scholarly journals Carbon Nanofibers Have IgE Adjuvant Capacity but Are Less Potent Than Nanotubes in Promoting Allergic Airway Responses

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Unni Cecilie Nygaard ◽  
Mari Samuelsen ◽  
Calin Daniel Marioara ◽  
Martinus Løvik
Keyword(s):  
Lung Inflammation ◽  
Carbon Nanofiber ◽  
Inflammatory Cells ◽  
Health Impact ◽  
Specific Ige ◽  
Positive Control ◽  
Bronchoalveolar Fluid ◽  
Ige Response ◽  
Airway Responses ◽  
Airway Model

There is a growing concern for the possible health impact of nanoparticles. The main objective of this study was to investigate the allergy-promoting capacity of four different carbon nanofiber (CNF) samples in an injection and an airway mouse model of allergy. Secondly, the potency of the CNF was compared to the previously reported allergy-promoting capacity of carbon nanotubes (CNT) in the airway model. Ultrafine carbon black particles (ufCBP) were used as a positive control. Particles were given together with the allergen ovalbumin (OVA) either by subcutaneous injection into the footpad or intranasally to BALB/cA mice. After allergen booster, OVA-specific IgE, IgG1, and IgG2a in serum were measured. In the airway model, inflammation was determined as influx of inflammatory cells (eosinophils, neutrophils, lymphocytes, and macrophages) and by mediators (MCP-1 and TNF-αpresent in bronchoalveolar fluid (BALF)). CNF and CNT both increased OVA-specific IgE levels in the two models, but in the airway model, the CNT gave a significantly stronger IgE response than the CNF. Furthermore, the CNT and not the CNF promoted eosinophil lung inflammation. Our data therefore suggest that nanotube-associated properties are particularly potent in promoting allergic responses.

scholarly journals Vinpocetine alleviates lung inflammation via macrophage inflammatory protein-1β inhibition in an ovalbumin-induced allergic asthma model

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0251012
Author(s):  
Won Seok Choi ◽  
Hyun Sik Kang ◽  
Hong Jo Kim ◽  
Wang Tae Lee ◽  
Uy Dong Sohn ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Specific Ige ◽  
Control Group ◽  
Bronchial Disease ◽  
Inflammatory Protein ◽  
Bronchial Inflammation ◽  
Bronchial Mucus ◽  
Macrophage Inflammatory Protein

Asthma is a well-known bronchial disease that causes bronchial inflammation, narrowing of the bronchial tubes, and bronchial mucus secretion, leading to bronchial blockade. In this study, we investigated the association between phosphodiesterase (PDE), specifically PDE1, and asthma using 3-isobutyl-1-methylxanthine (IBMX; a non-specific PDE inhibitor) and vinpocetine (Vinp; a PDE1 inhibitor). Balb/c mice were randomized to five treatment groups: control, ovalbumin (OVA), OVA + IBMX, OVA + Vinp, and OVA + dexamethasone (Dex). All mice were sensitized and challenged with OVA, except for the control group. IBMX, Vinp, or Dex was intraperitoneally administered 1 h before the challenge. Vinp treatment significantly inhibited the increase in airway hyper-responsiveness (P<0.001) and reduced the number of inflammatory cells, particularly eosinophils, in the lungs (P<0.01). It also ameliorated the damage to the bronchi and alveoli and decreased the OVA-specific IgE levels in serum, an indicator of allergic inflammation increased by OVA (P<0.05). Furthermore, the increase in interleukin-13, a known Th2 cytokine, was significantly decreased by Vinp (P<0.05), and Vinp regulated the release and mRNA expression of macrophage inflammatory protein-1β (MIP-1β) increased by OVA (P<0.05). Taken together, these results suggest that PDE1 is associated with allergic lung inflammation induced by OVA. Thus, PDE1 inhibitors can be a promising therapeutic target for the treatment of asthma.

scholarly journals Anti-inflammatory effect of Helix aspersa extracts in sephadex-induced model of lung inflammation: possible modulation of neutrophils

2021 ◽  
Vol 12 (4) ◽  
pp. 2557-2565
Author(s):  
Mebirouk Romeila ◽  
Naimi Dalila
Keyword(s):  
Lung Inflammation ◽  
Leukocyte Count ◽  
Inflammatory Cells ◽  
Negative Control Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Measured Activity ◽  
Anti Inflammatory ◽  
Inflammatory Effect

The focus of our study is to compare the anti-inflammatory effect of extracts prepared from Algerian mollusk called Helix ,on induced lung inflammation in rats: aqueous AE, HE and organic OE extracts. Animals were classified into six groups: control group T was instilled with NaCl (0.9%) in the trachea, negative control group was instilled with in trachea (5mg//Kg), positive control group was instilled with and treated with an anti-inflammatory drug, groups SAE, SHE and SOE were instilled with and treated with aqueous, and organic extracts respectively (4mg//Kg). 24h after instillation, we sacrificed animals, blood samples and fluid lavage (BALF) were collected. Lungs were for investigation. We measured activity (MPO) in BALF. Results showed induces a massive in lungs. HE and OE decreased leukocyte count in BALF and blood. AE increased leukocyte count in blood and decreased it in BALF. The three extracts decreased MPO activity in BALF, reduced number of inflammatory cells in the and protected lung from beads injuries. Both AE and HE reduced edema in lung. We conclude that treatment with Helix had an anti-inflammatory effect on inflammation.

