Satratoxin-G from the Black Mold Stachybotrys chartarum Induces Rhinitis and Apoptosis of Olfactory Sensory Neurons in the Nasal Airways of Rhesus Monkeys

Author:

Carey Stephan A.12,Plopper Charles G.3,Hyde Dallas M.4,Islam Zahidul25,Pestka James J.25,Harkema Jack R.26

Affiliation:

1. Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, USA

2. Center for Integrative Toxicology, Michigan State University, East Lansing, Michigan, USA

3. Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California–Davis, Davis, California, USA

4. California National Primate Research Center, University of California–Davis, Davis, California, USA

5. Department of Food Science and Human Nutrition Michigan State University, East Lansing, Michigan, USA

6. Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, USA

Abstract

Satratoxin-G (SG) is a trichothecene mycotoxin of Stachybotrys chartarum, the black mold suggested to contribute etiologically to illnesses associated with water-damaged buildings. We have reported that intranasal exposure to SG evokes apoptosis of olfactory sensory neurons (OSNs) and acute inflammation in the nose and brain of laboratory mice. To further assess the potential human risk of nasal airway injury and neurotoxicity, we developed a model of SG exposure in monkeys, whose nasal airways more closely resemble those of humans. Adult, male rhesus macaques received a single intranasal instillation of 20 µg SG (high dose, n = 3), or 5 µg SG daily for four days (repeated low dose, n = 3) in one nasal passage, and saline vehicle in the contralateral nasal passage. Nasal tissues were examined using light and electron microscopy and morphometric analysis. SG induced acute rhinitis, atrophy of the olfactory epithelium (OE), and apoptosis of OSNs in both groups. High-dose and repeated low-dose SG elicited a 13% and 66% reduction in OSN volume density, and a 14-fold and 24-fold increase in apoptotic cells of the OE, respectively. This model provides new insight into the potential risk of nasal airway injury and neurotoxicity caused by exposure to water-damaged buildings.

Publisher

SAGE Publications

Subject

Cell Biology,Toxicology,Molecular Biology,Pathology and Forensic Medicine

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2. Mycotoxins;Haschek and Rousseaux's Handbook of Toxicologic Pathology, Volume 3;2023

3. Effects of nasal inflammation on the olfactory bulb;Journal of Neuroinflammation;2022-12-09

4. Fungal Metabolites in Human Health and Diseases—An Overview;Encyclopedia;2022-09-14

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