Polystyrene microplastics trigger intestinal inflammation through CXCL11-mediated T-cell recruitment

Area of Science:

• Environmental toxicology
• Molecular biology
• Aquatic ecotoxicology

Background:

• Polystyrene microplastics (PMs) are widespread aquatic pollutants.
• The molecular mechanisms of PMs' ecotoxicity, especially intestinal inflammation, are not well understood.

Purpose of the Study:

• To investigate the effects of environmentally relevant PMs concentrations on zebrafish (Danio rerio).
• To elucidate the molecular pathways involved in PMs-induced intestinal inflammation.

Main Methods:

• Zebrafish were exposed to PMs (1.0 μm) at 0, 25, and 250 μg/L for 4 weeks.
• Histopathology, cytokine analysis, transcriptomics, qPCR, immunofluorescence, and Western blotting were employed.
• The interferon-gamma (INFγ)-STAT1 pathway and downstream targets were analyzed.

Main Results:

• The intestine was identified as the primary site of PMs accumulation and inflammation.
• PM exposure led to significant histopathological damage and elevated pro-inflammatory cytokines (TNF-α, IL-2).
• Activation of the INFγ-STAT1-CXCL11 signaling axis promoted T-cell infiltration into the zebrafish intestine.

Conclusions:

• PMs disrupt intestinal homeostasis in zebrafish via the INFγ-STAT1-CXCL11 pathway.
• This pathway amplifies inflammation by increasing CXCL11 expression and T-cell recruitment.
• The study reveals a specific molecular mechanism of microplastic immunotoxicity in aquatic organisms.