Abstract
It was previously demonstrated that non-allergen-sensitized rodents born to mothers exposed to a high-fat diet (HFD) spontaneously develop lower respiratory compliance and higher respiratory resistance. In the present study, we sought to determine if mice born to mothers consuming HFD would exhibit changes in inflammatory response and lung remodeling when subjected to ovalbumin (OVA) sensitization/challenge in adult life. Mice born to dams consuming either HFD or standard chow had increased bronchoalveolar lavage (BAL) levels of IL-1β, IL-4, IL-5, IL-10, IL-13, TNF-α and TGF-β1 after challenge with OVA. IL-4, IL-13, TNF-α and TGF-β1 levels were further increased in the offspring of HFD-fed mothers. Mice born to obese dams also had exacerbated values of leukocyte infiltration in lung parenchyma, eosinophil and neutrophil counts in BAL, mucus overproduction and collagen deposition. The programming induced by maternal obesity was accompanied by increased expression of miR-155 in peripheral-blood mononuclear cells and reduced miR-133b in trachea and lung tissue in adult life. Altogether, the present data support the unprecedented notion that the progeny of obese mice display exacerbated responses to sensitization/challenge with OVA, leading to the intensification of the morphological changes of lung remodeling. Such changes are likely to result from long-lasting changes in miR-155 and miR-133b expression.
Highlights
The global prevalence of allergic asthma has continuously increased since the last decade of the20th century [1]
We initially assessed biochemical and body weight parameters to demonstrate that our experimental approach was efficient in inducing obesity and its metabolic consequences just before the beginning of pregnancy
Our data revealed that body weight, blood glucose and serum triglycerides, cholesterol and leptin were increased in pregnant mice fed a high-fat diet (HFD)
Summary
The global prevalence of allergic asthma has continuously increased since the last decade of the20th century [1]. The global prevalence of allergic asthma has continuously increased since the last decade of the. The inflammatory response of allergic asthma is classically recognized as a predominantly TH 2 activation that leads to IgE production and eosinophil development and infiltration in the lung parenchyma. Such features are granted by TH 2 cytokines such as interleukin (IL)-4 and IL-5 [2]. More recent is the notion that exacerbation of allergic asthma is supported by lung neutrophil accumulation, increased production of acute phase proteins, such as the proinflammatory cytokines tumor necrosis factor-α (TNF-α) and IL-1β, and activation of nuclear factor-κB (NF-κB) [6,7]
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