Aerobic Exercise Decreases Lung Inflammation by IgE Decrement in an OVA Mice Model

2017 ◽  
Vol 38 (06) ◽  
pp. 473-480
Author(s):  
Deborah Camargo Hizume-Kunzler ◽  
Flavia R. Greiffo ◽  
Bárbara Fortkamp ◽  
Gabriel Ribeiro Freitas ◽  
Juliana Keller Nascimento ◽  
...  
Keyword(s):  
Aerobic Exercise ◽  
Lung Inflammation ◽  
Inflammatory Cells ◽  
Specific Ige ◽  
Mice Model ◽  
Acute Lung Inflammation ◽  
Lung Function Decline ◽  
Total Ige ◽  
Asthmatic Patients ◽  
Cell Counts

AbstractAerobic exercise (AE) reduces lung function decline and risk of exacerbations in asthmatic patients. However, the inflammatory lung response involved in exercise during the sensitization remains unclear. Therefore, we evaluated the effects of exercise for 2 weeks in an experimental model of sensitization and single ovalbumin-challenge. Mice were divided into 4 groups: mice non-sensitized and not submitted to exercise (Sedentary, n=10); mice non-sensitized and submitted to exercise (Exercise, n=10); mice sensitized and exposed to ovalbumin (OVA, n=10); and mice sensitized, submitted to exercise and exposed to OVA (OVA+Exercise, n=10). 24 h after the OVA/saline exposure, we counted inflammatory cells from bronchoalveolar fluid (BALF), lung levels of total IgE, IL-4, IL-5, IL-10 and IL-1ra, measurements of OVA-specific IgG1 and IgE, and VEGF and NOS-2 expression via western blotting. AE reduced cell counts from BALF in the OVA group (p<0.05), total IgE, IL-4 and IL-5 lung levels and OVA-specific IgE and IgG1 titers (p<0.05). There was an increase of NOS-2 expression, IL-10 and IL-1ra lung levels in the OVA groups (p<0.05). Our results showed that AE attenuated the acute lung inflammation, suggesting immunomodulatory properties on the sensitization process in the early phases of antigen presentation in asthma.

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.

Attenuation of bleomycin-induced pneumopathy in mice by a caspase inhibitor

2001 ◽  
Vol 280 (2) ◽  
pp. L316-L325 ◽  
Author(s):  
Kazuyoshi Kuwano ◽  
Ritsuko Kunitake ◽  
Takashige Maeyama ◽  
Naoki Hagimoto ◽  
Masayuki Kawasaki ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Inflammation ◽  
Caspase 3 ◽  
Fas Ligand ◽  
Inflammatory Cells ◽  
Lung Epithelial Cells ◽  
Caspase Inhibitor ◽  
Hydroxyproline Content ◽  
Caspase 1 ◽  
Lung Epithelial

Caspases have been implicated in the effector process of apoptosis in several systems including the Fas-Fas ligand pathway. We previously demonstrated that excessive apoptosis of lung epithelial cells and the Fas-Fas ligand pathway were essential in the pathogenesis of bleomycin-induced pneumopathy in mice. Therefore, the purpose of this study was to investigate whether a caspase inhibitor could prevent the development of this model. The expression of caspase-1 and caspase-3 was upregulated on lung epithelial cells, alveolar macrophages, and infiltrating inflammatory cells in this model. We demonstrated that a broad-spectrum caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, decreased the caspase-1- and caspase-3-like activity, the number of apoptotic cells, the pathological grade of lung inflammation and fibrosis, and the hydroxyproline content in lung tissues in this model. We conclude that caspase inhibitors could be a new therapeutic approach against lung injury and pulmonary fibrosis.

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.

scholarly journals Epithelial Ablation of Miro1/Rhot1 GTPase Leads to Mitochondrial Dysfunction and Lung Inflammation by Cigarette Smoke

2021 ◽  
Author(s):  
Shikha Sharma ◽  
Qixin Wang ◽  
Thivanka Muthumalage ◽  
Irfan Rahman
Keyword(s):  
Quality Control ◽  
Mitochondrial Dysfunction ◽  
Cigarette Smoke ◽  
Calcium Binding ◽  
Lung Inflammation ◽  
Inflammatory Cells ◽  
Mouse Lung ◽  
Control Mechanisms ◽  
Histopathological Changes ◽  
Mitochondrial Quality Control

