Formaldehyde-Induced Aggravation of Pruritus and Dermatitis Is Associated with the Elevated Expression of Th1 Cytokines in a Rat Model of Atopic Dermatitis

Abstract

Atopic dermatitis is a complex disease of heterogeneous pathogenesis, in particular, genetic predisposition, environmental triggers, and their interactions. Indoor air pollution, increasing with urbanization, plays a role as environmental risk factor in the development of AD. However, we still lack a detailed picture of the role of air pollution in the development of the disease. Here, we examined the effect of formaldehyde (FA) exposure on the manifestation of atopic dermatitis and the underlying molecular mechanism in naive rats and in a rat model of atopic dermatitis (AD) produced by neonatal capsaicin treatment. The AD and naive rats were exposed to 0.8 ppm FA, 1.2 ppm FA, or fresh air (Air) for 6 weeks (2 hours/day and 5 days/week). So, six groups, namely the 1.2 FA-AD, 0.8 FA-AD, Air-AD, 1.2 FA-naive, 0.8 FA-naive and Air-naive groups, were established. Pruritus and dermatitis, two major symptoms of atopic dermatitis, were evaluated every week for 6 weeks. After that, samples of the blood, the skin and the thymus were collected from the 1.2 FA-AD, the Air-AD, the 1.2 FA-naive and the Air-naive groups. Serum IgE levels were quantified with ELISA, and mRNA expression levels of inflammatory cytokines from extracts of the skin and the thymus were calculated with qRT-PCR. The dermatitis and pruritus significantly worsened in 1.2 FA-AD group, but not in 0.8 FA-AD, compared to the Air-AD animals, whereas FA didn't induce any symptoms in naive rats. Consistently, the levels of serum IgE were significantly higher in 1.2 FA-AD than in air-AD, however, there was no significant difference following FA exposure in naive animals. In the skin, mRNA expression levels of Th1 cytokines such as TNF-α and IL-1β were significantly higher in the 1.2 FA-AD rats compared to the air-AD rats, whereas mRNA expression levels of Th2 cytokines (IL-4, IL-5, IL-13), IL-17A and TSLP were significantly higher in 1.2 FA-naive group than in the Air-naive group. These results suggested that 1.2 ppm of FA penetrated the injured skin barrier, and exacerbated Th1 responses and serum IgE level in the AD rats so that dermatitis and pruritus were aggravated, while the elevated expression of Th2 cytokines by 1.2 ppm of FA in naive rats was probably insufficient for clinical manifestation. In conclusion, in a rat model of atopic dermatitis, exposure to 1.2 ppm of FA aggravated pruritus and skin inflammation, which was associated with the elevated expression of Th1 cytokines.

Topical film prepared with Rhus verniciflua extract‐loaded pullulan hydrogel for atopic dermatitis treatment

“…Cutaneous lesions were carefully assessed by scoring systems as previously described . Skin condition at the designated shoulder area was assessed twice, just before the initial application of pullulan hydrogel or RVE@PH (PND 42) and just after the last application (PND 56), to determine changes in the extent and severity of the lesions ( n = 5 per group).…”

“…Cutaneous lesions were carefully assessed by scoring systems as previously described. 29,36 Skin condition at the designated shoulder area was assessed twice, just before the initial application of pullulan hydrogel or RVE@PH (PND 42) and just after the last application (PND 56), to determine changes in the extent and severity of the lesions (n = 5 per group). We divided all skin lesions within 3 cm 2 of the shoulder into the inspection units (0.25 cm 2 ), inspected and scored the severity of each unit, and summed the scores per unit to yield the total score per rat individual.…”

Pseudolaric acid B attenuates atopic dermatitis-like skin lesions by inhibiting interleukin-17-induced inflammation

“…Then, we further examined the effects of PB on IL-1β and TNF-α, which are important to accelerate the development of AD 10 . The data showed that PB significantly decreased IL-1β and TNF-α release in the serum and lesional skin of AD mice (Fig.…”

Home Remodeling and Food Allergy Interact Synergistically to Increase the Risk of Atopic Dermatitis

“…Only short-term exposure to formaldehyde can cause dysfunction of the skin barrier in children with and without AD; this is more prominent in the latter [ 19 ]. In an experimental rat model of AD, exposure to formaldehyde aggravated pruritus and dermatitis and was associated with an elevated expression of Th1 cytokines [ 20 ]. Exposure to nitrogen dioxide (NO 2 ) at domestic concentrations causes impairment of the skin barrier function in subjects with AD [ 21 ].…”