History of eczema herpeticum is associated with the inability to induce human β-defensin (HBD)-2, HBD-3 and cathelicidin in the skin of patients with atopic dermatitis

Conflicts of interest: None declared. Madam, Patients with atopic dermatitis (AD) with a history of eczema herpeticum (ADEH) represent a subset of individuals with AD who have more severe disease.1 It has previously been shown that the skin of patients with AD has defects in its capacity to increase maximally the antimicrobial peptides (AMPs), cathelicidin, human β‐defensin (HBD)‐2 and HBD‐3 in response to inflammation, in contrast to patients with psoriasis who also have inflammation of the skin, but no difficulty with AMP induction.2, 3 To date, however, previous studies have not examined HBD‐2 and HBD‐3 induction in the ADEH subset of patients.4 We sought to examine if subjects with ADEH exhibit an inhibition in induction of AMPs, compared with subjects without ADEH. A total of 81 subjects were recruited into the study: 26 patients with psoriasis, 21 with AD and nine with ADEH and 25 healthy subjects with no history of skin disease (Table S1, see Supporting information). Two 2‐mm punch biopsies were collected from lesional and nonlesional skin of the patients. Normal controls provided two 2‐mm punch biopsies from the skin of their upper inner arm. Quantification of cathelicidin, interleukin (IL)‐13, HBD‐2 and HBD‐3 in the skin was performed by quantitative reverse transcriptase–polymerase chain reaction (RT‐PCR) (Data S2, see Supporting information), and their expression was calculated as relative to glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) mRNA. All statistical analyses were performed using SAS v.9.1 or higher (SAS Institute, Cary, NC, U.S.A.) (Data S1, see Supporting information).