1 Definitions of Probiotics, Prebiotics, and Postbiotics

1.1 Probiotics: Live Microorganisms with Evidence of Health Benefits

The International Scientific Association for Probiotics and Prebiotics (ISAPP) defines probiotics as live microorganisms that, when administered in adequate amounts, confer a health benefit on the host.

This definition includes three essential requirements:

① The microorganisms must remain viable at the time of use;

② The number of viable microorganisms must be sufficient to produce the intended effect;

③ The relevant microorganism or specific strain should have evidence of health benefits that corresponds to its intended use and efficacy claims.

Therefore, names such as Lactobacillus and Bifidobacterium indicate only the taxonomic identity of a microorganism and, on their own, do not establish that it qualifies as a probiotic. Different strains within the same species may differ in their cell-surface structures, metabolic capabilities, and modes of interaction with skin cells. Findings obtained for one strain therefore cannot be directly generalized to the species as a whole.

In topical skin-care products, live microorganisms may affect skin condition by competing for nutrients and adhesion sites, producing organic acids or antimicrobial substances, modifying the local microenvironment, and interacting with keratinocytes and immune cells.

However, conventional water-containing skin-care products must be protected against microbial contamination. Preservative systems, oxygen exposure, water activity, temperature, and storage duration may all affect the survival of live microorganisms. A genuine topical probiotic product should therefore specify the strain, the effective viable count, and the viability of the microorganisms throughout the product’s shelf life. If the ingredient list identifies a Lactobacillus ferment, a Bifidobacterium lysate, or a microbial cell extract, the ingredient generally should not be regarded as a live probiotic.

1.2 Prebiotics: Substrates Selectively Utilized by Host Microorganisms

A prebiotic is a substrate that is selectively utilized by host microorganisms and thereby confers a health benefit.

The defining feature of a prebiotic is not simply that it “provides nutrients for bacteria.” It must satisfy both of the following conditions:

① The substrate can be selectively utilized by specific microorganisms;

② Utilization of the substrate by those microorganisms results in a verifiable health benefit to the host.

Topical prebiotics may alter the nutrient conditions on the skin surface, allowing certain commensal microorganisms to gain a competitive advantage and thereby influencing the composition or metabolic function of the local microbial community.

The basic process can be summarized as follows:

Prebiotic substrate → selective utilization by specific skin microorganisms → changes in microbial composition or metabolic activity → changes in the local microenvironment and skin responses → skin health benefits

This process is influenced by anatomical site, sebum level, humidity, pH, cleansing habits, and the pre-existing microbial community. The same prebiotic therefore may not produce identical effects on every individual’s skin.

Sugars, oligosaccharides, polysaccharides, and plant extracts should not be classified as prebiotics solely because they can be utilized by microorganisms. In the strict sense, a prebiotic must be shown to undergo selective utilization and must subsequently be shown to provide a skin health benefit through that process.

1.3 Postbiotics: Preparations of Inactivated Microorganisms That Confer Health Benefits

ISAPP defines a postbiotic as a preparation of inanimate microorganisms and/or their components that confers a health benefit on the host.

A postbiotic preparation may contain:

① Intact inactivated microbial cells;

② Cell walls, cell membranes, and intracellular components generated through microbial cell disruption;

③ Peptidoglycan, lipoteichoic acid, proteins, enzymes, exopolysaccharides, and other components retained together with inactivated cells or microbial lysates;

④ Certain microbial metabolites retained together with the inactivated cells or their structural components.

Postbiotics do not need to remain viable in the finished product and do not depend on reproduction or long-term colonization on the skin surface. They are therefore generally easier to control with respect to formulation stability, manufacturing quality, and storage conditions than live microorganisms.

Postbiotics are not a collective term for all fermented ingredients. Under the strict definition, a postbiotic must consist of inactivated microorganisms and/or their components and must have been shown to confer a health benefit on the host. Substances such as lactic acid, short-chain fatty acids, proteins, peptides, or exopolysaccharides cannot, on their own, be called postbiotics if they have been isolated and purified to the point that the final preparation no longer contains inactivated microbial cells or their components, even when those substances were originally produced through microbial fermentation. Likewise, a fermentation filtrate that contains neither microbial cells nor their components cannot be classified as a postbiotic merely because it was produced through a fermentation process.

1.4 Core Differences Among the Three Ingredient Categories

The three categories can be summarized as three distinct modes of action:

Probiotics introduce live microorganisms, prebiotics modify the nutrients available to microorganisms, and postbiotics directly provide inactivated microorganisms and their functional components.

2 Mechanisms Underlying Skin Dryness, Roughness, and Itching

Whether probiotic-related ingredients can improve a skin concern depends on whether they act on the mechanisms that actually cause the condition. Skin dryness, roughness, and itching commonly involve four interconnected elements: the skin barrier, microorganisms, immune responses, and sensory nerves.

2.1 Barrier Damage Is an Important Basis of Dryness and Roughness

The skin barrier is primarily formed by the stratum corneum and epidermal tight junctions.

