scholarly journals Anti-Interleukin-1 Beta/Tumor Necrosis Factor-Alpha IgY Antibodies Reduce Pathological Allergic Responses in Guinea Pigs with Allergic Rhinitis

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hu Wei-xu ◽  
Zhou Wen-yun ◽  
Zhu Xi-ling ◽  
Wen Zhu ◽  
Wu Li-hua ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Treatment Group ◽  
Nasal Mucosa ◽  
Guinea Pigs ◽  
Interleukin 1 ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Ar Model ◽  
Necrosis Factor Alpha

This study aims to determine whether the combined blockade of IL-1βand TNF-αcan alleviate the pathological allergic inflammatory reaction in the nasal mucosa and lung tissues in allergic rhinitis (AR) guinea pigs. Healthy guinea pigs treated with saline were used as the healthy controls. The AR guinea pigs were randomly divided into (1) the AR model group treated with intranasal saline; (2) the 0.1% nonspecific IgY treatment group; (3) the 0.1% anti-TNF-αIgY treatment group; (4) the 0.1% anti-IL-1βIgY treatment group; (5) the 0.1% combined anti-IL-1βand TNF-αIgY treatment group; and (6) the fluticasone propionate treatment group. The inflammatory cells were evaluated using Wright’s staining. Histopathology was examined using hematoxylin-eosin staining. The results showed that the number of eosinophils was significantly decreased in the peripheral blood, nasal lavage fluid, and bronchoalveolar lavage fluid (P<0.05), and eosinophil, neutrophil, and lymphocyte infiltration and edema were significantly reduced or absent in the nasal mucosa and lung tissues (P<0.05) in the combined 0.1% anti-IL-1β- and TNF-αIgY-treated guinea pigs. The data suggest that topical blockade of IL-1βand TNF-αcould reduce pathological allergic inflammation in the nasal mucosa and lung tissues in AR guinea pigs.

scholarly journals The extract of black cumin, licorice, anise, and black tea alleviates OVA-induced allergic rhinitis in mouse via balancing activity of helper T cells in lung

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Chengsong Liao ◽  
Yangyang Han ◽  
Zhijing Chen ◽  
Huricha Baigude
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Aqueous Extract ◽  
Nigella Sativa ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Lavage Fluid ◽  
Ar Model ◽  
Control Group ◽  
Black Cumin

Abstract Background A formulation of black cumin (Nigella sativa L.), licorice (Glycyrrhiza glabra L.), anise (Pimpinella anisum L.) and tea (Camellia sinensis (L.) Kuntze) (denoted BLAB tea) is traditionally used to relief allergy reaction including allergic rhinitis. However, little is known about its underlining mechanism of anti-allergic effects. Methods To investigate the anti-allergenic mechanism of BLAB tea, we treated ovalbumin (OVA)-induced allergic rhinitis (AR) model of mice with BLAB tea, and elucidated its possible mechanism of action. Mice in the control group were treated with phosphate-buffered saline only. Subsequently, the infiltration of different inflammatory cells was measured. In addition, histopathological changes in the nasal mucosa, and the levels of allergen-specific cytokines and OVA-specific immunoglobulins were measured. Results The aqueous extract of BLAB significantly alleviated the nasal symptoms and reduced the accumulation of inflammatory cells in the nasal mucosa and nasal lavage fluid of AR model of mice. Conclusion The aqueous extract of BLAB induced the production of Th1 and Treg cytokines and inhibited the release of Th2 cytokines and histamine in nasal mucosa and serum of mice while decreasing the serum levels of OVA-specific IgE, IgG1, and IgG2a. These results suggest the potential of the aqueous extract of BLAB as a treatment option for allergic diseases.

scholarly journals Release of tumour necrosis factor alpha into bronchial alveolar lavage fluid following antigen challenge in passively sensitized guinea-pigs

1992 ◽  
Vol 1 (6) ◽  
pp. 425-428 ◽  
Author(s):  
D. E. Kelly ◽  
M. Denis ◽  
D. F. Biggs
Keyword(s):  
Tumour Necrosis Factor ◽  
Guinea Pigs ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Lavage Fluid ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Α ◽  
Bronchial Alveolar Lavage ◽  
Necrosis Factor

