scholarly journals Samsoeum water extract attenuates allergic airway inflammation via modulation of Th1/Th2 cytokines and decrease of iNOS expression in asthmatic mice

Author(s):  
Woo-Young Jeon ◽  
In-Sik Shin ◽  
Hyeun-Kyoo Shin ◽  
Mee-Young Lee
2018 ◽  
Vol 32 ◽  
pp. 205873841877489 ◽  
Author(s):  
Eiko Koike ◽  
Rie Yanagisawa ◽  
Tin-Tin Win-Shwe ◽  
Hirohisa Takano

Bisphenol A (BPA) is used in the production of polycarbonate plastics and epoxy resins and found in many consumer products. Previous studies have reported that perinatal exposure to BPA through the oral route promotes the development of allergic airway inflammation. We investigated the effects of exposure to low-dose BPA during the juvenile period of development on allergic airway inflammation. Six-week-old male C3H/HeJ mice were intratracheally administered ovalbumin (OVA, 1 μg) every 2 weeks and/or BPA (0, 0.0625, 1.25, and 25 pmol/animal/week) once per week for 6 weeks. Following the final intratracheal instillation, we examined the cellular profile of the bronchoalveolar lavage fluid, histological changes and expression of inflammatory/anti-inflammatory mediators in the lungs, OVA-specific immunoglobulin (Ig) production, serum corticosterone levels, and changes in the lymphoid tissues (mediastinal lymph node (MLN) and spleen). Exposure to OVA + BPA enhanced inflammatory cell infiltration and protein expression of Th2 cytokines/chemokines (e.g. interleukin (IL)-13 and IL-33) in the lungs, OVA-specific immunoglobulin E (IgE) production, the numbers of total cells and activated antigen-presenting cells (MHC class II+ CD86+, CD11c+), as well as the production of Th2 cytokines (i.e. IL-4 and IL-5) and stromal cell-derived factor-1α in MLN cells compared to OVA exposure alone. These effects were more prominent with 0.0625 or 1.25 pmol/animal/week of BPA. Furthermore, exposure to OVA + BPA altered serum levels of anti-inflammatory corticosterone, estrogen receptor 2 messenger RNA (mRNA) expression in the lungs and spleen functionality. These findings suggest that low-dose BPA exposure may aggravate allergic airway inflammation by enhancing Th2 responses via disruption of the immune system.


2021 ◽  
Vol 15 (10) ◽  
pp. 2512-2515
Author(s):  
Asma Inam ◽  
Muhammad Sair ◽  
Sadia Ikram ◽  
Sadia Majeed ◽  
Gul-E- Nazish ◽  
...  

Background: Asthma is a chronic inflammatory disease affecting smaller airways. Airflow obstruction leading to airway hyper-responsiveness and increased mucus production are salient features of asthma pathophysiology. Generally, Th2 cytokines are increased in allergic asthma. Aim: To propose the molecular mechanisms by which Carica Papaya Leaves Extract (CPLE) alleviates pulmonary edema in animal model of allergic airway inflammation comparable to methylprednisolone. Place and duration of study: Pharmacology Department, University of Health Sciences Lahore for 1 year. Methods: We took twenty four male BALB/c mice and divided them equally into four groups. The control group was given PBS only, while Group II served as diseased group and induced airway inflammation by ovalbumin. Group III and IV were first induced with airway inflammation and side by side treated with Carica papaya leaf extract (CPLE) 100mg/kg body weight orally and methylprednisolone 15 mg/kg body weight intraperitoneally for seven consecutive days respectively. At the end of the experimental protocol, mice were euthanized and lung wet/dry ratio was measured. mRNA expression of AQP1 and AQP5 in lung tissue were also determined using RT-PCR. Results: Ethanolic extract of Carica Papaya leaves decreased all markers of pulmonary edema in mouse model of allergic airway inflammation comparable to methylprednisolone by decreasing lung wet/dry ratio and enhancing AQP1 and AQP5 mRNA expression. Conclusion: Carica Papaya leaves extract may diminish pulmonary edema in mice associated with allergic asthma. Keywords: AQP1, AQP5 (Aquaporins), Carica Papaya Leaves Extract (CPLE), Pulmonary Edema, Th2 cytokines.


