Psychological stress delays inflammatory resolution and promotes sustained sensory sensitization during recovery from atopic dermatitis

Qiaofeng Zhao, Alberto Leguina-Ruzzi, Mitsutoshi Tominaga, Yayoi Kamata, Atsuko Kamo, Huiying Wan, Yuping Ran, Kenji Takamori

Atopic dermatitis (AD) is a chronic inflammatory disorder characterized by pruritus, eczematous
lesions, and epidermal barrier dysfunction, with substantial impact on quality of life (Weidinger
and Novak 2016). Its pathogenesis reflects a complex interplay between barrier impairment,
immune dysregulation, and environmental triggers, resulting in heterogeneous phenotypes (Kim,
Kim et al. 2019). While mechanisms driving onset and exacerbation have been extensively studied,
the processes governing disease resolution remain poorly understood. Inflammatory resolution is
increasingly recognized as an active process involving immune reprogramming, tissue repair, and
restoration of homeostasis rather than a passive decline in inflammation (Oetjen, Mack et al. 2017).
Disruption of this process may contribute to persistent symptoms and chronic disease activity.
However, the factors that impair inflammatory resolution in AD remain poorly understood.
Psychological stress is a recognized modifier of AD, associated with worsened pruritus and disease
persistence. Experimental incorporation of stress paradigms has improved the translational
relevance of AD models (Hall, Cruser et al. 2012). Restraint stress (RS), a model of psychological
stress in rodents, activates the hypothalamic-pituitary-adrenal (HPA) axis and may enhance DRG
neuronal excitability through glucocorticoid and sympathetic signaling, thereby facilitating Aβ
fiber–mediated mechanical alloknesis (Buynitsky and Mostofsky 2009). However, prior work has
focused largely on stress during active inflammation, emphasizing exacerbation rather than
recovery. We hypothesized that psychological stress disrupts the transition to resolution without
amplifying peak inflammation, thereby sustaining sensory sensitization during recovery.

Chaeeun Lee

Can aged Camellia oleifera Abel oil truly be used to treat atopic dermatitis?

Abstract

Xi-Lin Ouyang1, Zhang-Lin Yuan1, Xiao-Bing Chen1, Hong-Wan Gan2, Sen-Hui Guo1, Juan Cai1 and Jing-Jing Zhong2
1Department of Pharmacy, Gannan Healthcare Vocational College, Ganzhou, China, 2Department of
Dermatology, Ganzhou People’s Hospital, Ganzhou, China

Atopic dermatitis is an inflammatory skin condition characterized by erythema,
eruption, lichenification, and pruritus. Aged Camellia oleifera Abel oil, an effective
empirical plant oil utilized by the Gannan Hakka people in China to alleviate the
symptomsofatopicdermatitis.However,noscientificstudieshavebeenreported
to prove whether this oil is truly effective. We conducted this study to confirm
whether aged C. oleifera oil could alleviate the symptoms of 2,4
dinitrochlorobenzene (DNCB)-induced atopic dermatitis in mice. Differences
in the thickness and weight of the right and left ears were measured. ELISA
wasusedtodeterminetheserumlevelsoftheinflammatoryfactorsIL-4,IgE,IFN
γ, and TNF-α. HEstaining was performed to observe inflammatory cell infiltration
in the mouseskinlesions.Inaddition, themetabolitesofagedC.oleiferaoils were
analyzed, and molecular docking was used to assess the binding affinity of the
major metabolites to filaggrin, a protein involved in skin barrier function. Animal
studies showed that aged C. oleifera oil significantly improved the symptoms of
atopic dermatitis. HE staining and measurement of inflammatory factor levels
revealed similar results. A total of 41 metabolites were tentatively identified in the
oil, with fatty acids emerging as the major metabolites. Molecular docking
confirmed that the three most abundant fatty acids, i.e., oleic acid,
n-hexadecanoic acid, and octadecanoic acid, bind well to filaggrin. Our
results suggest that aged C. oleifera oils can be used to ameliorate the
symptoms of atopic dermatitis. Fatty acids may be the major active
metabolites responsible for the observed therapeutic effects by reducing
transdermal water loss, increasing skin hydration, alleviating DNCB-induced
skin barrier alterations, and eliminating itchy scratching caused by dry skin.