Corneocytes in the stratum corneum are embedded within intercellular lipids composed mainly of ceramides, cholesterol, and free fatty acids. Together, these structures limit the outward loss of water from the body and reduce the penetration of external irritants into the skin. Tight junctions in the granular layer further regulate the movement of water and exogenous substances between cells by sealing the spaces between adjacent cells.

When stratum corneum lipids are insufficient, natural moisturizing factors are reduced, corneocyte cohesion is impaired, or the desquamation process becomes disrupted, transepidermal water loss (TEWL) may increase. As the water content of the stratum corneum declines, corneocytes become less flexible and normal desquamation is impaired, resulting in flaking, tightness, and a rough skin texture.

2.2 The Skin Barrier and Microorganisms Influence Each Other

Healthy skin is inhabited by a wide range of bacteria, fungi, viruses, and other microorganisms. Differences in sebum, humidity, temperature, and pH across anatomical sites are accompanied by corresponding differences in microbial composition.

Skin microorganisms cannot be divided simplistically into “beneficial” and “harmful” organisms. The same microorganism may have different effects depending on the strain, abundance, and surrounding skin environment. Some strains of Staphylococcus epidermidis, for example, can produce antimicrobial substances that restrict the growth of other microorganisms. Research has also shown that S. epidermidis can secrete sphingomyelinase, thereby promoting host ceramide production and contributing to the maintenance of skin-barrier homeostasis.

Conversely, when certain microorganisms proliferate excessively under particular conditions, they may produce proteases, toxins, or pro-inflammatory stimuli. Staphylococcus aureus can increase serine protease activity in keratinocytes and affect barrier-related structures such as filaggrin and desmogleins.

Skin dysbiosis therefore does not merely refer to an increase in the abundance of a particular microorganism. Rather, it reflects altered relationships among microbial composition, microbial function, the skin environment, and host responses.

2.3 Immune Responses and Sensory Nerves Jointly Contribute to Itching

When the skin barrier is impaired, irritants, allergens, and microbial components can enter the epidermis more readily. In response to stimulation, keratinocytes and immune cells may release a range of inflammatory and pruritogenic mediators.

Interleukin-31 (IL-31) is an important cytokine associated with pruritus. IL-31 can act on sensory nerves and promote the elongation and branching of sensory nerve fibers, potentially making the skin more sensitive to mild stimuli.

Microorganisms may also stimulate sensory nerves directly. Studies have shown that V8 serine protease produced by S. aureus can activate protease-activated receptor 1 (PAR1) on sensory nerves, triggering itching and scratching behavior.

Skin itching may therefore develop into the following cycle:

Barrier damage → increased water loss and penetration of irritants → release of pruritogenic mediators by keratinocytes and immune cells → increased sensory nerve sensitivity → itching and scratching → further barrier damage

3 Primary Sites of Action of the Three Ingredient Categories in the Skin

3.1 Probiotics Primarily Affect Living Microorganisms and Host Responses

After coming into contact with the skin, live microorganisms may exert effects through the following mechanisms:

① Competing with other microorganisms for nutrients and adhesion sites;

② Producing organic acids, bacteriocins, or other antimicrobial substances;

③ Modifying local pH and the metabolic environment;

④ Interacting with keratinocytes and immune cells.

However, topical probiotics must still contain an adequate number of viable microorganisms at the time of actual use. Even if a particular strain demonstrates beneficial activity under experimental conditions, the finished product cannot continue to be evaluated according to a probiotic mechanism of action if most of the microorganisms become inactivated during storage.

When evaluating a topical probiotic product, it is therefore necessary to determine:

What the specific strain is, whether it remains viable at the time of use, what the effective viable count is, and whether corresponding human skin studies are available.

3.2 Prebiotics Primarily Modify the Nutritional Conditions of Skin Microorganisms

Prebiotics generally do not directly replenish stratum corneum lipids or directly block sensory nerve signaling. Their primary targets are the microorganisms already present on the skin.

Whether a prebiotic produces a meaningful effect depends on whether the following sequence occurs:

① The target microorganism can utilize the substrate;

② Utilization of the substrate demonstrates a degree of selectivity;

③ Microbial composition or metabolic function changes as a result;

④ Those changes subsequently improve the skin barrier, inflammation, or other skin-related outcomes.

If a study shows only that a particular sugar can promote bacterial growth, without demonstrating selectivity or improvement in the skin barrier, symptoms, or human outcomes, the evidence is insufficient to establish a complete prebiotic effect on the skin.

3.3 Postbiotics Primarily Act on Skin Cells and Local Defense Responses

Components in inactivated microbial preparations or microbial lysates, including cell structures, proteins, enzymes, and exopolysaccharides, may come into contact with keratinocytes and influence tight junctions, antimicrobial peptide expression, inflammatory mediators, and epidermal repair processes.

Cell-based studies have shown that certain Lactobacillus or Bifidobacterium lysates can enhance tight-junction function in keratinocytes. However, these effects demonstrate clear strain dependence. In one comparative study, lysates from several strains enhanced tight-junction function, whereas a lysate from one Lactobacillus fermentum strain reduced cell viability.