2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Kyu-Sup Cho ◽  
Mi-Kyung Park ◽  
Shin-Ae Kang ◽  
Hee-Young Park ◽  
Sung-Lyong Hong ◽  
...  

Although several studies have demonstrated that mesenchymal stem cells derived from adipose tissue (ASCs) can ameliorate allergic airway inflammation, the immunomodulatory mechanism of ASCs remains unclear. In this study, we investigated whether regulatory T cells (Tregs) induction is a potential mechanism in immunomodulatory effects of ASCs on allergic airway disease and how these induced Tregs orchestrate allergic inflammation. Intravenous administration of ASCs significantly reduced allergic symptoms and inhibited eosinophilic inflammation. Airway hyperresponsiveness, total immune cell and eosinophils in the bronchoalveolar lavage fluid, mucus production, and serum allergen-specific IgE and IgG1 were significantly reduced after ASCs administration. ASCs significantly inhibited Th2 cytokines (IL-4, IL-5, and IL-13) and enhanced Th1 cytokine (IFN-γ) and regulatory cytokines (IL-10 and TGF-β) in the bronchoalveolar lavage fluid and lung draining lymph nodes. Furthermore, levels of IDO, TGF-β, and PGE2were significantly increased after ASCs administration. Interestingly, this upregulation was accompanied by increased Treg populations. In conclusion, ASCs ameliorated allergic airway inflammation and improved lung function through the induction of Treg expansion. The induction of Treg by ASCs involves the secretion of soluble factors such as IDO, TGF-β, and PGE2and Treg might be involved in the downregulation of Th2 cytokines and upregulation of Th1 cytokines production.


2005 ◽  
Vol 288 (4) ◽  
pp. L741-L748 ◽  
Author(s):  
Carla M. Prado ◽  
Edna A. Leick-Maldonado ◽  
Vanessa Arata ◽  
David I. Kasahara ◽  
Mílton A. Martins ◽  
...  

In the present study we evaluated the role of neurokinins in the modulation of inducible nitric oxide synthase (iNOS) inflammatory cell expression in guinea pigs with chronic allergic airway inflammation. In addition, we studied the acute effects of nitric oxide inhibition on this response. Animals were anesthetized and pretreated with capsaicin (50 mg/kg sc) or vehicle 10 days before receiving aerosolized ovalbumin or normal saline twice weekly for 4 wk. Animals were then anesthetized, mechanically ventilated, given normal saline or N G-nitro-l-arginine methyl ester (l-NAME, 50 mg/kg ic), and challenged with ovalbumin. Prechallenge exhaled NO increased in ovalbumin-exposed guinea pigs ( P < 0.05 compared with controls), and capsaicin reduced this response ( P < 0.001). Compared with animals inhaled with normal saline, ovalbumin-exposed animals presented increases in respiratory system resistance and elastance and numbers of total mononuclear cells and eosinophils, including those expressing iNOS ( P < 0.001). Capsaicin reduced all these responses ( P < 0.05) except for iNOS expression in eosinophils. Treatment with l-NAME increased postantigen challenge elastance and restored both resistance and elastance previously attenuated by capsaicin treatment. Isolated l-NAME administration also reduced total eosinophils and mononuclear cells, as well as those cells expressing iNOS ( P < 0.05 compared with ovalbumin alone). Because l-NAME treatment restored lung mechanical alterations previously attenuated by capsaicin, NO and neurokinins may interact in controlling airway tone. In this experimental model, NO and neurokinins modulate eosinophil and lymphocyte infiltration in the airways.


Pneumologie ◽  
2013 ◽  
Vol 67 (S 01) ◽  
Author(s):  
M Idzko ◽  
K Ayata ◽  
T Müller ◽  
T Dürk ◽  
M Grimm ◽  
...  

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