Five groups of ten female guinea-pigs were passively sensitized against ovalbumin (OA) (n = 9) or control guinea-pig serum (n = 1). 24 h later, they received mepyramine (0.5 mg/kg, i.p.) and 30 min later inhaled aerosols of: (A) OA (2 in 0.9% saline, 8 min, n = 4/9); (B) saline (40 min, n = 4/9); (C) LPS (40 min, Escherichia coli 0111:B4, 150 ng/kg in PBS, n = 1/9); and (D) the control animal was treated as in (C) (n = 1). Their tracheas were cannulated under pentobarbital anaesthesia and bronchial alveolar lavage (BAL) was performed with 2 × 5 ml PBS containing BSA (1%) (n = 1 group), or BSA (1%) and aprotinin (1000 KIU/ml) (n = 4 groups), at 30, 60, 90 or 120 min post-inhalations. BAL fluids recovered were centrifuged, the supernatants recovered and frozen until assayed for tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6). No TNF-α could be detected unless aprotinin was present in the lavaging solution. BAL fluid from OA-sensitized and control animals that had inhaled LPS contained high levels of TNF-α that peaked at 90 min. BAL fluid from OA sensitized animals that inhaled OA aerosols contained no detectable TNF-α at 30 min, but it was found in increasing amounts at 60, 90 and 120 min; TNF-α was not detected in fluid from any of the animals that inhaled saline. As BAL fluids were toxic to the cells used in the assays, neither IL-1 nor IL-6 could be measured. We conclude that the monokine TNF-α is released into BAL fluid following anaphylactic challenge of passively sensitized guinea-pigs. The presence of the antiprotease, aprotinin, in the lavaging solution is essential for the detection and measurement of TNF-α in BAL fluid.

Effect of Astragalus membranaceus in Ovalbumin-Induced Allergic Rhinitis Mouse Model

2019 ◽  
Vol 33 (4) ◽  
pp. 420-432
Author(s):  
Zhong Bing ◽  
Du Jin-Tao ◽  
Liu Feng ◽  
Luo Ba ◽  
Liu Ya-Feng ◽  
...  
Keyword(s):  
T Cells ◽  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Lymphoid Tissue ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Nasal Lavage Fluid ◽  
Ifn Γ

Background Astragalus membranaceus (AM), a traditional Chinese medicine, has been used to treat allergic diseases, but the mechanism for treating allergic rhinitis (AR) remains unclear. Objective The purpose of this study was to look at the anti-inflammatory effect of AM on AR and the mechanism of anti-allergy. Methods The mouse model of AR was induced by ovalbumin. Allergic symptoms, number of eosinophils in nasal mucosa, and levels of inflammatory cells in nasal lavage fluid were analyzed. We explored the serum immunoglobulin E (IgE), interleukin-4 (IL-4), IL-5, IL-13, interferon-γ (IFN-γ), and IL-10. Besides, the relative mRNA of IL-4, IL-5, and IL-13 was also detected in nasal mucosa tissue. The proportion of CD4+ CD25+ Foxp3+ T cells in the spleen and nasal lymphoid tissue were analyzed. The mRNA levels of nuclear factor-kappa B p65 (NF-κB p65) and inhibitory kappa B alpha (IκBα), as well as NF-κB p65 DNA binding activity, were tested. We also measured the protein levels of NF-κB p65 and p-NF-κB p65 in nasal mucosa. Results AM could reduce the number of eosinophils in the nasal mucosa and decrease the levels of inflammatory cells in nasal lavage fluid. The serum IgE, IL-4, IL-5, and IL-13 were also decreased, while levels of IFN-γ and IL-10 were increased. The relative mRNA of IL-4, IL-5, and IL-13 was decreased by AM. AM increased the proportion of CD4+ CD25+ Foxp3+ T cells in the spleen and nasal lymphoid tissue. In addition, AM could reduce the activity of NF-kB by inhibiting the mRNA expression and DNA binding activity of NF-κB p65. However, AM had no significant effect on mRNA of IκBα. Above all, AM could reduce the p-NF-κB p65 protein expression of nasal mucosa. Conclusions AM could reduce the secretion of inflammatory cytokines by increasing the level of CD4+ CD25+ Foxp3+ T cells and inhibiting the activation of the NF-κB.

scholarly journals MicroRNA-29 mediates anti-inflammatory effects and alleviation of allergic responses and symptoms in mice with allergic rhinitis

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Jia Wang ◽  
Jinshu Yin ◽  
Hong Peng ◽  
Aizhu Liu
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Immunoglobulin E ◽  
Underlying Mechanism ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Ar Model ◽  
Protein Levels ◽  
Mucosa Cell

