Genomic approach to explore altered signaling networks of olfaction in response to diesel exhaust particles in mice

Sci Rep. 2020 Oct 12;10(1):16972. doi: 10.1038/s41598-020-74109-6.

Abstract

Airborne pollutants have detrimental effect on the human body and the environment. Diesel exhaust particles (DEPs) are known to be major component of particulate matter (PM) and cause respiratory diseases and neurotoxicity. However, the effects of air pollutants on the sensory nervous system, especially on the olfactory sense, have not been well studied. Herein, we aimed to explore DEP-induced changes in the olfactory perception process. Olfactory sensitivity test was performed after DEP inhalation in mice. Microarray was conducted to determine the differentially expressed genes, which were then utilized to build a network focused on neurotoxicity. Exposure to DEPs significantly reduced sniffing in mice, indicating a disturbance in the olfactory perception process. Through network analysis, we proposed five genes (Cfap69, Cyp26b1, Il1b, Il6, and Synpr) as biomarker candidates for DEP-mediated olfactory dysfunction. Changes in their expression might provoke malfunction of sensory transduction by inhibiting olfactory receptors, neurite outgrowth, and axonal guidance as well as lead to failure of recovery from neuroinflammatory damage through inhibition of nerve regeneration. Thus, we suggest the potential mechanism underlying DEPs-mediated olfactory disorders using genomic approach. Our study will be helpful to future researchers to assess an individual's olfactory vulnerability following exposure to inhalational environmental hazards.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytoskeletal Proteins / genetics*
  • Cytoskeletal Proteins / metabolism*
  • Environmental Exposure / adverse effects*
  • Female
  • Gene Expression / drug effects*
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Mice, Inbred BALB C
  • Microarray Analysis / methods
  • Olfaction Disorders / chemically induced*
  • Olfaction Disorders / genetics*
  • Particulate Matter / toxicity*
  • Retinoic Acid 4-Hydroxylase / genetics*
  • Retinoic Acid 4-Hydroxylase / metabolism*
  • Signal Transduction / genetics*
  • Signal Transduction / physiology*
  • Smell / drug effects*
  • Smell / genetics*
  • Smell / physiology
  • Synaptophysin / genetics
  • Synaptophysin / metabolism
  • Vehicle Emissions / toxicity*

Substances

  • CFAP69 protein, mouse
  • Cytoskeletal Proteins
  • IL1B protein, mouse
  • Interleukin-1beta
  • Interleukin-6
  • Particulate Matter
  • Synaptophysin
  • Synpr protein, mouse
  • Vehicle Emissions
  • interleukin-6, mouse
  • Cyp26b1 protein, mouse
  • Retinoic Acid 4-Hydroxylase