular mechanisms involved in a protective activation of the immune system. In this study, we aimed to evaluate the participation of Dectin-1 receptor in the induction of IL-8, TNF-α, IL-12, IL-10 and IL-17A secretion by human monocytes activated with different cytokines, and challenged in vitro with Paracoccidioides brasiliensis (P. brasiliensis). Our results show that monocytes challenged with P. brasiliensis (Pb265) are able to produce IL-12, IL-8, IL-17, IL-10 and TNF-α. Dectin-1 receptor blockage decreased the IL-12, IL-17, IL-10 and TNF-α levels indicating the participation of such receptor in the induction of these cytokines. Only IL-8 production was not affected by the blockage. Cells activation with different cytokines showed that GM-CSF was able to induce secretion of all cytokines and the receptor blockage prior to the challenge also decreased the cytokine secretion, except IL-8. Monocytes activated with TNF-α promoted IL-8, IL-10 and TNF-α production, whereas stimulation with IFN-γ promoted mainly IL-12 and TNF-α. Thus, these findings bring new and important knowledge about Dectin-1 participation in cytokines production by monocytes challenged with Pb265.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of Dectin‐1 receptor on cytokine production by human monocytes challenged with Paracoccidioides brasiliensis

Romagnolo

Silva

Coletta

et al. 2018

Mycoses

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“…Recent investigations have shed light on the importance of NET release for control of candidiasis and other invasive fungal infections 22,53–56 . This neutrophil effector mechanism delivers antimicrobial proteins and peptides while preventing dissemination of infection 19,21 .…”

Section: Discussionmentioning

confidence: 99%

Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth

Johnson

Kernien

Hoyer

et al. 2017

Sci Rep

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Candida spp. adhere to medical devices, such as catheters, forming drug-tolerant biofilms that resist killing by the immune system. Little is known about how C. glabrata, an emerging pathogen, resists attack by phagocytes. Here we show that upon encounter with planktonic (non-biofilm) C. glabrata, human neutrophils initially phagocytose the yeast and subsequently release neutrophil extracellular traps (NETs), complexes of DNA, histones, and proteins capable of inhibiting fungal growth and dissemination. When exposed to C. glabrata biofilms, neutrophils also release NETs, but significantly fewer than in response to planktonic cells. Impaired killing of biofilm parallels the decrease in NET production. Compared to biofilm, neutrophils generate higher levels of reactive oxygen species (ROS) when presented with planktonic organisms, and pharmacologic inhibition of NADPH-oxidase partially impairs NET production. In contrast, inhibition of phagocytosis nearly completely blocks NET release to both biofilm and planktonic organisms. Imaging of the host response to C. glabrata in a rat vascular model of infection supports a role for NET release in vivo. Taken together, these findings show that C. glabrata triggers NET release. The diminished NET response to C. glabrata biofilms likely contributes to the resilience of these structured communities to host defenses.

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“…NETs contained neutrophil antimicrobial factors, including neutrophil elastase and myeloperoxidase [9], and played an important role in trapping extracellular killing [9,17,18]. Wartha et al indicated that capsules of Streptococcus pneumoniae reduced trapping and protected bacteria from killing by NETs [19].…”

Section: Discussionmentioning

confidence: 99%

Resistance of hypervirulent Klebsiella pneumoniae to both intracellular and extracellular killing of neutrophils

Wang¹,

Shen²,

Wu³

et al. 2017

PLoS ONE

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Hypervirulent Klebsiella pneumoniae (HvKP) is hypermucoviscous organism, carrying genes of rmpA and aerobactin, causing serious community-acquired infection and metastatically spread in young healthy hosts. Neutrophils play an important role during innate immune response against bacterial infection by phagocytosis and neutrophil extracellular traps (NETs). Whether neutrophils can effectively defend against HvKP remains unclear. In this study, we observed that the HvKP was significantly more resistant to neutrophil-mediated phagocytosis and intracellular killing than classic Klebsiella pneumoniae (cKP) isolates. Although both HvKP and cKP induced NETs under scanning electron microscopy and confocal microscopy, more cKP than HvKP were trapped in NETs, and the killing by intracellular and extracellular mechanisms of neutrophils was detected only on cKP. Together, our results demonstrated that HvKP resisted to both intracellular and extracellular killing of neutrophils.

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Participation of dectin-1 receptor on NETs release against Paracoccidioides brasiliensis: Role on extracellular killing

Cited by 35 publications

References 63 publications

Role of Dectin‐1 receptor on cytokine production by human monocytes challenged with Paracoccidioides brasiliensis

Role of Dectin‐1 receptor on cytokine production by human monocytes challenged with Paracoccidioides brasiliensis

Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth

Resistance of hypervirulent Klebsiella pneumoniae to both intracellular and extracellular killing of neutrophils

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