Modulation of Autophagy on Cinnamaldehyde Induced THP-1 Cell Activation.

Summary

Using a THP-1 dendritic cell model, cinnamaldehyde increased activation markers and ROS while upregulating autophagy-related genes and proteins. Blocking autophagy exaggerated activation, whereas activating autophagy with rapamycin dampened responses, implicating autophagy as a key regulator of fragrance allergen-induced sensitization.

Key Findings

• Cinnamaldehyde increased THP-1 activation markers (CD54, CD86) and ROS.
• Autophagy-related genes and proteins (LC3B, p62, ATG5) were upregulated after exposure.
• Autophagy inhibition (Baf-A1) amplified activation and oxidative stress, while rapamycin reduced both via mTOR suppression.

Clinical Implications

Suggests that enhancing autophagy might mitigate sensitization responses to fragrance allergens; supports integrating autophagy readouts into in vitro assays for cosmetic ingredient safety testing.

Limitations

• In vitro single-cell line model may not fully recapitulate in vivo skin immune microenvironment.
• Dose-response and time-course generalizability to consumer exposure scenarios require further validation.

Future Directions

Validate findings in primary human dendritic cells and ex vivo skin models; assess other fragrance allergens; explore autophagy-targeted prophylaxis for high-risk individuals.