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Epidermal growth factor receptor inhibitors selectively inhibit the expressions of human β-defensins induced by

Kio Park1, Rie Ommori2, Kyoko Imoto2

  • 1Department of Dermatology, Yamato Takada Municipal Hospital, Nara, Japan; Department of Dermatology, Nara Medical University, Nara, Japan.

Journal of Dermatological Science
|May 17, 2014
PubMed
Abstract

Insights

Epidermal growth factor receptor inhibitors (EGFRIs) can alter skin immunity. These cancer drugs may cause side effects by affecting human beta-defensins (hBDs) in response to bacteria.

Area of Science:

  • Dermatology
  • Oncology
  • Immunology

Background:

  • Epidermal growth factor receptor inhibitors (EGFRIs) are used to treat various cancers.
  • Dermatological side effects, like acneiform eruptions, are common with EGFRIs, but their mechanisms are unclear.

Purpose of the Study:

  • To investigate how EGFRIs affect human beta-defensin (hBD) expression against staphylococci.
  • To elucidate the pathomechanism of EGFRIs-induced cutaneous adverse reactions.

Main Methods:

  • Human beta-defensins 1, 2, and 3 (hBD1, hBD2, hBD3) expression was studied in normal human epidermal keratinocytes (NHEKs).
  • NHEKs were stimulated with Staphylococcus aureus and S. epidermidis (live or supernatant) with or without gefitinib and erlotinib (EGFRIs).
  • hBD levels in culture supernatants were measured using enzyme-linked immunosorbent assay (ELISA).

Main Results:

  • EGFRIs did not inhibit hBD1 and hBD3 expression induced by S. aureus.
  • EGFRIs suppressed hBD2 and hBD3 expression induced by S. epidermidis.

Conclusions:

  • EGFRIs may induce cutaneous adverse effects by selectively disrupting innate immune responses.
  • This disruption involves altered responses to both commensal and pathogenic bacteria.
Keywords:
ErlotinibGefitinibHuman β-defensins

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