A bacterium once known as Propionibacterium acnes has been reclassified and is now scientifically referred to as Cutibacterium acnes (C. acnes). This bacterium is a standard member of the skin’s microbial community, living harmlessly on most individuals where its presence goes unnoticed. The central question is how this common bacterium shifts from a quiet inhabitant to a contributor to the development of acne.
The Role of Sebum and Hair Follicles
Acne begins within the skin’s hair follicles, also known as pores. Each follicle contains a hair and is connected to sebaceous glands that produce an oily substance called sebum. Normally, sebum travels up the follicle to the skin’s surface, providing a protective, moisturizing layer.
This environment within the follicle is the natural habitat for C. acnes. The bacterium thrives in these lipid-rich surroundings, using sebum as its primary source of energy. The base of the follicle provides a low-oxygen setting, which is ideal for this anaerobe, an organism that flourishes in the absence of air.
Here, the bacterium exists as a commensal organism, meaning it benefits from living on the skin without harming its host. This is part of a healthy skin microbiome where diverse microorganisms coexist. The presence of C. acnes is not inherently problematic; it is a normal part of the skin’s ecosystem, waiting for conditions to change.
How Bacteria Proliferate and Clog Pores
The transition to an acne lesion begins when sebum production increases, often driven by hormonal fluctuations that signal the sebaceous glands to become overactive. The excess oil creates a more favorable environment for C. acnes. This surplus allows the bacteria to multiply far more rapidly than usual.
As the C. acnes population expands, it contributes to a physical blockage within the hair follicle. The bacteria, combined with surplus sebum and dead skin cells that fail to shed properly, form a sticky plug. This mixture prevents the normal flow of sebum to the surface and is known as a microcomedone, the precursor to a visible blemish.
This microcomedone marks the first non-inflammatory stage of acne. If the plug remains below the skin’s surface, it forms a closed comedone, or a whitehead. Should the pore open to the air, the contents can oxidize and darken, creating an open comedone, or a blackhead.
Triggering the Inflammatory Response
A clogged pore transforms into an inflamed pimple when the immune system is activated. Within the blocked follicle, the proliferating C. acnes bacteria metabolize sebum. As they feed, they secrete proteins and break down oils into byproducts. These substances act as irritants to the lining of the hair follicle.
The presence of these bacterial byproducts and cellular debris signals a threat to the body, triggering a localized immune response. The body dispatches white blood cells and other inflammatory mediators to the site to combat the bacteria. This defensive action causes the visible symptoms of inflammatory acne.
The resulting inflammation leads to the redness, swelling, and tenderness of a pimple, known as a papule. If the immune response intensifies, pus—a mixture of dead white blood cells, bacteria, and cellular debris—can accumulate, forming a pustule. This inflammatory reaction is primarily responsible for the appearance and discomfort of an acne lesion.
This process can escalate, causing pressure within the follicle. If the follicle wall ruptures, its inflammatory contents can spill into the surrounding dermal tissue. This can lead to larger, painful lesions like nodules and cysts, which form deeper in the skin and carry a higher risk of scarring.
Factors That Influence Bacterial Activity
Acne severity varies between individuals due to factors that influence C. acnes activity. A primary driver is hormones, particularly androgens. These hormones stimulate the sebaceous glands to produce more sebum. This is why acne is common during puberty, when androgen levels surge in both sexes.
A person’s genetic makeup also plays a part. Genetics can influence the size and activity of sebaceous glands and the sensitivity of the immune system. Some individuals may be genetically predisposed to react more aggressively to C. acnes, leading to a more intense inflammatory response.
Not all C. acnes are the same, as there are different strains, or phylotypes. Some strains are more strongly associated with acne than others. Certain strains possess genes that produce more potent inflammatory triggers, while other strains are commonly found on healthy skin. This helps explain why some people can have high levels of the bacteria without developing significant acne.