Cigarette smoke (CS) exposure results in lung damage and inflammation through mitochondrial dysfunction. Mitochondria quality control is sustained by Miro1 (Rhot1), a calcium-binding membrane-anchored GTPase by its interaction with PINK1/Parkin during mitophagy. However, the exact mechanism that operates this interaction of mitophagy machinery in Miro1 degradation and CS-induced mitochondrial dysfunction that results in lung inflammation remains unclear. We hypothesized that mitochondrial Miro1 plays an important role in regulating mitophagy machinery and resulting lung inflammation by CS in mouse lung. We showed a role of Miro1 in CS-induced mitochondrial dysfunction and quality control mechanisms. The Rhot1Fl/Fl (WT) and lung epithelial cell-specific Rhot1 KO were exposed to mainstream CS for 3 days (acute) and 4 months (chronic). The cellular infiltration, cytokines, and lung histopathology were studied for the inflammatory response in the lungs. Acute CS exposure showed a notable increase in the total inflammatory cells, macrophages, and neutrophils associated with inflammatory mediators and Miro1 associated mitochondrial quality control proteins Parkin and OPA1. Chronic exposure showed an increase infiltration of total inflammatory cells and neutrophils versus air controls. Histopathological changes, such as pulmonary macrophages and neutrophils were increased in CS exposed mice. The epithelial Miro1 ablation led to augmentation of inflammatory cell infiltration with alteration in the levels of pro-inflammatory cytokines and histopathological changes. Thus, CS induces disruption of mitochondrial quality control mechanisms, and Rhot1/Miro1 mediates the process of CS-induced mitochondrial dysfunction ensuing lung inflammatory responses.

scholarly journals Enterotoxin-Specific Immunoglobulin E Responses in Humans after Infection or Vaccination with Diarrhea-Causing Enteropathogens

2000 ◽  
Vol 68 (10) ◽  
pp. 6077-6081 ◽  
Author(s):  
Firdausi Qadri ◽  
Muhammad Asaduzzaman ◽  
Christine Wennerås ◽  
Golam Mohi ◽  
M. John Albert ◽  
...  
Keyword(s):  
North American ◽  
Immunoglobulin E ◽  
Specific Ige ◽  
Cholera Vaccine ◽  
Total Ige ◽  
B Subunit ◽  
The North ◽  
Specific Immunoglobulin E ◽  
Oral Cholera Vaccine ◽  
Ige Response

ABSTRACT Cholera toxin (CT)-specific antibody responses of the immunoglobulin E (IgE) isotype in the sera of adult patients suffering from infection with either Vibrio cholerae O1, V. cholerae O139, or enterotoxigenic Escherichia coli(ETEC) were analyzed and compared with those in the sera of volunteers immunized with a bivalent B subunit O1/O139 whole-cell cholera vaccine. A significant IgE response to CT was observed in 90% of the patients with V. cholerae O1 infection (18 of 20; P = <0.001) and 95% of the patients with V. cholerae O139 infection (19 of 20; P = <0.001). Similarly, the majority of the patients with ETEC diarrhea (83%; 13 of 15) showed a positive IgE response to CT. Eight of 10 North American volunteers (80%) orally challenged with V. cholerae O1 showed CT-specific IgE responses (P = 0.004). In contrast, Swedish volunteers immunized with the oral cholera vaccine showed no IgE responses to CT (P value not significant). During the study period, total IgE levels in the sera of the diarrheal patients, the North American volunteers, and the Swedish cholera vaccinees alike remained unchanged. However, the total IgE levels in the sera of patients and healthy Bangladeshi controls were on average 89-fold higher than those in the sera of the healthy Swedish volunteers and 34-fold higher than those in the sera of the North American volunteers.

scholarly journals Lack of evidence of IgE allergic sensitisation from working with lactic acid bacteria in the dairy foods industry

2018 ◽  
Vol 85 (3) ◽  
pp. 355-357
Author(s):  
Coralie Barrera ◽  
Gabriel Reboux ◽  
Audrey Laboissière ◽  
Laurence Millon ◽  
Anne Oppliger
Keyword(s):  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Preventive Measures ◽  
Immunoglobulin E ◽  
Milk Powder ◽  
Medical Practitioner ◽  
Specific Ige ◽  
Adverse Health Effects ◽  
High Concentrations ◽  
Ige Response

This research communication aimed to evaluate the level of immunoglobulin E from lactic acid bacteria (LAB) that are used in dairy industries. Previous studies have demonstrated that workers report symptoms of irritation and are frequently IgG-sensitised to LAB. Workers (n = 44) from a probiotic production unity and the control lab were seen by a medical practitioner and responded to an occupational questionnaire. Specific IgE by the DELFIA® technique against 6 strains of LAB were measured on 44 exposed workers and 31 controls sera. Levels of specific IgE were low and no difference was observed between the two groups. This lack of IgE response could be explained by a healthy worker effect, an efficient implementation of personal protective equipment or by an absence of allergic mechanisms to account for the self-reported irritative symptoms. Despite the high concentrations of LAB, preventive measures are effective enough to guarantee no allergic effect and to prevent other adverse health effects. The implementation of preventive measures to avoid or reduce exposure to dust of LAB, and more generally to milk powder, is recommended in all dairy industry.

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