Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Sep;163(3):659-61.
doi: 10.1111/j.1365-2133.2010.09892.x. Epub 2010 Jun 9.

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

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

T R Hata et al. Br J Dermatol. 2010 Sep.
No abstract available

PubMed Disclaimer

Figures

Fig 1
Fig 1
(a)Ability to induce antimicrobial peptides (AMPs) as evidenced by lesional minus nonlesional expression analysed by quantitative reverse transcriptase–polymerase chain reaction (RT-PCR). Skin biopsy samples from lesional and nonlesional skin of subjects were collected and analysed for expression of AMPs. Values of the AMPs were normalized to the housekeeping gene glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and the data plotted are presented as relative AMP expression. Differences separated by diagnostic group reveal cathelicidin expression in patients with atopic dermatitis (AD) with a history of eczema herpeticum (ADEH) to be significantly depressed compared with patients with AD (P = 0.014) or psoriasis (P = 0.001). (b) Ability to induce human β-defensin (HBD)-2 as evidenced by lesional minus nonlesional expression, analysed by quantitative RT-PCR and normalized to the housekeeping gene GAPDH reveal HBD-2 to be significantly suppressed in patients with ADEH in comparison to those with AD (P = 0.003) or psoriasis (P < 0.001). (c) Ability to induce HBD-3 as evidenced by lesional and nonlesional differences, analysed by quantitative RT-PCR and normalized to the housekeeping gene GAPDH reveal HBD-3 expression in patients with ADEH to be depressed compared with that in patients with psoriasis (P = 0.003), while showing a trend towards lower levels than subjects with AD (P = 0.06). (a–c) Differences were calculated using the ΔΔCt method (see Supporting information).
Fig 2
Fig 2
(a) Nonlesional skin values for cathelicidin analysed by quantitative reverse transcriptase–polymerase chain reaction (RT-PCR) and normalized to the housekeeping gene glyceraldehyde 3-phosphate dehydrogenase (GAPDH) revealed no significant differences between the four groups. (b) Analysis of human β-defensin (HBD)-2 in nonlesional skin revealed significantly higher HBD-2 levels in subjects with atopic dermatitis (AD) with a history of eczema herpeticum (ADEH) compared with patients with AD (P < 0.001) or psoriasis (P < 0.001), or normal control subjects (P = 0.001). (c) Analysis of HBD-3 in nonlesional skin revealed significantly higher HBD-3 levels in subjects with ADEH compared with those with AD (P = 0.002) or psoriasis (P = 0.003). CATH, cathelicidin; NonLes, nonlesional; Psor, psoriasis; Cont, control.

Similar articles

Cited by

References

    1. Beck LA, Boguniewicz M, Hata T, et al. Phenotype of atopic dermatitis subjects with a history of eczema herpeticum. J Allergy Clin Immunol. 2009;124:260–9. 269.e1–7. - PMC - PubMed
    1. Ong PY, Ohtake T, Brandt C, et al. Endogenous antimicrobial peptides and skin infections in atopic dermatitis. N Engl J Med. 2002;347:1151–60. - PubMed
    1. Nomura I, Goleva E, Howell MD, et al. Cytokine milieu of atopic dermatitis, as compared to psoriasis, skin prevents induction of innate immune response genes. J Immunol. 2003;171:3262–9. - PubMed
    1. Howell MD, Wollenberg A, Gallo RL, et al. Cathelicidin deficiency predisposes to eczema herpeticum. J Allergy Clin Immunol. 2006;117:836–41. - PMC - PubMed
    1. Schauber J, Dorschner RA, Coda AB, et al. Injury enhances TLR2 function and antimicrobial peptide expression through a vitamin D-dependent mechanism. J Clin Invest. 2007;117:803–11. - PMC - PubMed

Publication types

MeSH terms