scholarly journals Pediococcus Pentosaceus from the Sweet Potato Fermented Ger-Minated Brown Rice Can Inhibit Type I Hypersensitivity in RBL-2H3 Cell and BALB/c Mice Models

2021 ◽  
Vol 9 (9) ◽  
pp. 1855
Author(s):  
Kyu-Ree Dhong ◽  
Hye-Jin Park
Keyword(s):  
Mrna Expression ◽  
Brown Rice ◽  
Allergic Diseases ◽  
Nuclear Factor Κb ◽  
Treated Group ◽  
Interleukin 4 ◽  
Type I ◽  
Pediococcus Pentosaceus ◽  
Factor Α ◽  
Type I Hypersensitivity

In this study, the effect of GBR fermented with the Pediococcus pentosaceus SP024 strain on IgE/Ag mediated passive cutaneous anaphylaxis (PCA) was investigated. Protocatechuic acid and trans-ferulic acid levels in GBR-SP024 increased more than those in unfermented GBR, respec-tively. The inhibitory activity of GBR-SP024 on β-hexosaminidase release and the level of proin-flammatory cytokine mRNA expression (tumor necrosis factor-α (TNF-α) and interleukin 4 (IL-4)) was observed in IgE/Ag-stimulated RBL-2H3 cells. Western blot analysis showed that GBR-SP024 significantly inhibited the phosphorylation of the linker for activation of T cell (LAT) and nuclear factor-κB (NF-κB) in IgE/Ag-stimulated RBL-2H3 cells. Further, we investigated the anti-allergic effect of GBR-SP024 using PCA murine model. The number of infiltrated immune cells and degranulated mast cells in GBR-SP024 treated dermis was lower than that in the GBR-treated mice. In addition, mRNA expression of 5-lipoxygenase (5-LOX) in the dermis of ear tissue declined in the GBR-SP024–treated group, compared to that in the GBR group. GBR-SP024 was also more effective than GBR at reducing the levels of IL-33 protein expression in IgE/Ag-stimulated BALB/c mice. Our study suggests the potential usage of GBR-SP024 as a dietary supplement or an adjuvant for treating IgE-dependent-allergic diseases.

scholarly journals Hispidulin Inhibits Mast Cell-Mediated Allergic Inflammation through Down-Regulation of Histamine Release and Inflammatory Cytokines

Molecules ◽  
2019 ◽  
Vol 24 (11) ◽  
pp. 2131 ◽  
Author(s):  
Dong Eun Kim ◽  
Kyoung-jin Min ◽  
Min-Jong Kim ◽  
Sang-Hyun Kim ◽  
Taeg Kyu Kwon
Keyword(s):  
Mast Cells ◽  
Inflammatory Cytokines ◽  
Immunoglobulin E ◽  
Inflammatory Diseases ◽  
Allergic Inflammation ◽  
Interleukin 4 ◽  
Type I ◽  
Ige Mediated ◽  
Factor Α ◽  
Jnk Activation

Hispidulin (4′,5,7-trihydroxy-6-methoxyflavone) is a natural compound derived from traditional Chinese medicinal herbs, and it is known to have an anti-inflammatory effect. Here, we investigated the effect of hispidulin on the immunoglobulin E (IgE)-mediated allergic responses in rat basophilic leukemia (RBL)-2H3 mast cells. When RBL-2H3 cells were sensitized with anti-dinitrophenyl (anti-DNP) IgE and subsequently stimulated with DNP-human serum albumin (HSA), histamine and β-hexosaminidase were released from the cells by degranulation of activated mast cells. However, pretreatment with hispidulin before the stimulation of DNP-HSA markedly attenuated release of both in anti-DNP IgE-sensitized cells. Furthermore, we investigated whether hispidulin inhibits anti-DNP IgE and DNP-HSA-induced passive cutaneous anaphylaxis (PCA), as an animal model for Type I allergies. Hispidulin markedly decreased the PCA reaction and allergic edema of ears in mice. In addition, activated RBL-2H3 cells induced the expression of inflammatory cytokines (tumor necrosis factor-α and interleukin-4), which are critical for the pathogenesis of allergic disease, through the activation of c-Jun N-terminal kinase (JNK). Inhibition of JNK activation by hispidulin treatment reduced the induction of cytokine expression in the activated mast cells. Our results indicate that hispidulin might be a possible therapeutic candidate for allergic inflammatory diseases through the suppression of degranulation and inflammatory cytokines expression.

scholarly journals Anti-Inflammatory Property of the Essential Oil from Cinnamomum camphora (Linn.) Presl Leaves and the Evaluation of Its Underlying Mechanism by Using Metabolomics Analysis