Abstract Background To investigate the role of microRNA-29 (miR-29) in mice with allergic rhinitis (AR) and its underlying mechanism. Methods AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). miRNA expression was examined in the nasal mucosa tissues of mice and patients with AR, and miRNA-29 was found to be downregulated. To unveil the role of miRNA-29 in AR, it was overexpressed in the nasal mucosa of AR mice by intranasal administration of miRNA-29 agomir. The symptoms of nasal rubbing and sneezing were recorded and evaluated. miR-29 expression, OVA-specific immunoglobulin E (IgE) concentration, pro-inflammatory cytokines levels, eosinophils number, and cleaved caspase-3 and CD276 expression were examined in nasal mucosa tissues and nasal lavage fluid (NALF) by qRT-PCR, ELISA, hematoxylin and eosin staining, western blotting, or immunohistochemistry, respectively. TUNEL assay was used to analyze nasal mucosa cells apoptosis. Results Decreased expression of miR-29 was observed in AR, the symptoms of which were alleviated by overexpressing miR-29. In addition, overexpression of miR-29 markedly reduced the concentration of OVA-specific IgE, the levels of IL-4, IL-6, IL-10, and IFN-γ, the pathological alterations and eosinophils infiltration in the nasal mucosa. Furthermore, restoration of miR-29 expression reduced nasal mucosa cell apoptosis. Moreover, overexpression of miR-29 significantly attenuated CD276 mRNA and protein levels in nasal mucosa cells. Conclusion MiR-29 mediated antiallergic effects in OVA-induced AR mice by decreasing inflammatory response, probably through targeting CD276. MiRNA-29 may serve as a potential novel therapeutic target for the treatment of AR.

scholarly journals MicroRNA-182-5p relieves murine allergic rhinitis via TLR4/NF-κB pathway

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 1202-1212
Author(s):  
Aichun Zhang ◽  
Yangzi Jin
Keyword(s):  
Allergic Rhinitis ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Inflammatory Factors ◽  
Pcr Analysis ◽  
Reverse Transcription Pcr ◽  
Pathway Activation ◽  
Nasal Lavage Fluid

AbstractAllergic rhinitis (AR) is one of the most common chronic diseases. This study examined whether microRNA (miR)-182-5p plays a role in AR by regulating toll-like receptor 4 (TLR4). First, data demonstrated that TLR4 was a target of miR-182-5p. Subsequently, AR mouse model was established to explore the role of miR-182-5p and TLR4 in AR in vivo. Initially, quantitative reverse transcription-PCR (qRT-PCR) analysis indicated that miR-182-5p was downregulated, while TLR4 expression was upregulated in AR mice. Then we found that miR-182-5p mimic reduced the frequency of sneezing and nose rubbing of the AR mice. In addition, miR-182-5p mimic significantly increased ovalbumin (OVA)-specific IgE and leukotriene C4 expression levels in nasal lavage fluid (NLF) and serum of AR mice. miR-182-5p mimic decreased the number of inflammatory cells in NLF of AR mice. It also reduced the levels of inflammatory factors in the serum of AR mice, such as interleukin (IL)-4, IL-5, IL-13, IL-17 and tumor necrosis factor (TNF)-α, while increasing the release of IFN-γ and IL-2. Finally, miR-182-5p mimic inhibited NF-κB signaling pathway activation in AR mice. However, all effects of miR-182-5p mimic on AR mice were reversed by TLR4-plasmid. In conclusion, miR-182-5p/TLR4 axis may represent a novel therapeutic target for AR.

scholarly journals Allergic Inflammation Caused by Dimerized Translationally Controlled Tumor Protein is Attenuated by Cardamonin

2021 ◽  
Vol 12 ◽  
Author(s):  
Haejun Pyun ◽  
Joo-Won Nam ◽  
Hyunsoo Cho ◽  
Jiyoung Park ◽  
Eun Kyoung Seo ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage Fluid ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Allergic Diseases ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Translationally Controlled Tumor Protein ◽  
Dimeric Form ◽  
Allergic Mouse ◽  
Inflammatory Effect

