scholarly journals Exposure to low-dose bisphenol A during the juvenile period of development disrupts the immune system and aggravates allergic airway inflammation in mice

2018 ◽  
Vol 32 ◽  
pp. 205873841877489 ◽  
Author(s):  
Eiko Koike ◽  
Rie Yanagisawa ◽  
Tin-Tin Win-Shwe ◽  
Hirohisa Takano
Keyword(s):  
Immune System ◽  
Bisphenol A ◽  
Airway Inflammation ◽  
Low Dose ◽  
Allergic Airway Inflammation ◽  
Lymphoid Tissues ◽  
Th2 Cytokines ◽  
Juvenile Period ◽  
Specific Immunoglobulin ◽  
Anti Inflammatory

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.

scholarly journals Oral exposure to low dose bisphenol A aggravates allergic airway inflammation in mice

2019 ◽  
Vol 6 ◽  
pp. 1253-1262 ◽  
Author(s):  
Rie Yanagisawa ◽  
Eiko Koike ◽  
Tin-Tin Win-Shwe ◽  
Hirohisa Takano
Keyword(s):  
Bisphenol A ◽  
Airway Inflammation ◽  
Low Dose ◽  
Allergic Airway Inflammation ◽  
Oral Exposure

Adjuvant and Anti-Inflammatory Properties of Cigarette Smoke in Murine Allergic Airway Inflammation

2009 ◽  
Vol 40 (1) ◽  
pp. 38-46 ◽  
Author(s):  
Nancy J. Trimble ◽  
Fernando M. Botelho ◽  
Carla M. T. Bauer ◽  
Ramzi Fattouh ◽  
Martin R. Stämpfli
Keyword(s):  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Allergic Airway Inflammation ◽  
Anti Inflammatory

scholarly journals An anti-inflammatory eicosanoid switch mediates the suppression of type-2 inflammation by helminth larval products

2020 ◽  
Vol 12 (540) ◽  
pp. eaay0605 ◽  
Author(s):  
Marta de los Reyes Jiménez ◽  
Antonie Lechner ◽  
Francesca Alessandrini ◽  
Sina Bohnacker ◽  
Sonja Schindela ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Mitogen Activated Protein Kinase ◽  
Metabolic Enzyme ◽  
Prostaglandin E ◽  
Lipoxygenase Pathway ◽  
Anti Inflammatory ◽  
Type 2 Inflammation ◽  
Allergy And Asthma

Eicosanoids are key mediators of type-2 inflammation, e.g., in allergy and asthma. Helminth products have been suggested as remedies against inflammatory diseases, but their effects on eicosanoids are unknown. Here, we show that larval products of the helminth Heligmosomoides polygyrus bakeri (HpbE), known to modulate type-2 responses, trigger a broad anti-inflammatory eicosanoid shift by suppressing the 5-lipoxygenase pathway, but inducing the cyclooxygenase (COX) pathway. In human macrophages and granulocytes, the HpbE-driven induction of the COX pathway resulted in the production of anti-inflammatory mediators [e.g., prostaglandin E2 (PGE2) and IL-10] and suppressed chemotaxis. HpbE also abrogated the chemotaxis of granulocytes from patients suffering from aspirin-exacerbated respiratory disease (AERD), a severe type-2 inflammatory condition. Intranasal treatment with HpbE extract attenuated allergic airway inflammation in mice, and intranasal transfer of HpbE-conditioned macrophages led to reduced airway eosinophilia in a COX/PGE2-dependent fashion. The induction of regulatory mediators in macrophages depended on p38 mitogen-activated protein kinase (MAPK), hypoxia-inducible factor-1α (HIF-1α), and Hpb glutamate dehydrogenase (GDH), which we identify as a major immunoregulatory protein in HpbE. Hpb GDH activity was required for anti-inflammatory effects of HpbE in macrophages, and local administration of recombinant Hpb GDH to the airways abrogated allergic airway inflammation in mice. Thus, a metabolic enzyme present in helminth larvae can suppress type-2 inflammation by inducing an anti-inflammatory eicosanoid switch, which has important implications for the therapy of allergy and asthma.

scholarly journals Low-Dose Intestinal Trichuris muris Infection Alters the Lung Immune Microenvironment and Can Suppress Allergic Airway Inflammation

2015 ◽  
Vol 84 (2) ◽  
pp. 491-501 ◽  
Author(s):  
Alistair L. Chenery ◽  
Frann Antignano ◽  
Kyle Burrows ◽  
Sebastian Scheer ◽  
Georgia Perona-Wright ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Cross Talk ◽  
Low Dose ◽  
Intestinal Inflammation ◽  
Allergic Airway Inflammation ◽  
Interleukin 10 ◽  
Th1 Cell ◽  
Trichuris Muris ◽  
Airway Pathology

Immunological cross talk between mucosal tissues such as the intestine and the lung is poorly defined during homeostasis and disease. Here, we show that a low-dose infection with the intestinally restricted helminth parasiteTrichuris murisresults in the production of Th1 cell-dependent gamma interferon (IFN-γ) and myeloid cell-derived interleukin-10 (IL-10) in the lung without causing overt airway pathology. This cross-mucosal immune response in the lung inhibits the development of papain-induced allergic airway inflammation, an innate cell-mediated type 2 airway inflammatory disease. Thus, we identify convergent and nonredundant roles of adaptive and innate immunity in mediating cross-mucosal suppression of type 2 airway inflammation during low-dose helminth-induced intestinal inflammation. These results provide further insight in identifying novel intersecting immune pathways elicited by gut-to-lung mucosal cross talk.

scholarly journals Anti-oxidant and Anti-inflammatory Effects of Aquatic Exercise in Allergic Airway Inflammation in Mice

2019 ◽  
Vol 10 ◽  
Author(s):  
Boae Lee ◽  
Yeonye Kim ◽  
Young Mi Kim ◽  
Jaehoon Jung ◽  
Taehyung Kim ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Aquatic Exercise ◽  
Anti Oxidant ◽  
Anti Inflammatory
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