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4796
Author(s):  
Jiali Chen ◽  
Cailin Tang ◽  
Yang Zhou ◽  
Rongfei Zhang ◽  
Shaoxia Ye ◽  
...  
Keyword(s):  
Essential Oil ◽  
Mrna Expression ◽  
Underlying Mechanism ◽  
Treated Group ◽  
Microglial Cells ◽  
Cinnamomum Camphora ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Bv2 Microglial Cells

Cinnamomum camphora (Linn.) Presl has been widely used in traditional Chinese medicine for a variety of purposes. Our previous study indicated the antibacterial mechanism of the essential oil (EO) from C. camphora leaves; however, its anti-inflammatory activity and the underlying mechanism have not been clearly demonstrated. Thus, the present study investigated its anti-inflammatory property. Our data revealed that EO significantly decreased the release of nitric oxide (NO) and the mRNA expression of inducible NO synthase (iNOS) in lipopolysaccharide (LPS)-induced BV2 microglial cells. EO also attenuated LPS-induced increase in the mRNA expression and secretion of inflammatory cytokines including interleukin-6 (IL-6), IL-18, IL-1β and tumor necrosis factor-α (TNF-α). Furthermore, the metabolic profiles of LPS-induced BV2 microglial cells treated with or without EO were explored. Thirty-nine metabolites were identified with significantly different contents, including 21 upregulated and 18 downregulated ones. Five pathways were enriched by shared differential metabolites. Compared with the control cells, the glucose level was decreased, while the lactate level was increased, in the culture supernatant from LPS-stimulated cells, which were reversed by EO treatment. Moreover, compared to the LPS-treated group, the activities of phosphofructokinase (PFK) and pyruvate kinase (PK) in EO group were decreased. In summary, the current study demonstrated that EO from C. camphora leaves acts as an anti-inflammatory agent, which might be mediated through attenuating the glycolysis capacity of microglial cells.

scholarly journals HIF-1α is a negative regulator of interferon regulatory factors: Implications for interferon production by hypoxic monocytes

2021 ◽  
Vol 118 (26) ◽  
pp. e2106017118
Author(s):  
Travis Peng ◽  
Shin-Yi Du ◽  
Myoungsun Son ◽  
Betty Diamond
Keyword(s):  
Inflammatory Cytokines ◽  
Cell Function ◽  
Hypoxia Inducible Factor ◽  
Human Monocyte ◽  
Nuclear Factor Κb ◽  
Negative Regulator ◽  
Type I ◽  
Hypoxic Conditions ◽  
Stressed Cells ◽  
Factor Α

Patients with severe COVID-19 infection exhibit a low level of oxygen in affected tissue and blood. To understand the pathophysiology of COVID-19 infection, it is therefore necessary to understand cell function during hypoxia. We investigated aspects of human monocyte activation under hypoxic conditions. HMGB1 is an alarmin released by stressed cells. Under normoxic conditions, HMGB1 activates interferon regulatory factor (IRF)5 and nuclear factor-κB in monocytes, leading to expression of type I interferon (IFN) and inflammatory cytokines including tumor necrosis factor α, and interleukin 1β, respectively. When hypoxic monocytes are activated by HMGB1, they produce proinflammatory cytokines but fail to produce type I IFN. Hypoxia-inducible factor-1α, induced by hypoxia, functions as a direct transcriptional repressor of IRF5 and IRF3. As hypoxia is a stressor that induces secretion of HMGB1 by epithelial cells, hypoxia establishes a microenvironment that favors monocyte production of inflammatory cytokines but not IFN. These findings have implications for the pathogenesis of COVID-19.

scholarly journals PI3K is critical for the nuclear translocation of IRF-7 and type I IFN production by human plasmacytoid predendritic cells in response to TLR activation

2008 ◽  
Vol 205 (2) ◽  
pp. 315-322 ◽  
Author(s):  
Cristiana Guiducci ◽  
Cristina Ghirelli ◽  
Marie-Annick Marloie-Provost ◽  
Tracy Matray ◽  
Robert L. Coffman ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Cell Types ◽  
Nuclear Factor Κb ◽  
Type I ◽  
Endosomal Trafficking ◽  
Type I Ifn ◽  
Protein Levels ◽  
Proinflammatory Responses ◽  
Novel Target ◽  
Factor Α

