Ragweed pollen extract intensifies lipopolysaccharide‐induced priming of <scp>NLRP</scp>3 inflammasome in human macrophages

Varga, Alíz; Budai, Marietta Margit; Milesz, Sándor; Bácsi, Attila; Tőzsér, József; Benkő, Szilvia

doi:10.1111/imm.12052

Cited by 26 publications

(16 citation statements)

References 35 publications

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“…The cells responded similarly to the cells that were pre‐exposed to LPS, but the secretion was lower than when the cells were pre‐exposed to LPS before adding NaHS. A reduced IL‐1β secretion without LPS treatment is in agreement with a previous report where ragweed pollen extract exposure in THP1 macrophages was studied (Varga et al, ). A previous study showed that NaHS exposure increased Akt phosphorylation, regulated by PI3K (Cai et al, ).…”

Section: Discussionsupporting

confidence: 92%

Hydrogen sulfide exposure induces NLRP3 inflammasome‐dependent IL‐1β and IL‐18 secretion in human mononuclear leukocytes in vitro

Basic

Alizadehgharib

Dahlén

et al. 2017

Clinical & Exp Dental Res

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The aim was to investigate if hydrogen sulfide (H2S) induces the formation of the NLRP3 inflammasome and subsequent IL‐1β and IL‐18 secretion in human peripheral blood mononuclear cells (PBMCs) and in the human monocyte cell line THP1. Bacterial production of H2S has been suggested to participate in the inflammatory host response in periodontitis pathogenesis. H2S is a toxic gas with pro‐inflammatory properties. It is produced by bacterial degradation of sulfur‐containing amino acids, for example, cysteine. We hypothesize that H2S affects the inflammatory host response by inducing formation of the NLRP3 inflammasome and thereby causes the secretion of IL‐1ß and IL‐18. PBMCs from eight healthy blood donors, the human monocyte cell line THP1 Null, and two variants of the THP1 cell line unable to form the NLRP3 inflammasome were cultured in the presence or absence of 1 mM sodium hydrosulfide (NaHS) in 24‐well plates at 37°C for 24 hr. Supernatants were collected and the IL‐1β and IL‐18 concentrations were measured with DuoSet ELISA Development kit. PBMCs exposed to NaHS produced more IL‐1ß and IL‐18 than unexposed control cells (p = .023 and p = .008, respectively). An increase of extracellular potassium ions (K+) inhibited the secretion of IL‐1ß and IL‐18 (p = .008). Further, NaHS triggered the secretion of IL‐1ß and IL‐18 in human THP1‐Null monocytes (p = .0006 and p = .002, respectively), while the NaHS‐dependent secretion was reduced in the monocyte cell lines unable to form the NLRP3 inflammasome. Hence, the results suggest that NaHS induces the formation of the NLRP3 inflammasome and thus the secretion of IL‐1ß and IL‐18. Enhanced NLRP3 inflammasome‐dependent secretion of IL‐1β and IL‐18 in human mononuclear leukocytes exposed to NaHS in vitro is reported. This may be a mode for H2S to contribute to the inflammatory host response and pathogenesis of periodontal disease.

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Section: Discussionsupporting

confidence: 92%

Hydrogen sulfide exposure induces NLRP3 inflammasome‐dependent IL‐1β and IL‐18 secretion in human mononuclear leukocytes in vitro

Basic

Alizadehgharib

Dahlén

et al. 2017

Clinical & Exp Dental Res

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“…Many studies provided increasing evidence for the central role of ROS in NLRP3 inflammasome activation [19, 24, 45–46]. Additional studies have demonstrated, through the use of either NADPH oxidase inhibitors or general ROS scavengers such as diphenylene iodonium (DPI) and N-acetyl-cysteine (NAC), that IL-1β production in response to even more diverse stimuli could be prevented [47–50].…”

Section: Discussionmentioning

confidence: 99%

Contribution of endogenously produced reactive oxygen species to the activation of podocyte NLRP3 inflammasomes in hyperhomocysteinemia

