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Deoxynivalenol triggers the expression of IL-8-related signaling cascades and decreases protein biosynthesis in primary monocyte-derived cells

Constanze Nossol; P. Landgraf; M. Oster; S. Kahlert; A. Barta-Böszörmenyi; J. Kluess; K. Wimmers; B. Isermann; O. Stork; D. C. Dieterich; S. Dänicke; H.-J. Rothkötter
Mycotoxin Research · Vol. 40, Issue 2 · pp. 279-293 · 2024

Abstract

Humans and their immune system are confronted with mold-contaminated food and/or mold-contaminated air in daily life and indoor activities. This results in metabolic stress and unspecific disease symptoms. Other studies provided evidence that exposure to mold is associated with the etiology of allergies. Deoxynivalenol (DON) is of great concern due to its frequent occurrence in toxically relevant concentrations. The exposure to this toxin is a permanent health risk for both humans and farm animals because DON cannot be significantly removed during standard milling and processing procedures. However, the direct effect on immunity or hematology is poorly defined because most investigations could not separate the effect of DON-contaminated feed intake. Due to the widespread distribution of DON after rapid absorption, it is not surprising that DON is known to affect the immune system. The immune system of the organism has one important function, to defend against the invasion of unknown substances/organisms. This study shows for the first time a synergistic effect of both—low physiological DON-doses in combination with low LPS-doses with the focus on the IL-8 expression on protein and RNA level. Both doses were found in vivo. IL-8 together with other anorectic cytokines like IL-1β can affect the food intake and anorexia. We could also show that a calcium-response is not involved in the increased IL-8 production after acute DON stimulation with high or low concentrations.

Bibliographic Information

JournalMycotoxin Research
PublisherSpringer
Publication Date2024-05-01
Publication Year2024
Volume40
Issue2
Pages279-293
Document TypeJournal Article
Print ISSN0178-7888
eISSN1867-1632
DOI10.1007/s12550-024-00528-3

Access Information

NARA Access Coverage1985-01-01~Current
Journal Homepagehttps://www.springer.com/journal/12550
Publisher PageOpen Publisher Page
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