We demonstrated in our previous reports that dimeric form of translationally controlled tumor protein (dTCTP) initiates a variety of allergic phenomena. In the present study, we examined whether and how dTCTP’s role in allergic inflammation can be modulated or negated. The possible potential of cardamonin as an anti-allergic agent was assessed by ELISA using BEAS-2B cells and OVA-challenged allergic mouse model. The interaction between cardamonin and dTCTP was confirmed by SPR assay. Cardamonin was found to reduce the secretion of IL-8 caused by dTCTP in BEAS-2B cells by interacting with dTCTP. This interaction between dTCTP and cardamonin was confirmed through kinetic analysis (KD = 4.72 ± 0.07 μM). Also, cardamonin reduced the migration of various inflammatory cells in the bronchoalveolar lavage fluid (BALF), inhibited OVA specific IgE secretion and bronchial remodeling. In addition, cardamonin was observed to have an anti-allergic response by inhibiting the activity of NF-κB. Cardamonin exerts anti-allergic anti-inflammatory effect by inhibiting dTCTP, suggesting that it may be useful in the therapy of allergic diseases.

Overexpression of the Superoxide Anion and NADPH Oxidase Isoforms 1 and 4 (NOX1 and NOX4) in Allergic Nasal Mucosa

2009 ◽  
Vol 23 (4) ◽  
pp. 370-376 ◽  
Author(s):  
Joon Hwan Moon ◽  
Tae Hoon Kim ◽  
Heung Man Lee ◽  
Seung Hoon Lee ◽  
Whan Choe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Allergic Rhinitis ◽  
Nadph Oxidase ◽  
Nasal Mucosa ◽  
Vascular Endothelium ◽  
Superoxide Anion ◽  
Nasal Polyps ◽  
Inflammatory Cells ◽  
Submucosal Glands ◽  
Cellular Source

Background The purpose of this study was to investigate the expression and distribution of superoxide anion, NADPH oxidase (NOX)1, and NOX4 in healthy, allergic nasal mucosa and nasal polyps to evaluate the possible influence of oxidative stress on the development of allergic rhinitis and nasal polyps. Methods The expression and distribution of superoxide anion, NOX1 and NOX4 were evaluated in healthy and allergic nasal mucosa and nasal polyps, using dihydroethidium fluorescence, semiquantitative reverse transcriptase-polymerase chain reaction, immunohistochemistry, and Western blot. Results NOX1 and NOX4 were localized mainly in the epithelial layer, submucosal glands, vascular endothelium, and inflammatory cells in healthy and allergic nasal mucosa and nasal polyps. The cellular source that generated superoxide anion is also localized in the epithelial cells, submucosal glands, vascular endothelium, and inflammatory cells, demonstrating the similar sites of expression of NOX1 and NOX4 in healthy and allergic nasal mucosa and nasal polyps. NOX1 and NOX4 mRNA and proteins and superoxide anions had increased levels of expression in allergic nasal mucosa and nasal polyps compared with healthy nasal mucosa. Conclusions These results indicate that NOX1 and NOX4 may play an important role in reactive oxygen species production, contributing to the oxidative stress in allergic rhinitis and nasal polyp tissues.

scholarly journals Honeysuckle extract relieves ovalbumin-induced allergic rhinitis by inhibiting AR-induced inflammation and autoimmunity

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Bin Lin ◽  
Bijuan Cai ◽  
Huige Wang
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Inflammatory Reaction ◽  
Lavage Fluid ◽  
Nasal Lavage ◽  
Autoimmune Response ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protein Levels ◽  
Nasal Lavage Fluid ◽  
Ifn Γ

Abstract Honeysuckle has antiviral, antioxidative and anti-inflammatory properties. Allergic rhinitis (AR) is induced by immunoglobulin E (IgE)-mediated inflammatory reaction. Our study investigates whether honeysuckle extract (HE) has therapeutic effect on AR. An AR model of mice was established by ovalbumin (OVA). Hematoxylin–Eosin staining was used to assess nasal mucosa damage. Enzyme-linked immunosorbent assay (ELISA) was performed to determine serum histamine, IgE and interleukin (IL)-2, IL-4, IL-17 and interferon-γ (IFN-γ) from nasal lavage fluid. Western blot was carried out to analyze the protein level from nasal mucosa tissue. We found that HE not only decreased nasal rubbing and sneezing in AR mice, but also reduced AR-induced damage to nasal mucosa. Moreover, HE lowered the levels of serum IgE and histamine and inhibited IL-4 and IL-17 levels from AR mice but raised IL-2 and IFN-γ levels in AR-induced nasal lavage fluid. Our results also showed that HE elevated the protein levels of forkhead box P3 (Foxp3) and T-box transcription factor (T-bet) in AR-induced nasal mucosa tissue, whereas it inhibited signal transducer and activator of transcription (STAT) 3 and GATA binding protein 3 (GATA-3) protein levels. By regulating AR-induced inflammatory reaction and autoimmune response, HE also relieved OVA-induced AR. Thus, HE could be used as a potential drug to treat AR.