Plasmacytoid predendritic cells (pDCs) are the main producers of type I interferon (IFN) in response to Toll-like receptor (TLR) stimulation. Phosphatidylinositol-3 kinase (PI3K) has been shown to be activated by TLR triggering in multiple cell types; however, its role in pDC function is not known. We show that PI3K is activated by TLR stimulation in primary human pDCs and demonstrate, using specific inhibitors, that PI3K is required for type I IFN production by pDCs, both at the transcriptional and protein levels. Importantly, PI3K was not involved in other proinflammatory responses of pDCs, including tumor necrosis factor α and interleukin 6 production and DC differentiation. pDCs preferentially expressed the PI3K δ subunit, which was specifically involved in the control of type I IFN production. Although uptake and endosomal trafficking of TLR ligands were not affected in the presence of PI3K inhibitors, there was a dramatic defect in the nuclear translocation of IFN regulatory factor (IRF) 7, whereas nuclear factor κB activation was preserved. Thus, PI3K selectively controls type I IFN production by regulating IRF-7 nuclear translocation in human pDCs and could serve as a novel target to inhibit pathogenic type I IFN in autoimmune diseases.

scholarly journals Lipopolysaccharide Analogs Improve Efficacy of Acellular Pertussis Vaccine and Reduce Type I Hypersensitivity in Mice

2007 ◽  
Vol 14 (7) ◽  
pp. 821-829 ◽  
Author(s):  
Jeroen Geurtsen ◽  
H. Alexander Banus ◽  
Eric R. Gremmer ◽  
Henke Ferguson ◽  
Liset J. J. de la Fonteyne-Blankestijn ◽  
...  
Keyword(s):  
Lipid A ◽  
Ex Vivo ◽  
Lavage Fluid ◽  
Interleukin 4 ◽  
Type I ◽  
Monophosphoryl Lipid A ◽  
Endotoxin Activity ◽  
Lung Eosinophilia ◽  
Bronchial Lymph Node ◽  
Type I Hypersensitivity

ABSTRACT Pertussis is an infectious disease of the respiratory tract that is caused by the gram-negative bacterium Bordetella pertussis. Although acellular pertussis (aP) vaccines are safe, they are not fully effective and thus require improvement. In contrast to whole-cell pertussis (wP) vaccines, aP vaccines do not contain lipopolysaccharide (LPS). Monophosphoryl lipid A (MPL) and Neisseria meningitidis LpxL2 LPS have been shown to display immune-stimulating activity while exerting little endotoxin activity. Therefore, we evaluated whether these LPS analogs could increase the efficacy of the aP vaccine. Mice were vaccinated with diphtheria-tetanus-aP vaccine with aluminum, MPL, or LpxL2 LPS adjuvant before intranasal challenge with B. pertussis. Compared to vaccination with the aluminum adjuvant, vaccination with either LPS analog resulted in lower colonization and a higher pertussis toxin-specific serum immunoglobulin G level, indicating increased efficacy. Vaccination with either LPS analog resulted in reduced lung eosinophilia, reduced eosinophil numbers in the bronchoalveolar lavage fluid, and the ex vivo production of interleukin-4 (IL-4) by bronchial lymph node cells and IL-5 by spleen cells, suggesting reduced type I hypersensitivity. Vaccination with either LPS analog increased serum IL-6 levels, although these levels remained well below the level induced by wP, suggesting that supplementation with LPS analogs may induce some reactogenicity but reactogenicity considerably less than that induced by the wP vaccine. In conclusion, these results indicate that supplementation with LPS analogs forms a promising strategy that can be used to improve aP vaccines.

scholarly journals The Type II Heat-Labile Enterotoxins LT-IIa and LT-IIb and Their Respective B Pentamers Differentially Induce and Regulate Cytokine Production in Human Monocytic Cells

2004 ◽  
Vol 72 (11) ◽  
pp. 6351-6358 ◽  
Author(s):  
George Hajishengallis ◽  
Hesham Nawar ◽  
Richard I. Tapping ◽  
Michael W. Russell ◽  
Terry D. Connell
Keyword(s):  
Cytokine Production ◽  
Nuclear Factor Κb ◽  
Type I ◽  
Type Ii ◽  
Cytokine Induction ◽  
Heat Labile ◽  
Tnf Α ◽  
A Subunit ◽  
Anti Inflammatory ◽  
Factor Α