Abais

Xia

et al. 2014

Free Radical Biology and Medicine

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Hyperhomocysteinemia (hHcys) is an important pathogenic factor contributing to the progression of end-stage renal disease. Recent studies have demonstrated the implication of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-mediated NLRP3 inflammasome activation in the development of podocyte injury and glomerular sclerosis during hHcys. However, it remains unknown which reactive oxygen species (ROS) are responsible for this activation of NLRP3 inflammasomes and how such action of ROS is controlled. The present study tested the contribution of common endogenous ROS including superoxide (O2•−), hydrogen peroxide (H2O2), and hydroxyl radical (•OH) to the activation of NLRP3 inflammasomes in mouse podocytes and glomeruli. In vitro, confocal microscopy and size exclusion chromatography demonstrated that dismutation of O2•− by 4-Hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL) and decomposition of H2O2 by catalase prevented Hcys-induced aggregation of NLRP3 inflammasome proteins and inhibited Hcys-induced caspase-1 activation and IL-1β production in mouse podocytes. However, •OH scavenger tetramethylthiourea (TMTU) had no significant effect on either Hcys-induced NLRP3 inflammasome formation or activation. In vivo, scavenging of O2•− by TEMPOL and removal of H2O2 by catalase substantially inhibited NLRP3 inflammasome formation and activation in glomeruli of hHcys mice as shown by reduced colocalization of NLRP3 with ASC or caspase-1 and inhibition of caspase-1 activation and IL-1β production. Furthermore, TEMPOL and catalase significantly attenuated hHcys-induced glomerular injury. In conclusion, endogenously produced O2•− and H2O2 primarily contribute to NLRP3 inflammasome formation and activation in mouse glomeruli resulting in glomerular injury or consequent sclerosis during hHcys.

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“…Accumulating evidence indicates that inflammasomes are involved in the pathogenesis of AD. Activation of the inflammasome in keratinocytes by allergens and S. aureus , as well as in Mɸs after exposure to ragweed pollen allergen, has been shown . Current knowledge suggests inflammasomes promote Th1‐ or Th17‐mediated inflammation that may be important for acute AD .…”

Section: Immune Reactivitymentioning

confidence: 99%

Pathogenesis of atopic dermatitis

Peng

Novak

2015

Clin Experimental Allergy

221

155

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SummaryAtopic dermatitis (AD) is the most common allergic inflammatory skin disease. Interactions of genetic, environmental and immunological factors result in the initiation and progress of AD. Although the clinical picture, characterized by acute flare-ups of eczematous, pruritic lesions on dry skin at typical predilection such as the flexural folds, is quite homogenous, the trigger factors of the disease are diverse and the pathophysiologic network involved is complex. Therefore, first attempts have been made to classify subtypes of AD based on the most relevant causal factors in the individual patient. To optimize such a stratification of patients, detailed knowledge about cofactors impacting on manifestation of AD as well as impairment of the course of the disease is indispensable. AD shares general features of barrier dysfunction and skin inflammation with other inflammatory diseases of the skin such as psoriasis or allergic contact dermatitis, but a plethora of disease-specific genetic, immunologic and environmental factors have been identified in AD as well. It is the purpose of this review to illustrate key concepts of the pathogenesis of AD. Important findings of recent years will be summarized and cofactors of the pathogenesis will be controversially discussed. We will summarize knowledge on pathogenic factors on the immunologic level contributing to skin barrier dysfunction in AD and the role of the microbiome as first line of defence. Furthermore, we will elucidate the role of innate lymphoid cells in AD and outline the pattern of T helper cell subtypes present in the skin during different stages of AD.

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Ragweed pollen extract intensifies lipopolysaccharide‐induced priming of NLRP3 inflammasome in human macrophages

Cited by 26 publications

References 35 publications

Hydrogen sulfide exposure induces NLRP3 inflammasome‐dependent IL‐1β and IL‐18 secretion in human mononuclear leukocytes in vitro

Hydrogen sulfide exposure induces NLRP3 inflammasome‐dependent IL‐1β and IL‐18 secretion in human mononuclear leukocytes in vitro

Contribution of endogenously produced reactive oxygen species to the activation of podocyte NLRP3 inflammasomes in hyperhomocysteinemia

Pathogenesis of atopic dermatitis

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