Introduction

Chronic eczema is a major challenge in dermatology due to its high prevalence, severe course, frequent relapses, significant burden affecting patients of different ages and both sexes. Effective treatment requires understanding environmental factors, especially microbial influences, which affect the patient’s condition. These triggers are detected and mediated by transmembrane Toll-like receptors located in barrier tissues.

Objective

To investigate changes in Toll-like receptor 2 and Toll-like receptor 4 expression during recurrence of chronic eczema before and after treatment.

Material and methods

The study included 80 patients with chronic eczema (54 women, 26 men; aged 24–81 years) without severe somatic or infectious diseases and a control group of 20 individuals. Peripheral blood Toll-like receptor 2 and Toll-like receptor 4 expression was measured by flow cytometry using monoclonal antibodies conjugated with phycoerythrin.

Results

The study demonstrated increased colonization of eczema lesions with Enterococcus faecalis and Streptococcus pyogenes. Toll-like receptor 2 expression was elevated across all age groups and reached the highest values in men aged 61–81 years (118.00 ±9.54 conventional units), particularly in patients with prolonged disease duration (15–20 years) and very severe eczema. Lower Toll-like receptor 2 expression was observed in patients with shorter disease duration. Toll-like receptor 4 expression was elevated in both men and women aged 41–60 years. Following treatment, Toll-like receptor 2 expression decreased to values comparable to controls, whereas Toll-like receptor 4 expression declined but remained at the upper limit of the reference range in men aged 41–60 years.

Conclusions

Toll-like receptor 2 and Toll-like receptor 4 expression was associated with eczema severity, disease duration, and patient age. Toll-like receptor 2 may represent a marker of disease activity and treatment response, whereas persistent Toll-like receptor 4 expression after therapy may reflect ongoing immune activation or skin barrier repair processes.