Activation of aryl hydrocarbon receptor by benzo[a]pyrene increases interleukin 33 expression and eosinophil infiltration in a mouse model of allergic airway inflammation.

We recently demonstrated that benzo[a]pyrene (BaP), the aryl hydrocarbon receptor (AhR) ligand, directly contributes to aggravation of cutaneous allergy in a mouse model of allergic dermatitis. The present study aimed to determine whether BaP-induced AhR activation results in development of airway inflammation. Initially, the potential for a direct relationship between BaP-induced AhR activation and airway inflammation was investigated in vivo, using a mouse model of type 2 helper T cell (Th2) hapten toluene-2,4-diisocyanate (TDI)-induced airway inflammation.

Rapid adaptation of to acetylcholinesterase inhibitors (pyraclofos and pirimicarb) in a multi-generation study.

We evaluated the real effects of pollutants through a multi-generation study. We tested whether short-term exposure (48 h) of successive (first and second) generations of neonates (<24-h-old) to two acetylcholinesterase inhibitor insecticides, pyraclofos, and pirimicarb, would change insecticide sensitivity and life-cycle parameters over four generations. Additionally, we tested whether acetylcholinesterase (AChE) activity levels would be associated with this sensitivity change.

Subacute oral administration of folic acid elicits anti-inflammatory response in a mouse model of allergic dermatitis.

Folic acid (FA) deficiency is associated with several health problems, including megaloblastic anemia and fetal neural tube defects. Therefore, supplementation with FA is strongly recommended by governments worldwide. Recent published reports indicate that FA functions in immune system maintenance.

Effect of prenatal exposure to combined immunosuppressive agrochemicals in a mouse model of allergic airway inflammation.

The aim of this study is to identify the combined effect of multiple chemicals to the development of allergy. In this study, the effect of prenatal exposure to an organochlorine agent methoxychlor (MXC) and/or an organophosphate agent parathion (PARA) on trimellitic anhydride-induced allergic airway inflammation was examined in mice. Eosinophil infiltration in the bronchoalveolar lavage fluid (BALF) was significantly enhanced by MXC + PARA exposure compared to that of the control, MXC, and PARA groups.

Direct activation of aryl hydrocarbon receptor by benzo[a]pyrene elicits T-helper 2-driven proinflammatory responses in a mouse model of allergic dermatitis.

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that binds to various environmental chemicals and contributes to numerous toxicological effects. However, the direct effects of AhR on the development of allergic diseases are not fully understood. The main aim of this study was to elucidate the action of AhR in the development of cutaneous allergies.

Role of estrogen receptors α and β in the development of allergic airway inflammation in mice: A possible involvement of interleukin 33 and eosinophils.

Recent studies have shown that the estrogen receptor α (ERα), but not ERβ, is involved in the proinflammatory and propruritic responses in cutaneous allergy. In addition, results from our recent study showed that while oral administration of the rather ERβ-selective agonist bisphenol A exacerbated the respiratory allergic inflammation, the potential inflammatory reaction in the skin was decreased after administration of bisphenol A. This study aimed to elucidate whether ERα and ERβ are involved in the progression of an allergic airway inflammation.

Involvement of estrogen receptor α in pro-pruritic and pro-inflammatory responses in a mouse model of allergic dermatitis.

It has been reported that endogenous or exogenous estrogens can affect the immune system, resulting in immune disorders; however, their direct involvement in such conditions remains to be demonstrated. The purpose of this study was to investigate whether estrogen receptors (ER) are directly implicated in pro-pruritic and pro-inflammatory reactions in cutaneous allergy. Initially, enhancement of the pro-inflammatory response by several ER agonists [methoxychlor (MXC), β-estradiol (E2), propylpyrazoletriol (PPT; an ERα agonist), and diarylpropionitrile (DPN; an ERβ agonist)] was examined in vivo using a male BALB/c mouse model of allergic dermatitis induced by toluene-2,4-diisocyanate administration.

Oral Administration of Bisphenol A Directly Exacerbates Allergic Airway Inflammation but Not Allergic Skin Inflammation in Mice.

Bisphenol A (BPA) is used in various areas of daily life as a major component of plastic products. However, it is also known as a strong endocrine disruptor that affects the human immune system. Studies have indicated that BPA possibly exacerbates allergic diseases such as atopic dermatitis and asthma.