Complement system is activated in acute inflammatory response to environmental particulates in the lungs

Area of Science:

• Environmental Health
• Immunology
• Toxicology

Background:

• Short-term exposure to particulate matter (PM) triggers acute inflammatory responses and complement component C5 activation.
• The precise links between PM-induced complement activation, inflammation, and causative factors require further elucidation.

Purpose of the Study:

• To investigate acute inflammatory responses and complement C5 activation levels following exposure to different PM types.
• To identify specific PM components contributing to complement activation and pulmonary inflammation.

Main Methods:

• Mice were intratracheally administered four types of PM: titanium dioxide (TiO₂), diesel exhaust particles (DEP), Asian sand dust (ASD), and ambient PM2.5.
• Complement activation markers (C5, C5aR1, C5b-9) and inflammatory responses were assessed.
• Raman microscopy, ICP-MS, and EDXRF were used to analyze PM components and their proximity to neutrophils.

Main Results:

• Exposure to ASD, DEP, and PM2.5 significantly increased C5b-9 deposition in lung tissues.
• All PM types upregulated C5aR1 expression, predominantly in neutrophils.
• ASD exposure revealed mineral components (Si, K, Mg, Al, Fe) near neutrophils; Si, Mg, Al, and K were potent contributors to inflammation and complement activation.
• ASD induced the most severe acute inflammatory response and complement system activation.

Conclusions:

• ASD-induced complement system activation, driven by its mineral components, plays a critical role in neutrophil activation and acute pulmonary inflammation.
• PM composition significantly influences complement system activation and the severity of air pollution-related health risks, especially acute lung inflammation.