Abstract
Despite their distinct clinical manifestation, frontal fibrosing alopecia (FFA) and lichen planopilaris (LPP) display similar histopathologic features. Aberrant innate immune responses to endogenous or exogenous triggers have been discussed as factors that could drive inflammatory cascades and the collapse of the stem cell niche. In this exploratory study, we investigate the bacterial composition of scalp skin and plucked hair follicles (HF) of patients with FFA, LPP and alopecia areata circumscripta (AAc), as well as healthy individuals, in relation to cellular infiltrates and the expression of defense mediators. The most abundant genus in lesional and non-lesional HFs of LPP and FFA patients was Staphylococcus, while Lawsonella dominated in healthy individuals and in AAc patients. We observed statistically significant differences in the ratio of Firmicutes to Actinobacteria between healthy scalp, lesional, and non-lesional sites of FFA and LPP patients. This marked dysbiosis in FFA and LPP in compartments close to the bulge was associated with increased HβD1 and HβD2 expression along the HFs from lesional sites, while IL-17A was increased in lesional HF from AAc patients. The data encourage further studies on how exogenous factors and molecular interactions across the HF epithelium could contribute to disease onset and propagation.
Highlights
We investigate the presence of bacteria on the skin surface and in deeper parts of hair follicles (HF) from lesional and non-lesional scalps of lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) patients in comparison to healthy individuals, and patients with alopecia areata circumscripta (AAc)
Hematoxylin and eosin, Giemsa and immunohistochemical stainings were performed on 2–4 μm sections of formalin-fixed, paraffin-embedded diagnostic biopsies obtained from lesional scalp sites of 22 alopecia patients (n = 11 LPP, n = 8 FFA)
Staphylococcus, Lawsonella, and Cutibacterium were the nating taxa found on healthy skin [37]
Summary
LPP, lichen planopilaris; FFA, frontal fibrosing alopecia; AAc, alopecia areata circumscripta; HF, hair follicle; I.P., immune privilege. In the neutrophilic cicatricial alopecia subtype folliculitis decalvans (FD), Staphylococcus aureus colonization, along with a deficient host immune response, are recognized pathogenetic factors [20,21] Beyond their typical role in infection or clinically relevant inflammation, evidence has been emerging that cutaneous microbes help calibrate the responses of innate and adaptive immune cells [22], and that HFs provide the environment for such calibration, affecting tissue homeostasis and HF cycling, e.g., via the involvement of regulatory T cells [22,23]. We investigate the presence of bacteria on the skin surface and in deeper parts of HFs from lesional and non-lesional scalps of LPP and FFA patients in comparison to healthy individuals, and patients with alopecia areata circumscripta (AAc). The study was complemented by immunohistochemical staining and ELISA analyses for human beta-defensins (HβD1, HβD2) and interleukin-17A (IL-17A)
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