The number of malassezia yeasts probably also increases.
However, the severity of a person's acne does not depend on the number of bacteria on the skin surface or in the sebaceous ducts (the passageway from the oil glands).
The number and activity of C acnes bacteria varies according to oxygen supply, nutrient supply and the pH level of the skin. Some acne lesion are colonised by C acnes and others are not.
The C acnes bacteria can produce active enzymes and innate inflammatory mediators and these may contribute to the activity of acne in some patients. Activation triggers expression of immune response genes. Inflammatory mediators detected in acne lesions colonised by C acnes include:
Lipases (enzymes that break down fats)
Proteases (enzymes that break down proteins)
Hyaluronate lyase (enzyme that breaks down skin ground substance)
Phosphatase (enzyme that breaks down phosphates)
Smooth-muscle contracting substances
Cytokines, such as IL-12 and IL-8, and defensins (these are chemical messengers).
The lipases can convert triglyceride in sebum to free fatty acids. The free fatty acids increase clumping of bacteria in sebaceous ducts and thus the colonisation of the ducts by more of them. The inflammatory mediators provoked by the bacteria penetrate surrounding skin and are a cause of inflammation.
What is the effect of treatment on acne bacteria?
Antimicrobials such as topical benzoyl peroxide and oral tetracyclines suppress C acnes in patients with acne. They also have non-antibiotic anti-inflammatory activity.