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Leucocyte entry and endothelial E-selectin expression following intradermal Propionibacterium acnes administration
Journal of Comparative Pathology
|February 24, 2000
Summary
This study investigated immune responses in pig skin to heat-killed Propionibacterium acnes (HKPA), a key factor in acne. Findings reveal dose-dependent and antigen-specific immune cell influx, mirroring human inflammatory acne.
Area of Science:
- Dermatology
- Immunology
- Microbiology
Background:
- Propionibacterium acnes (P. acnes) is a major bacterial agent implicated in human inflammatory acne.
- Porcine skin shares structural and compositional similarities with human skin, making pigs a suitable model.
- Genetically inbred pigs allow for leucocyte transfer without rejection, facilitating immune response studies.
Purpose of the Study:
- To investigate the immune responses in porcine skin following intradermal inoculation of heat-killed P. acnes (HKPA).
- To characterize the cellular infiltrate and endothelial changes in response to HKPA challenge.
- To compare the induced immune response with that observed in human inflammatory acne.
Main Methods:
- Intradermal inoculation of heat-killed P. acnes (HKPA) in sensitized pigs.
- Dose-ranging challenge with HKPA and purified protein derivative (PPD) in control pigs.
- Tracking of chromium-51 (51Cr)-labeled peripheral blood lymphocytes (PBLs) and indium-111 (111In)-labeled neutrophils.
Main Results:
- Peak PBL entry into challenge sites occurred at 4 hours, sustained up to 24 hours.
- HKPA induced a dose-dependent and antigen-specific influx of PBLs and neutrophils.
- Predominant lymphocyte subset was CD3(+)CD2(+)T-cells, with gammadelta TCR(+)cells noted later; E-selectin was upregulated on dermal endothelium.
Conclusions:
- The porcine model effectively mimics human inflammatory acne immune responses.
- HKPA triggers a specific, dose-dependent inflammatory infiltrate involving lymphocytes and neutrophils.
- Upregulation of E-selectin suggests a role for endothelial adhesion molecules in P. acnes-induced skin inflammation.