Impact of Mycotoxins Secreted by Aspergillus Molds on the Inflammatory Response of Human Corneal Epithelial Cells

Toxins (Basel). 2017 Jun 22;9(7):197. doi: 10.3390/toxins9070197.

Abstract

Exposure to molds and mycotoxins not only contributes to the onset of respiratory disease, it also affects the ocular surface. Very few published studies concern the evaluation of the effect of mycotoxin exposure on ocular cells. The present study investigates the effects of aflatoxin B₁ (AFB₁) and gliotoxin, two mycotoxins secreted by Aspergillus molds, on the biological activity of the human corneal epithelial (HCE) cells. After 24, 48, and 72 h of exposure, cellular viability and inflammatory response were assessed. Both endpoint cell viability colorimetric assays and continuous cell impedance measurements, providing noninvasive real-time assessment of the effect on cells, were performed. Cytokine gene expression and interleukin-8 release were quantified. Gliotoxin appeared more cytotoxic than AFB₁ but, at the same time, led to a lower increase of the inflammatory response reflecting its immunosuppressive properties. Real-time cell impedance measurement showed a distinct profile of cytotoxicity for both mycotoxins. HCE cells appeared to be a well-suited in vitro model to study ocular surface reactivity following biological contaminant exposure. Low, but persistent inflammation, caused by environmental factors, such as fungal toxins, leads to irritation and sensitization, and could be responsible for allergic manifestations which, in turn, could lead to mucosal hyper-reactivity.

Keywords: aflatoxin B1; cellular impedance; gliotoxin; in vitro; inflammatory response; mycotoxin; ocular surface.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aflatoxin B1 / toxicity*
  • Aspergillus / metabolism
  • Cell Line
  • Cell Survival / drug effects
  • Cornea / cytology
  • Cytokines / genetics
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Gene Expression
  • Gliotoxin / toxicity*
  • Humans
  • Inflammation / chemically induced*
  • Inflammation / genetics

Substances

  • Cytokines
  • Gliotoxin
  • Aflatoxin B1