Critical roles of NLRP3 inflammasome in IL-1β secretion induced by Corynebacterium pseudotuberculosis in vitro

Zhou, Zhixiong; Li, Hexian; Tian, Shangquan; Yi, Wenyi; Zhou, Yang; Yang, Haoyue; Li, Xiao; Wu, Bi; Li, Xiaoxia; Wu, Junjun; Wang, Zhiying; Hu, Shijun; Fang, Rendong

doi:10.1016/j.molimm.2019.09.016

Cited by 13 publications

(15 citation statements)

References 34 publications

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“…125 Prevotella, Porphyromonas and Corynebacterium genera, which are increased in HS skin, can activate TLR2 and/or TLR4 in various cell types, including professional APCs. [126][127][128][129][130][131] Further, Prevotella exposure is associated with the increased production of IL-8 and IL-6 by epithelial cells. 132 This supports the hypothesis that dysbiosis favouring these bacteria may promote inflammation in HS skin via glycolipid-sensing TLRs expressed by innate immune cells and keratinocytes.…”

Section: Immune Re S P On S E To the MI Crob I Ome In H S 71 | Pattern Recognition Receptorsmentioning

confidence: 99%

Yin and Yang: A disrupted skin microbiome and an aberrant host immune response in hidradenitis suppurativa

Schell

Schneider

Nelson

2021

Experimental Dermatology

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Hidradenitis suppurativa (HS) is a chronic multifaceted, potentially scarring, inflammatory skin disease affecting the pilosebaceous units (PSU) of the axilla, inframammary folds, groin and buttocks. Clinical features include painful inflammatory nodules, abscesses and draining sinus tracts that produce a purulent, foul-smelling discharge. The estimated prevalence of HS is 0.2-0.6% globally, but the prevalence varies by geographic location: 0.5-1.3% in Europe, 0.7-1.2% in the United States and 0.01%-2.2% in the Asia-Pacific region. 1,2 Common comorbidities and behaviours associated with HS include diabetes, pulmonary disease, metabolic syndrome, obesity, polycystic ovary syndrome, inflammatory bowel disease, smoking and mechanical stress on skin. 1,3-5 HS negatively impacts patients' quality of life and causes significant economic burden on patients and the healthcare system. [6][7][8][9][10] The pathogenesis of HS is not fully understood. However, evidence supports the hypothesis that hair follicle occlusion leads to follicle rupture and an aberrant immune response to follicular and bacterial debris, triggering a cycle of damage and chronic inflammation. 7,[11][12][13][14] Factors involved in HS pathogenesis include genetics, hormones, local environmental factors (eg sweating, skin friction), abnormal host responses to skin bacteria and impaired wound healing. [15][16][17][18] Approximately 30% of patients have a family history of HS, and of these, about 10% of these familial cases have an inactivating mutation in the γ-secretase enzyme complex. 19,20 These γ-secretase mutations are relatively uncommon in sporadic cases of HS (~6%). 21 γ-secretase activity in the skin

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Section: Immune Re S P On S E To the MI Crob I Ome In H S 71 | Pattern Recognition Receptorsmentioning

confidence: 99%

Yin and Yang: A disrupted skin microbiome and an aberrant host immune response in hidradenitis suppurativa

Schell

Schneider

Nelson

2021

Experimental Dermatology

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“…MAPKs, highly conserved in all eukaryotes, control a variety of cellular processes, including cell differentiation, proliferation, survival, and stress responses. It has been reported that the MAPK pathway remains associated with in ammasome activation [17][18][19]. We evaluated the roles of MAPK signaling pathways in NLRP3 and NLRP6 in ammasome activation by subjecting the T. gondii-infected FHs 74 Int cells to pretreatment with SB203580 and SP600125, inhibitors of p38 MAPK and JNK, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…in ammasome activation and IL-1β secretion [18,19]. Wang et al [24] reported that T. gondii infection and MAPKs are associated with the in ammasome activation in mice.…”

Section: Discussionmentioning

confidence: 99%

“…Release of LDH signi cantly increased in the T. gondii-infected groups compared to that in the mock-infected control group. Cytotoxicities of FHs 74 Int cells infected with T. gondii for 0, 4, in ammasome activation and IL-1β secretion [18,19]. Wang et al [24] reported that T. gondii infection and MAPKs are associated with the in ammasome activation in mice.…”

Section: Effects Of T Gondii Infection On Cell Morphology and Cytotomentioning

confidence: 99%

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Expression Profiles of NOD-Like Receptors and Regulation of NLRP3 Inflammasome Activation in Toxoplasma Gondii-Infected Human Small Intestinal Epithelial Cells

