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Polymorphonuclear leukocyte lysosomal release in response to Propionibacterium acnes in vitro and its enhancement by
Abstract:
Propionibacterium acnes cells were tested for the ability to trigger lysosomal hydrolase release from human polymorphonuclear leukocytes. Representative strains of P. acnes serotype I and II failed to stimulate lysosomal release in the absence of serum. P. acnes growth culture supernatants failed to trigger release under any test condition. Addition of fresh or heat-inactivated human serum resulted in lysosomal hydrolase release directly proportional to the number of P. acnes/PMN. Pooled sera from acne patients, with a high anti-P. acnes titer stimulated release to P. acnes. Preabsorption of this reagent with P. acnes cells reduced the anti-P. acnes titer and produced 93.37 +/- 11.49% inhibition of lysosomal enzyme release compared to unabsorbed anti-serum. Electron microscopy indicated that P. acnes was readily phagocytosed by PMNs when fresh or heated serum was present.
Insights
Propionibacterium acnes (P. acnes) requires human serum to activate lysosomal hydrolase release from polymorphonuclear leukocytes (PMNs). This interaction is crucial for the inflammatory response in acne.
Area of Science:
- Immunology
- Microbiology
- Dermatology
Background:
- Propionibacterium acnes (P. acnes) is implicated in inflammatory skin conditions like acne.
- The precise mechanisms by which P. acnes triggers inflammation are not fully understood.
Purpose of the Study:
- To investigate the role of P. acnes in stimulating lysosomal hydrolase release from human polymorphonuclear leukocytes (PMNs).
- To determine the influence of human serum on this interaction.
Main Methods:
- Human PMNs were incubated with P. acnes serotypes I and II.
- Lysosomal hydrolase release was measured with and without human serum.
- P. acnes specific antibody titers in patient sera were assessed.
- Electron microscopy was used to visualize PMN-P. acnes interactions.
Main Results:
- P. acnes alone did not induce lysosomal hydrolase release.
- Addition of fresh or heat-inactivated human serum significantly increased lysosomal hydrolase release, proportional to P. acnes concentration.
- Sera from acne patients with high anti-P. acnes titers enhanced release.
- Pre-absorption of these sera with P. acnes reduced enzyme release, indicating antibody involvement.
- Electron microscopy confirmed phagocytosis of P. acnes by PMNs in the presence of serum.
Conclusions:
- Human serum factors, potentially antibodies, are essential for P. acnes to trigger lysosomal hydrolase release from PMNs.
- This serum-dependent activation of PMNs by P. acnes may contribute to the inflammatory processes observed in acne vulgaris.