Acne care is no longer limited to clearing excess sebum and dead skin cells. A new approach to acne care also considers how skin and microorganisms interact to shape the environment within the pore, offering fresh insight into acne pathogenesis.
A Shifting Perspective on Acne Bacteria
Acne results from a complex interplay of factors, including sebum, dead skin cells, hormonal changes, inflammatory responses, and the skin microbiome. When sebum production increases or dead skin cells fail to shed properly, pores can become more prone to blockage, potentially altering the interaction between resident microorganisms and the skin.
C. acnes bacteria naturally exist on skin with well-developed sebaceous glands. Since they are also found on healthy skin, their mere presence or quantity alone cannot fully explain acne development. Recent research has moved beyond simply controlling bacterial proliferation, focusing instead on how C. acnes establishes itself within the pore and when it begins to act collectively. This means examining not just bacterial counts, but also the process of signal exchange and collective bacterial behavior.
How Acne Bacteria Recognize Each Other’s Presence
Bacteria, including C. acnes, release signaling molecules into their surroundings. When many bacteria cluster closely together, these signals accumulate and increase in concentration. This process—bacteria detecting the concentration of accumulated signaling molecules to regulate collective behavior—is called quorum sensing.
Quorum refers to a state in which bacterial signals have accumulated enough to influence the activity of multiple bacteria. Signal concentration depends not only on bacterial count but also on how much signaling molecule each bacterium produces, the distance between bacteria, and the rate at which signals diffuse or lose activity.
Therefore, even with the same number of C. acnes present, concentration is unlikely to rise if the bacteria are widely dispersed or if signals dissipate quickly. Conversely, in environments where bacteria cluster closely and signals tend to remain localized, individual signals accumulate repeatedly. In confined spaces such as pores, signals may accumulate locally.
Quorum matters not simply because bacterial numbers increase, but because it can trigger a shift in the activity of multiple bacteria in a similar direction.
From Accumulated Signal to Behavioral Change
Even when signals accumulate sufficiently, actual change occurs only when C. acnes detects them and translates them into an internal response. During this process, changes may occur in how bacteria attach to the inner surface of the follicle, form clusters with neighboring C. acnes, and produce external substances or enzymes.
Reaching quorum does not mean a biofilm—a protective structure built by bacteria—forms immediately. However, signal-driven behavioral changes are linked to biofilm formation, and actual formation involves multiple factors, including C. acnes attachment characteristics, specific strain type, and conditions within the follicle.
A biofilm is a structure formed when C. acnes attaches to a surface such as the inner follicle, forms clusters, and becomes surrounded by substances the bacteria produce or release extracellularly. Formation broadly occurs in three stages.
Stage 1: The Beginning of Biofilm Formation—Initial Attachment
Biofilm formation begins as some C. acnes settle onto the inner surface of the follicle. Not all C. acnes attach to the same degree; attachment varies depending on bacterial strain and surrounding conditions such as sebum, dead skin cells, and moisture levels within the follicle.
Stage 2: Bacterial Clustering and Colony Expansion
A colony forms around the initially attached C. acnes. As bacteria increase, the colony expands and bacterial density in that area gradually rises. Signals accumulated during this process help regulate collective bacterial activity.
Stage 3: Formation of an External Structure Connecting the Bacteria
As the C. acnes colony forms, sugars, proteins, and extracellular genetic material begin to accumulate around it. These substances fill the spaces between bacteria and connect them, forming the biofilm’s external structure.
How Quorum Sensing Works in Acne Bacteria
From Passive Presence to Inflammatory Trigger: C. acnes is a resident bacterium naturally present on skin with well-developed sebaceous glands. When conditions within the pore change and C. acnes cluster closely, signaling molecules such as AI-2 can accumulate, potentially leading to collective bacterial activity.
Biofilm Formation: As quorum signals accumulate, C. acnes may form a biofilm, creating conditions that allow it to remain stably within the pore. This structure can act as a protective barrier against antimicrobial agents or external stimuli, making it easier for bacteria to persist in one location than when dispersed.
Enzyme and Inflammatory Mediator Release: At this stage, C. acnes activity in producing enzymes and inflammation-related substances that can irritate surrounding skin tissue also changes. These changes may influence the progression of comedonal acne toward pustular or inflammatory acne.
Where Can Quorum Signals Be Regulated?
