Effects of oral administration of Ocimum basilicum on goblet cell hyperplasia and upstream cytokine gene expression in allergic asthma

2020 ◽  
Vol 60 (2) ◽  
pp. 64-68
Author(s):  
E. Mehrabi Nasaba ◽  
S.M. Athari ◽  
B. Motlagh ◽  
S.S. Athari
Keyword(s):  
Gene Expression ◽  
Oral Administration ◽  
Allergic Asthma ◽  
Goblet Cell ◽  
Ocimum Basilicum ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia

scholarly journals Study Effect of Vitamin D on the Immunopathology Responses of the Bronchi in Murine Model of Asthma

2021 ◽  
Author(s):  
Linlin Feng ◽  
Tingting Meng ◽  
Yunyun Qi ◽  
Seyyed Shamsadin Athari ◽  
Xiaoyun Chen
Keyword(s):  
Vitamin D ◽  
Allergic Asthma ◽  
Goblet Cell ◽  
Murine Model ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Asthmatic Patients ◽  
Genetic And Environmental Factors

  Allergic asthma is a complicated respiratory problem characterized by airway inflammation, airway hyperresponsiveness (AHR), breathlessness, mucus hyper-secretion, and goblet cell hyperplasia. Asthma is controlled by genetic and environmental factors. Allergy is the main trigger of asthma and is mediated by Th2 cytokines along with IgE production. Vitamin D (Vit D) is the main supplementary factor for the immune system. In the present study, we investigated the effect of Vit D on the exacerbation of allergic asthma. A murine model of allergic asthma was induced by ovalbumin (OVA) in four of five groups of studied female BALB/c mice (each group, n=20). One group was considered as control. Of OVA-induced mice, two groups received Vit D via oral (10,000 IU/kg diet) or intranasal (inhalation) forms (30 min on days 25, 27, and 29), and the third group received budesonide. At least, AHR, the levels of IL-4, IL-5, IL-13, and INF-g in bronchoalveolar lavage fluid (BALF), serum IgE and histamine, IL-25 and IL-33 gene expression, as well as histopathology study of the lung were done. The Penh values, type2 Cytokines in BALF (in both protein and molecular levels), total IgE and histamine, perivascular and peribronchial inflammation, goblet cell hyperplasia, and mucus hypersecretion decreased significantly in both oral and intranasal Vit D-treated asthmatic mice groups, especially on day 38 of orally treated mice. Here, we found Vit D as a promising agent in control of allergic asthma with a remarkable ability to decrease the severity of inflammation. Therefore, Vit D sufficiency is highly recommended in asthmatic patients.

Intestinal phenotype of variable-weight cystic fibrosis knockout mice

2007 ◽  
Vol 293 (1) ◽  
pp. G222-G229 ◽  
Author(s):  
Juan C. Canale-Zambrano ◽  
Maya C. Poffenberger ◽  
Sean M. Cory ◽  
Daryl G. Humes ◽  
Christina K. Haston
Keyword(s):  
Gene Expression ◽  
Cystic Fibrosis ◽  
Cell Proliferation ◽  
Mast Cell ◽  
Body Weight ◽  
Goblet Cell ◽  
Knockout Mice ◽  
Expression Profiling ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia

Cystic fibrosis (CF) transmembrane conductance regulator ( Cftr) knockout mice present the clinical features of low body weight and intestinal disease permitting an assessment of the interrelatedness of these phenotypes in a controlled environment. To identify intestinal alterations that are affected by body weight in CF mice, the histological phenotypes of crypt-villus axis height, goblet cell hyperplasia, mast cell infiltrate, crypt cell proliferation, and apoptosis were measured in a population of 12-wk-old (C57BL/6 × BALB/cJ) F2 Cftrtm1UNC and non-CF mice presenting a range of body weight. In addition, cardiac blood samples were assessed, and gene expression profiling of the ileum was completed. Crypt-villus axis height decreased with increasing body weight in CF but not control mice. Intestinal crypts from CF mice had fewer apoptotic cells, per unit length, than did non-CF mice, and normalized cell proliferation was similar to control levels. Goblet cell hyperplasia and mast cell infiltration were increased in the CF intestine and identified to be independent of body weight. Blood triglyceride levels were found to be significantly lower in CF mice than in control mice but were not dependent on CF mouse weight. By expression profiling, genes of DNA replication and lipid metabolism were among those altered in CF mice relative to non-CF controls, and no differences in gene expression were measured between samples from CF mice in the 25th and 75th percentile for weight. In this CF mouse model, crypt elongation, due to an expanded proliferative zone and decreased apoptosis, was identified to be dependent on body weight.

scholarly journals NOTCH3 contributes to rhinovirus-induced goblet cell hyperplasia in COPD airway epithelial cells

Thorax ◽  
2018 ◽  
Vol 74 (1) ◽  
pp. 18-32 ◽  
Author(s):  
Yaxun Jing ◽  
Joao Antonio Gimenes ◽  
Rahul Mishra ◽  
Duc Pham ◽  
Adam T Comstock ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cultures ◽  
Goblet Cell ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Mucin Gene ◽  
Airways Obstruction ◽  
Secretase Inhibitor