ABSTRACT The type II heat-labile enterotoxins, LT-IIa and LT-IIb, exhibit potent adjuvant properties. However, little is known about their immunomodulatory activities upon interaction with innate immune cells, unlike the widely studied type I enterotoxins that include cholera toxin (CT). We therefore investigated interactions of LT-IIa and LT-IIb with human monocytic THP-1 cells. We found that LT-II enterotoxins were inactive in stimulating cytokine release, whereas CT induced low levels of interleukin-1β (IL-1β) and IL-8. However, all three enterotoxins potently regulated cytokine induction in cells activated by bacterial lipopolysaccharide or fimbriae. Induction of proinflammatory (tumor necrosis factor α [TNF-α]) or chemotactic (IL-8) cytokines was downregulated, whereas induction of cytokines with anti-inflammatory (IL-10) or mucosal adjuvant properties (IL-1β) was upregulated by the enterotoxins. These effects appeared to depend on their A subunits, because isolated B-pentameric subunits lacked regulatory activity. Enterotoxin-mediated inhibition of proinflammatory cytokine induction in activated cells was partially attributable to synergism for endogenous production of IL-10 and to an IL-10-independent inhibition of nuclear factor κB (NF-κB) activation. In sharp contrast to the holotoxins, the B pentamers (LT-IIaB and, to a greater extent, LT-IIbB) stimulated cytokine production, suggesting a link between the absence of the A subunit and increased proinflammatory properties. In this regard, the ability of LT-IIbB to activate NF-κB and induce TNF-α and IL-8 was antagonized by the LT-IIb holotoxin. These findings support distinct immunomodulatory roles for the LT-II holotoxins and their respective B pentamers. Moreover, the anti-inflammatory properties of the holotoxins may serve to suppress innate immunity and promote the survival of the pathogen.

Regulation of progranulin expression in myeloid cells

2006 ◽  
Vol 291 (6) ◽  
pp. R1602-R1612 ◽  
Author(s):  
Colin H. P. Ong ◽  
Zhiheng He ◽  
Leonid Kriazhev ◽  
Xiaochuan Shan ◽  
Roger G. E. Palfree ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Mrna Stability ◽  
De Novo ◽  
Myeloid Cells ◽  
Nuclear Factor Κb ◽  
Interleukin 4 ◽  
Mrna Levels ◽  
All Trans Retinoic Acid ◽  
Myelomonocytic Cells ◽  
Differential Control

Progranulin (pgrn; granulin-epithelin precursor, PC-cell-derived growth factor, or acrogranin) is a multifunctional secreted glycoprotein implicated in tumorigenesis, development, inflammation, and repair. It is highly expressed in macrophage and monocyte-derived dendritic cells. Here we investigate its regulation in myeloid cells. All- trans retinoic acid (ATRA) increased pgrn mRNA levels in myelomonocytic cells (CD34+progenitors; monoblastic U-937; monocytic THP-1; progranulocytic HL-60; macrophage RAW 264.7) but not in nonmyeloid cells tested. Interleukin-4 impaired basal expression of pgrn in U-937. Differentiation agents DMSO, and, in U-937 only, phorbol ester [phorbol 12-myristate,13-acetate (PMA)] elevated pgrn mRNA expression late in differentiation, suggestive of roles for pgrn in more mature terminally differentiated granulocyte/monocytes rather than during growth or differentiation. The response of pgrn mRNA to ATRA differs in U-937 and HL-60 lineages. In U-937, ATRA and chemical differentiation agents greatly increased pgrn mRNA stability, whereas, in HL-60, ATRA accelerated pgrn mRNA turnover. The initial upregulation of pgrn mRNA after stimulation with ATRA was independent of de novo protein synthesis in U-937 but not HL-60. Chemical blockade of nuclear factor-κB (NF-κB) activation impaired ATRA-stimulated pgrn expression in HL-60 but not U-937, whereas in U-937 it blocked PMA-induced pgrn mRNA expression, suggestive of cell-specific roles for NF-κB in determining pgrn mRNA levels. We propose that: 1) ATRA regulates pgrn mRNA levels in myelomonocytic cells; 2) ATRA acts in a cell-specific manner involving the differential control of mRNA stability and differential requirement for NF-κB signaling; and 3) elevated pgrn mRNA expression is characteristic of more mature cells and does not stimulate differentiation.

Type I interferons in combination with bacterial stimuli induce apoptosis of monocyte-derived dendritic cells

Blood ◽  
2001 ◽  
Vol 98 (3) ◽  
pp. 736-742 ◽  
Author(s):  
Manfred Lehner ◽  
Thomas Felzmann ◽  
Katharina Clodi ◽  
Wolfgang Holter
Keyword(s):  
Cell Death ◽  
Lipoteichoic Acid ◽  
Type I Interferons ◽  
Interleukin 4 ◽  
Type I ◽  
Cell Recovery ◽  
Activation Induced Cell Death ◽  
Tnf Α ◽  
Macrophage Colony ◽  
Factor Α

