Hang Zhao

Atopic dermatitis (AD) is a chronic inflammatory skin disease driven by immune dysregulation and epidermal barrier dysfunction, in which eosinophils act as key effector cells contributing to tissue damage and persistent inflammation. This comprehensive review elucidates the multifaceted contributions of eosinophils to the progression of AD. Driven by key type 2 cytokines (notably IL-4, IL-5, and IL-13) and specific chemokines, eosinophils infiltrate lesional skin and undergo IgE-mediated degranulation. The subsequent release of cytotoxic granule proteins, including major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil-derived neurotoxin (EDN), and eosinophil peroxidase (EPX), directly induces keratinocyte apoptosis, exacerbates tissue remodeling, and sustains the local inflammatory cascade. Furthermore, we explore the intricate crosstalk between eosinophils and sensory neurons, which, alongside cytokines like IL-31, profoundly aggravates chronic pruritus. Consequently, modulating eosinophil activation and recruitment has emerged as a vital therapeutic approach. We systematically evaluate current and emerging pharmacological interventions, ranging from conventional topical corticosteroids to advanced targeted therapies. Particular emphasis is placed on the mechanistic impact of novel biologics and small-molecule Janus kinase (JAK) inhibitors, demonstrating how they attenuate eosinophilic inflammation. By identifying current gaps in this field, this review provides valuable insights for future research and clinical practice in the field of AD.

Introduction: C-X-C motif chemokine ligand 1 (CXCL1) is a potent neutrophil chemoattractant that plays a pivotal role in recruiting neutrophils during inflammatory conditions. This study explored the role of CXCL1 in modulating the gut microbiota, influencing neutrophil infiltration, and contributing to the development of colitis. Methods: We employed quantitative PCR to assess CXCL1 expression in colon samples. A mouse model of dextran sulfate sodium (DSS)-induced colitis was utilized to explore the progression of colitis in wild-type (WT) and CXCL1-deficient (CXCL1−/−) mice. Results: Colitis attenuation was evident in CXCL1−/− mice. Significant alterations were observed in the gut microbiome, as revealed by 16S rRNA gene sequencing. Furthermore, CXCL1−/− mice exhibited reduced gut permeability and diminished endotoxin levels in peripheral blood following DSS treatment compared to WT mice. In response to DSS treatment, WT mice showed a clear increase in neutrophil infiltration, while CXCL1−/− mice exhibited lower levels of infiltration. Fecal microbiota transplantation (FMT) using stools from CXCL1−/− mice alleviated DSS-induced colitis. Interestingly, FMT from patients with colitis increased CXCL1 and Ly6G expression in the colons of gut-sterilized mice. Clinical data analysis revealed elevated CXCL1 and CD15 expression in patients with colitis, with a positive correlation between the severity of colitis and the expression of CXCL1 and CD15. Conclusion: These findings shed light on the pivotal role of CXCL1 in promoting colitis by modulating the gut microbiota.

Under the action of natural products, microorganisms participate in a complete cycle of the “gut-brain-skin” axis linkage mechanism, thereby regulating the development of atopic dermatitis.