Particulate matter inflammation and receptor sensitivity are target cell specific

Area of Science:

• Environmental Health
• Toxicology
• Cell Biology

Background:

• Inhaled particulate matter (PM) is a complex mixture that can activate various cell types in the respiratory tract.
• Epithelial cells lining the airways and sensory C fibers are initial targets of inhaled PM.
• Cellular activation, indicated by intracellular calcium ([Ca(2+)](i)) increases, is a key signaling event.

Purpose of the Study:

• To compare the in vitro biological responses of epithelial cells and sensory neurons to PM from diverse sources.
• To investigate the role of acid-sensitive pathways in PM-induced cellular activation and inflammatory cytokine release.

Main Methods:

• Single-cell calcium imaging of human bronchial epithelial cells (BEAS-2B) exposed to various PM types.
• Measurement of intracellular calcium ([Ca(2+)](i)) and interleukin-6 (IL-6) release in BEAS-2B cells and mouse dorsal root ganglia (DRG).
• Pretreatment with vanilloid (VR1) receptor antagonist (capsazepine) or acid-sensitive pathway antagonist (amiloride) to assess pathway involvement.

Main Results:

• BEAS-2B cells exhibited variable increases in [Ca(2+)](i) and IL-6 release in response to PM, correlating significantly with [Ca(2+)](i) increases.
• PM exposure led to significantly higher IL-6 release in DRG sensory neurons compared to BEAS-2B epithelial cells.
• Antagonists reduced IL-6 release in both cell types, but with less inhibition in DRG, indicating differential pathway sensitivity.

Conclusions:

• Particulate matter from different sources induces differential activation of epithelial cells and sensory neurons.
• The cellular target and PM source significantly influence the degree of biological response.
• Differential sensitivity of target cells to PM may contribute to the organism's overall inflammatory response.