RationaleGoblet cell hyperplasia (GCH) is one of the cardinal features of chronic obstructive pulmonary disease (COPD) and contributes to airways obstruction. Rhinovirus (RV), which causes acute exacerbations in patients with COPD, also causes prolonged airways obstruction. Previously, we showed that RV enhances mucin gene expression and increases goblet cell number in a COPD mouse model. This study examines whether RV causes sustained GCH in relevant models of COPD.MethodsMucociliary-differentiated COPD and normal airway epithelial cell cultures and mice with normal or COPD phenotype were infected with RV or sham and examined for GCH by immunofluorescence and/or mucin gene expression. In some experiments, RV-infected COPD cells and mice with COPD phenotype were treated with γ-secretase inhibitor or interleukin-13 neutralising antibody and assessed for GCH. To determine the contribution of NOTCH1/3 in RV-induced GCH, COPD cells transduced with NOTCH1/3 shRNA were used.ResultsRV-infected COPD, but not normal cell cultures, showed sustained GCH and increased mucin genes expression. Microarray analysis indicated increased expression of NOTCH1, NOTCH3 and HEY1 only in RV-infected COPD cells. Blocking NOTCH3, but not NOTCH1, attenuated RV-induced GCH in vitro. Inhibition of NOTCH signalling by γ-secretase inhibitor, but not neutralising antibody to IL-13, abrogated RV-induced GCH and mucin gene expression.ConclusionsRV induces sustained GCH via NOTCH3 particularly in COPD cells or mice with COPD phenotype. This may be one of the mechanisms that may contribute to RV-induced prolonged airways obstruction in COPD.

Platelet-activating Factor Induces Goblet Cell Hyperplasia and Mucin Gene Expression in Airways

1998 ◽  
Vol 157 (6) ◽  
pp. 1927-1934 ◽  
Author(s):  
YA-PING LOU ◽  
KIYOSHI TAKEYAMA ◽  
KATHLEEN M. GRATTAN ◽  
JAMES A. LAUSIER ◽  
IRIS F. UEKI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Goblet Cell ◽  
Platelet Activating Factor ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Mucin Gene

scholarly journals Simvastatin inhibits goblet cell hyperplasia and lung arginase in a mouse model of allergic asthma: a novel treatment for airway remodeling?

2010 ◽  
Vol 156 (6) ◽  
pp. 335-349 ◽  
Author(s):  
Amir A. Zeki ◽  
Jennifer M. Bratt ◽  
Michelle Rabowsky ◽  
Jerold A. Last ◽  
Nicholas J. Kenyon
Keyword(s):  
Mouse Model ◽  
Allergic Asthma ◽  
Goblet Cell ◽  
Airway Remodeling ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Novel Treatment

Mild and Moderate Asthma Is Associated with Airway Goblet Cell Hyperplasia and Abnormalities in Mucin Gene Expression

2001 ◽  
Vol 163 (2) ◽  
pp. 517-523 ◽  
Author(s):  
CLAUDIA L. ORDOÑEZ ◽  
RAMIN KHASHAYAR ◽  
HOFER H. WONG ◽  
RON FERRANDO ◽  
REEN WU ◽  
...  
Keyword(s):  
Gene Expression ◽  
Goblet Cell ◽  
Cell Hyperplasia ◽  
Moderate Asthma ◽  
Goblet Cell Hyperplasia ◽  
Mucin Gene

scholarly journals A Synthetic Curcuminoid Analogue, 2,6-Bis-4-(Hydroxyl-3-Methoxybenzylidine)-Cyclohexanone (BHMC) Ameliorates Acute Airway Inflammation of Allergic Asthma in Ovalbumin-Sensitized Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Chau Ling Tham ◽  
Sin Yee Yeoh ◽  
Chun Hao Ong ◽  
Hanis Hazeera Harith ◽  
Daud Ahmad Israf
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Goblet Cell ◽  
Bronchoalveolar Lavage Fluid ◽  
Intraperitoneal Administration ◽  
Lavage Fluid ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Cellular Models

2,6-Bis-(4-hydroxyl-3-methoxybenzylidine) cyclohexanone (BHMC), a synthetic curcuminoid analogue, has been shown to exhibit anti-inflammatory properties in cellular models of inflammation and improve the survival of mice from lethal sepsis. We further evaluated the therapeutic effect of BHMC on acute airway inflammation in a mouse model of allergic asthma. Mice were sensitized and challenged with ovalbumin (OVA), followed by intraperitoneal administration of 0.1, 1, and 10 mg/kg of BHMC. Bronchoalveolar lavage fluid, blood, and lung samples were collected, and the respiratory function was measured. OVA sensitization and challenge increased airway hyperresponsiveness (AHR) and pulmonary inflammation. All three doses of BHMC (0.1-10 mg/kg) significantly reduced the number of eosinophils, lymphocytes, macrophages, and neutrophils, as well as the levels of Th2 cytokines (IL-4, IL-5 and IL-13) in bronchoalveolar lavage fluid (BALF) as compared to OVA­challenged mice. However, serum level of IgE was not affected. All three doses of BHMC (0.1-10 mg/kg) were effective in suppressing the infiltration of inflammatory cells at the peribronchial and perivascular regions, with the greatest effect observed at 1 mg/kg which was comparable to dexamethasone. Goblet cell hyperplasia was inhibited by 1 and 10 mg/kg of BHMC, while the lowest dose (0.1 mg/kg) had no significant inhibitory effect. These findings demonstrate that BHMC, a synthetic nonsteroidal small molecule, ameliorates acute airway inflammation associated with allergic asthma, primarily by suppressing the release of inflammatory mediators and goblet cell hyperplasia to a lesser extent in acute airway inflammation of allergic asthma.

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