Abstract Both type I interferons (IFNs) as well as lipopolysaccharide (LPS) individually compromise selected monocytic or dendritic cell (DC) functions. This study investigates the influence of these agents on the differentiation and the regulation of cell death of monocyte-derived DCs generated in the presence of granulocyte-macrophage colony-stimulating factor plus interleukin-4 (IL-4). It is reported that excessive apoptosis occurred rapidly in monocyte-derived DC cultures, if IFN-α or IFN-β was added in combination with LPS or lipoteichoic acid (LTA). The small fraction of cells surviving in such cultures displayed a mature DC phenotype with expression of CD83, CD80, and CD86. IL-10 was found in the supernatants of monocyte-derived DC cultures, if supplemented with LPS or IFN-α plus LPS but not in control cultures. When monocyte-derived DCs were generated in the presence of IFN-α without LPS, these cells displayed an immature DC phenotype with a reduction of cell recovery but no overt apoptosis. However, the addition of LPS, LTA, LPS plus IFN-γ, or tumor necrosis factor α (TNF-α) plus prostaglandin E2 to such cells again resulted in the rapid induction of apoptosis in the majority of cells, together with a reduced production of IL-12 p70 and TNF-α. Together, these data indicate an exquisite sensitivity of monocyte-derived DCs to activation-induced cell death if generated in the presence of IFN-α, indicating the existence of an important mechanism of immunosuppression caused by IFN-α–inducing agents, such as viral or bacterial stimuli.

scholarly journals Diverse innate stimuli activate basophils through pathways involving Syk and IκB kinases

2021 ◽  
Vol 118 (12) ◽  
pp. e2019524118
Author(s):  
Christophe Pellefigues ◽  
Palak Mehta ◽  
Sally Chappell ◽  
Bibek Yumnam ◽  
Sam Old ◽  
...  
Keyword(s):  
Growth Factors ◽  
Signaling Pathways ◽  
Allergic Diseases ◽  
Basophil Activation ◽  
Interleukin 4 ◽  
Type I ◽  
Direct Effects ◽  
Gm Csf ◽  
Type 2 Cytokines

Mature basophils play critical inflammatory roles during helminthic, autoimmune, and allergic diseases through their secretion of histamine and the type 2 cytokines interleukin 4 (IL-4) and IL-13. Basophils are activated typically by allergen-mediated IgE cross-linking but also by endogenous “innate” factors. The aim of this study was to identify the innate stimuli (cytokines, chemokines, growth factors, hormones, neuropeptides, metabolites, and bacterial products) and signaling pathways inducing primary basophil activation. Basophils from naïve mice or helminth-infected mice were cultured with up to 96 distinct stimuli and their influence on basophil survival, activation, degranulation, and IL-4 or IL-13 expression were investigated. Activated basophils show a heterogeneous phenotype and segregate into distinct subsets expressing IL-4, IL-13, activation, or degranulation markers. We find that several innate stimuli including epithelial derived inflammatory cytokines (IL-33, IL-18, TSLP, and GM-CSF), growth factors (IL-3, IL-7, TGFβ, and VEGF), eicosanoids, metabolites, TLR ligands, and type I IFN exert significant direct effects on basophils. Basophil activation mediated by distinct upstream signaling pathways is always sensitive to Syk and IκB kinases-specific inhibitors but not necessarily to NFAT, STAT5, adenylate cyclase, or c-fos/AP-1 inhibitors. Thus, basophils are activated by very diverse mediators, but their activation seem controlled by a core checkpoint involving Syk and IκB kinases.

scholarly journals Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients

Science ◽  
2020 ◽  
Vol 369 (6504) ◽  
pp. 718-724 ◽  
Author(s):  
Jérôme Hadjadj ◽  
Nader Yatim ◽  
Laura Barnabei ◽  
Aurélien Corneau ◽  
Jeremy Boussier ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Nuclear Factor Κb ◽  
Type I ◽  
Therapeutic Approaches ◽  
Host Immune Responses ◽  
Interferon Activity ◽  
Critical Patients ◽  
Factor Α ◽  
Necrosis Factor ◽  
Blood Viral Load

Coronavirus disease 2019 (COVID-19) is characterized by distinct patterns of disease progression that suggest diverse host immune responses. We performed an integrated immune analysis on a cohort of 50 COVID-19 patients with various disease severity. A distinct phenotype was observed in severe and critical patients, consisting of a highly impaired interferon (IFN) type I response (characterized by no IFN-β and low IFN-α production and activity), which was associated with a persistent blood viral load and an exacerbated inflammatory response. Inflammation was partially driven by the transcriptional factor nuclear factor–κB and characterized by increased tumor necrosis factor–α and interleukin-6 production and signaling. These data suggest that type I IFN deficiency in the blood could be a hallmark of severe COVID-19 and provide a rationale for combined therapeutic approaches.

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