Oral Administration of Acrylamide Worsens the Inflammatory Responses in the Airways of Asthmatic Mice Through Agitation of Oxidative Stress in the Lungs

• Published in: Frontiers in immunology 2020-10, Vol.11, p.1940
• Main Authors: Hajimohammadi, Bahador, Athari, Seyyede Masoume, Abdollahi, Mohammad, Vahedi, Ghasem, Athari, Seyyed Shamsadin
• Format: Article
• Language: English
• Subjects: acrylamide; Acrylamide - administration & dosage; Acrylamide - toxicity; Administration, Oral; Airway Remodeling - drug effects; allergic asthma; Animals; Asthma - chemically induced; Asthma - immunology; Asthma - metabolism; Asthma - physiopathology; Bronchoalveolar Lavage Fluid - immunology; Bronchoconstriction - drug effects; Cytokines - metabolism; Female; Fibrosis; food contamination; Immunology; Inflammation Mediators - metabolism; Lung - drug effects; Lung - immunology; Lung - metabolism; Lung - physiopathology; Mice, Inbred BALB C; Ovalbumin; oxidative stress; Oxidative Stress - drug effects; Respiratory Hypersensitivity - chemically induced; Respiratory Hypersensitivity - immunology; Respiratory Hypersensitivity - metabolism; Respiratory Hypersensitivity - physiopathology; toxicology
• ISSN: 1664-3224; 1664-3224
• DOI: 10.3389/fimmu.2020.01940

Acrylamide is a toxic chemical substance produced when starch-rich foods are fried at high temperatures. Asthma is a chronic and complicated respiratory disease, of which genetic and environmental factors are the main triggers. Orally-received components may have an effect on asthma pathophysiology. The aim of this study was to investigate the role of AA as a stimulus in asthma. BALB/c mice were allocated into four groups as follows: two OVA-sensitized asthmatic groups, including one treated with AA by gavage feeding and one non-treated (asthma group), and two healthy (non-asthmatic) groups, one treated with AA by gavage feeding and one non-treated (negative control group). Airway hyperresponsiveness, cell count, cytokine levels in BAL fluid, lung histopathology, IgE levels, and oxidative stress indices including plasma level of MDA, pulmonary antioxidant enzymes (SOD and CAT) levels, HP content, and collagen fiber accumulation in lung tissue were measured. We found that the group of mice treated with both OVA and AA (asthmatic and AA-treated mice) experienced higher levels of asthma-associated biomarkers, including higher enhanced pause (Penh value), eosinophilic inflammation, mucus hyper secretion, goblet cell hyperplasia, total and OVA-specific IgE levels, IL-4, IL-5, and IL-13 levels than the group sensitized only with OVA (asthmatic mice). The OVA-AA-treated mice also experienced worsened levels of oxidative stress indicators. Healthy (non-asthmatic) mice that only received AA were in similar conditions to healthy untreated mice (negative control group). The OVA-AA-treated group showed more severe allergic asthma symptoms in comparison to the group only sensitized with OVA. Therefore, food/water contaminated with AA can act as a stimulant of allergic asthma and exacerbate the bronchial inflammatory responses.