Building on these findings, research is also examining approaches that regulate the process of signal generation, transmission, and response, rather than directly reducing C. acnes. This is called quorum inhibition, or quorum sensing inhibition (QSI).
01 Altering Signal Generation and Transmission
When C. acnes gathers closely at a certain density, it exchanges information with neighboring bacteria through signaling molecules such as AI-2, the chemical signal bacteria use to recognize each other’s presence. Quorum inhibition regulates this signaling process. Rather than eliminating bacteria directly, QSI interferes with how signaling molecules are transmitted to and recognized by bacteria, thereby reducing collective responses.
Some ingredients showing quorum-inhibiting activity may adsorb or degrade signaling molecules before they reach bacterial receptors, lowering their activity, or bind to receptors first to prevent signals from being properly read. If signaling molecules are not sufficiently transmitted or bacteria fail to recognize them properly, C. acnes may struggle to translate a densely populated environment into a collective response. This process may also affect subsequent colony formation and biofilm development.
02 Regulating Biofilm Formation
Regulating quorum signals can also affect the process by which C. acnes gathers to form a biofilm. When this process is regulated, biofilm-related responses may decrease, along with the bacteria’s ability to adhere stably to the pore wall. As a result, the colony structure within the pore may loosen, changing the conditions under which physical treatments such as sebum and dead skin cell clearing, extraction, and scaling can be effective.
Because biofilms also serve as a protective environment against external stimuli and antimicrobial ingredients, weakening this formation process may help slow C. acnes from firmly establishing itself in one location.
03 Altering Lipase and Other Enzyme Activity
When C. acnes recognizes quorum signals, collective activity intensifies, and production of lipase (a sebum-degrading enzyme) and protease (a protein-degrading enzyme) may change accordingly. Lipase breaks down triglycerides in sebum to produce free fatty acids, which, depending on skin conditions, can readily contribute to irritation or inflammation-related responses.
When quorum signals are regulated, production of enzymes such as lipase and protease may decrease, along with the amount of free fatty acids generated during sebum breakdown. This may help ease irritation to skin tissue or reduce the likelihood of comedonal acne progressing to red, painful pustular or nodular acne.
A New Approach That Doesn’t Attack Acne Bacteria Directly
Research is moving beyond simply reducing C. acnes toward examining the process by which bacteria gather and respond. Rather than eliminating bacteria, this approach examines changes in indicators such as signal generation, biofilm formation, and lipase activity.
Related ingredient research is also drawing attention. Green tea callus lysate has been reported to reduce biofilm formation, lipase activity, and AI-2 production under experimental conditions without directly killing C. acnes. Greek propolis extract and shikonin are also being studied as materials that may influence biofilm formation and pathogenicity-related indicators in C. acnes. Some ingredients, such as azelaic acid, are already used in acne care.
However, being used as an acne care ingredient is distinct from being established as a quorum-inhibiting ingredient. At present, it is more accurate to understand that the perspective on C. acnes is broadening from bacterial elimination toward signal and colony regulation. In the esthetics field, this can be considered alongside pore care, sebum and dead skin cell management, and barrier recovery.
Ultimately, what matters is not how many C. acnes are present, but the state in which they exist and act within the pore. Activity patterns differ depending on whether bacteria remain dispersed individually or form colonies through signal exchange. Directly reducing bacteria can affect not only C. acnes but also other resident bacteria coexisting on the skin.
Approaches focusing on quorum and biofilm are less about eliminating all bacteria and more about examining whether the collective activity of C. acnes, which shifts under specific conditions, can be regulated.
References 1. Vasam M. et al. “Acne vulgaris: A review of the pathophysiology, treatment, and recent nanotechnology based advances.” Biochemistry and Biophysics Reports, 36. 2023.
2. Niedźwiedzka A. et al. “The Role of the Skin Microbiome in Acne: Challenges and Future Therapeutic Opportunities.” International Journal of Molecular Sciences, 25(21). 2024.
3. Markowska K. et al. “Understanding Quorum-Sensing and Biofilm Forming in Anaerobic Bacterial Communities.” International Journal of Molecular Sciences, 25(23). 2024.
4. Hamada S. et al. “Heparinoid enhances the efficacy of a bactericidal agent by preventing Cutibacterium acnes biofilm formation via quorum sensing inhibition.” Journal of Microorganism Control, 29(1). 2024.
Editor JIWON, YANG
Image Shutterstock
The Signature Magazine – August 2026 Issue