scholarly journals Suppression of Tumorigenesis: Modulation of Inflammatory Cytokines by Oral Administration of Microencapsulated Probiotic Yogurt Formulation

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Aleksandra Malgorzata Urbanska ◽  
Arghya Paul ◽  
Jasmine Bhahena ◽  
Satya Prakash
Keyword(s):  
Treatment Group ◽  
Intestinal Inflammation ◽  
Interleukin 1 ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Western Blots ◽  
Reactive Protein ◽  
Probiotic Yogurt ◽  
Factor Alpha ◽  
Irritable Bowel

The objective of this study was to examine the ability of a novel microencapsulated probiotic yogurt formulation to suppress the intestinal inflammation. We assessed its anticancer activity by screening interleukin-1, 6, and 12 (IL-1, 6, 12), secretory levels of tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), prostaglandinE2  (PGE2), and thromboxane B2 in the digesta obtained from the duodenum, jejunum, proximal, and distal segments of the ileum of C57BL/6J-ApcMin/J mice. Formulation-receiving animals showed consistently lower proinflammatory cytokines' levels when compared to control group animals receiving empty alginate-poly-L-lysine-alginate (APA) microcapsules suspended in saline. The concentrations of IL-12 found in serum in control and treatment group animals were significant:46.58±16.96 pg/mL and158.58±28.56 pg/mL for control and treatment animals, respectively. We determined a significant change in plasma C-reactive protein:81.04±23.73 ng/mL in control group and64.21±16.64 ng/mL in treatment group. Western blots showed a 71% downregulation of cyclooxygenase-2 (COX-2) protein in treatment group animals compared to control. These results point to the possibility of using this yogurt formulation in anticancer therapies, in addition to chronic gut diseases such as Crohn's disease, irritable bowel syndrome (IBS), and inflammatory bowel disease (IBD) thanks to its inflammation lowering properties.

Anti-inflammatory effects of zinc and alterations in zinc transporter mRNA in mouse models of allergic inflammation

2007 ◽  
Vol 292 (2) ◽  
pp. L577-L584 ◽  
Author(s):  
Carol Lang ◽  
Chiara Murgia ◽  
Mary Leong ◽  
Lor-Wai Tan ◽  
Giuditta Perozzi ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Gene Array ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Mrna Levels ◽  
Solute Carrier Family ◽  
Zn Uptake ◽  
Solute Carrier

There is clinical evidence linking asthma with the trace element, zinc (Zn). Using a mouse model of allergic inflammation, we have previously shown that labile Zn decreases in inflamed airway epithelium (Truong-Tran AQ, Ruffin RE, Foster PS, Koskinen AM, Coyle P, Philcox JC, Rofe AM, Zalewski PD. Am J Respir Cell Mol Biol 27: 286–296, 2002). Moreover, mild nutritional Zn deficiency worsens lung function. Recently, a number of proteins belonging to the Solute Carrier Family 39 (ZIP) and Solute Carrier Family 30 (ZnT) have been identified that bind Zn and regulate Zn homeostasis. Mice were sensitized, and subsequently aerochallenged, with ovalbumin to induce acute and chronic airway inflammation. Mice received 0, 54, or 100 μg of Zn intraperitoneally. Tissues were analyzed for Zn content and histopathology. Inflammatory cells were counted in bronchoalveolar lavage fluid. Cytokine and Zn transporter mRNA levels were determined by cDNA gene array and/or real-time PCR. Zn supplementation decreased bronchoalveolar lavage fluid eosinophils by 40 and 80%, and lymphocytes by 55 and 66%, in the acute and chronic models, respectively. Alterations in Zn transporter expression were observed during acute inflammation, including increases in ZIP1 and ZIP14 and decreases in ZIP4 and ZnT4. Zn supplementation normalized ZIP1 and ZIP14, but it did not affect mRNA levels of cytokines or their receptors. Our results indicate that inflammation-induced alterations in Zn transporter gene expression are directed toward increasing Zn uptake. Increases in Zn uptake may be needed to counteract the local loss of Zn in the airway and to meet an increased demand for Zn-dependent proteins. The reduction of inflammatory cells by Zn in the airways provides support for Zn supplementation trials in human asthmatic individuals.

Sign in / Sign up

Export Citation Format

Share Document