Chu

Gao

et al. 2020

Preprint

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Background: Toxoplasma gondii is a parasite that majorly infects through the oral route. Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) play crucial roles in the immune responses generated during the parasitic infection and also drive the inflammatory response against invading parasites. However, little is known about the regulation of NLRs and inflammasome activation in T. gondii-infected human small intestinal epithelial (FHs 74 Int) cells. Methods: FHs 74 Int cells infected with T. gondii were subsequently evaluated for morphological changes, cytotoxicity, expression profiles of NLRs, inflammasome components, caspase-cleaved interleukins (ILs), and the mechanisms of NLRP3 and NLRP6 inflammasome activation. Immunocytochemistry, lactate dehydrogenase assay, reverse transcription polymerase chain reaction (RT-PCR), real-time quantitative RT-PCR, and western blotting techniques were utilized for the analysis purpose. Results: Under normal and T. gondii-infected conditions, members of the NLRs, inflammasome components, and caspase-cleaved ILs were expressed in the FHs Int 74 cells, except for NLRC3, NLRP5, and NLRP9. Among the NLRs, mRNA expression of NOD2, NLRP3, NLRP6, and NAIP1 were significantly increased in T. gondii-infected cells, whereas that of NLRP2, NLRP7, and CIITA mRNAs decreased significantly in a time-dependent manner. In addition, T. gondii infection induced NLRP3, NLRP6 and NLRC4 inflammasome activation and production of IL-1β, IL-18, and IL-33 in FHs 74 Int cells. T. gondii-induced NLRP3 inflammasome activation was strongly associated with the phosphorylation of p38 MAPK but not JNK1/2. NLRP6 inflammasome activation was not related to the MAPK pathway in FHs 74 Int cells. Conclusions: This study highlighted the expression profiles of NLRs and unraveled the underlying mechanisms of NLRP3 inflammasome activation in T. gondii-infected FHs 74 Int cells. These findings may contribute to understanding of the mucosal and innate immune responses induced by the NLRs and inflammasomes during T. gondii infection in FHs 74 Int cells.

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“…Previous studies have pointed out that extracellular HMGB1 can interact with a variety of cell surface receptors, including toll‐like receptor (TLR) 2, TLR4, or TLR9 and advanced glycation end product receptor (RAGE), to induce the production of pro‐inflammatory cytokines . Of course, NLRP3 inflammasome is the most studied members of the NLRP superfamily . NLRP3 inflammasome consists of NLRP3, apoptosis‐related spot‐like protein (ASC), and caspase‐1 .…”

Section: Introductionmentioning

confidence: 99%

Blockade of high mobility group box 1 involved in the protective of curcumin on myocardial injury in diabetes in vivo and in vitro

Yan

Zhou

et al. 2020

IUBMB Life

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The aim of this study was to investigate the protective effect of curcumin (Cu) on myocardial injury in diabetic cardiomyopathy in vivo and in vitro. Serum and myocardial glucose, inflammatory cytokines, and cardiac function indexes of type 2 diabetes db/db mice were measured. The mechanism of action was confirmed by immunohistochemistry, immunofluorescence, and western blot experiments. H9C2 cells stimulated by glucose (Glu) were used as cell models in vitro. Cu treatment improved glucose tolerance and lipid profile and reduced the production of inflammatory cytokines. In addition, Cu decreased the serum biochemical indexes. Cu inhibits high mobility group box 1 (HMGB1) signaling pathway in db/db mice. Cu treatment also significantly inhibited pa‐induced inflammatory signaling pathway in H9C2 cells. HMGB1 inhibitor or HMGB1 knockdown counteracted the effects of Cu on diabetic cardiomyopathy. The present study showed the protective effects of Cu on myocardial injury via HMGB1 pathway in diabetic cardiomyopathy in vivo and in vitro.

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Critical roles of NLRP3 inflammasome in IL-1β secretion induced by Corynebacterium pseudotuberculosis in vitro

Cited by 13 publications

References 34 publications

Yin and Yang: A disrupted skin microbiome and an aberrant host immune response in hidradenitis suppurativa

Yin and Yang: A disrupted skin microbiome and an aberrant host immune response in hidradenitis suppurativa

Expression Profiles of NOD-Like Receptors and Regulation of NLRP3 Inflammasome Activation in Toxoplasma Gondii-Infected Human Small Intestinal Epithelial Cells

Blockade of high mobility group box 1 involved in the protective of curcumin on myocardial injury in diabetes in vivo and in vitro

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