Immunological toxicity of mycotoxins

Author: Bondy, Genevieve S.

Source: Stewart Postharvest Review, Volume 4, Number 6, December 2008 , pp. 1-6(6)

Publisher: Stewart Postharvest Solutions

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Abstract:

Purpose of review: This review summarises advances in our understanding of the mechanisms by which key fungal toxins, which are present worldwide in crops and for which postharvest control strategies are critical, modulate immune responses.

Findings: Aflatoxins, fumonisins, ochratoxins and trichothecenes are structurally and mechanistically distinct classes of toxins, all of which may suppress or enhance immune responses. Recently, there has been a focus on defining the effects of fungal toxins on cells that mediate inflammatory responses. In addition, several toxins have been shown to alter dendritic cell function, and thus may modulate antigen presentation and the early stages of immune response. Increasingly, effects on cytokine and chemokine production in lymphoid and non-lymphoid cells are being examined to determine the pathways by which immune responses are modulated by fungal toxins.

Directions for future research: Further research in the following areas will provide insight into the immunomodulatory effects of fungal toxins, including: (1) research using non-continuous dosing strategies that would provide greater insight into the effects of fungal toxins on sporadically exposed populations; (2) research on dendritic cell responses to fungal toxin exposure that would clarify effects on early stages of immune responses; and (3) further research on the link between early pro- and anti-inflammatory responses, immunomodulation and non-lymphoid target organ toxicity for all fungal toxin classes.

Keywords: AFLATOXIN; FUMONISINS; OCHRATOXIN; TRICHOTHECENE; DEOXYNIVALENOL; IMMUNOTOXICITY

Document Type: Research article

DOI: http://dx.doi.org/10.2212/spr.2008.6.7

Affiliations: 1: Toxicology Research Division, Food Directorate, Health Products and Food Branch, Health Canada, Ottawa, ON, Canada

Publication date: 2008-12-01

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