Another study using a reconstructed human epidermis model found that a specific Lactobacillus rhamnosus lysate reduced the increase in barrier permeability and desmosomal damage induced by sodium lauryl sulfate (SLS). In vitro and ex vivo skin studies have also shown that certain inactivated Lactobacillus preparations or microbial lysates may promote tight-junction protein expression, epidermal repair, and local antimicrobial responses.

These findings demonstrate that the effects of a postbiotic cannot be inferred solely from the fact that it is “derived from lactic acid bacteria.” Changes in strain, culture conditions, inactivation method, degree of cell disruption, purification process, or dose may alter both the composition and the biological effects of the final preparation.

4 Effects of Postbiotics on Skin Roughness

 4.1 Postbiotics May Improve Dry Roughness Associated with Barrier Damage

Roughness caused by insufficient stratum corneum hydration, lipid deficiency, and abnormal desquamation is among the skin manifestations that postbiotics may be more likely to help improve.

Certain validated postbiotic preparations or specific inactivated microbial preparations may act through the following pathway:

Promotion of barrier-related proteins or tight-junction function → reduced entry of external irritants → decreased excessive water loss → improved hydration of the stratum corneum → reduced abnormal desquamation and surface roughness

Another possible pathway involves ceramide production.

A specific ultrasonically treated Streptococcus thermophilus preparation was found to contain relatively high levels of neutral sphingomyelinase. Studies observed that this preparation could promote sphingomyelin hydrolysis and increase ceramide levels in keratinocytes and the stratum corneum.

The reaction can be simplified as follows:

Sphingomyelin + H₂O —sphingomyelinase→ ceramide + phosphocholine

Ceramides are important components of the intercellular lipids in the stratum corneum. An increase in ceramide levels may help improve lipid organization and water-retention capacity. However, this mechanism was demonstrated using a specific S. thermophilus preparation and cannot be generalized to suggest that all postbiotics promote ceramide production.

The effects of postbiotics on roughness must also be considered in the context of the complete formulation. Humectants such as glycerol and urea primarily increase the water content of the stratum corneum; ceramides, cholesterol, and fatty acids help replenish barrier lipids; and occlusive ingredients such as petrolatum reduce water evaporation.

4.2 Postbiotics Are Not Appropriate for Every Type of Skin Roughness

Postbiotics are more likely to help improve roughness caused by dryness, mild irritation, or barrier instability. If roughness results from keratosis pilaris, abnormal keratinization, chronic photodamage, inflammatory skin disease, or fungal infection, the underlying mechanisms are different, and the use of a postbiotic product alone is unlikely to address the primary cause.

It is important to distinguish among:

① Simple dryness, fine scaling, and tightness;

② Roughness accompanied by papules, marked thickening, or follicular keratin plugs;

③ Roughness accompanied by persistent erythema, exudation, crusting, or clearly demarcated lesions.

The first condition is more likely to benefit from comprehensive barrier care. The latter two generally require further assessment to identify the underlying cause.

5 Effects of Postbiotics on Skin Itching

5.1 Postbiotics Primarily Reduce Upstream Triggers of Itching

Current mechanistic evidence more strongly supports the following conclusion: certain postbiotics may indirectly reduce itching by improving the skin barrier and the local inflammatory environment, but they should not be regarded as universally applicable, direct antipruritic ingredients.

A possible pathway is:

Postbiotic action on keratinocytes → improved barrier structure and local defense → reduced water loss, irritant penetration, and microbial pressure → decreased inflammation and release of pruritogenic mediators → reduced persistent stimulation of sensory nerves → reduced dryness-associated itching

A randomized, double-blind, placebo-controlled study showed that a cream containing 10% Bifidobacterium longum lysate improved irritation sensitivity, barrier resilience, and dryness in 66 women with reactive skin. Another small study involving 11 participants with atopic dermatitis who used a preparation continuously for two weeks observed improvements in stratum corneum ceramide levels and certain skin symptoms.

These findings suggest that validated, specific microbial lysates or inactivated microbial preparations may reduce skin discomfort through mechanisms related to the skin barrier and local responses. Overall, current human studies mainly support preliminary benefits of specific inactivated microbial preparations or complete formulations. However, these studies do not demonstrate that all postbiotics have antipruritic effects, nor do they establish that postbiotics directly block IL-31, PAR1, or other sensory nerve pathways involved in itching.

5.2 Postbiotics Cannot Address Every Type of Itching

Itching may have many causes, including skin dryness, atopic dermatitis, contact dermatitis, urticaria, fungal or bacterial infections, parasitic infections, adverse drug reactions, and neurological or systemic diseases.

Postbiotics may be more appropriate as supportive care in the following circumstances:

① Dryness-associated itching accompanied by mild scaling;

② Mild barrier instability caused by excessive cleansing or environmental irritation;

③ Daily barrier care after a clear diagnosis has been established and appropriate treatment has been initiated.

If itching continues to worsen or is accompanied by marked redness, swelling, exudation, crusting, skin breakdown, widespread lesions, or severe nighttime attacks, the underlying cause should be investigated rather than continuing to add microbiome-oriented skin-care products.

6 How to Evaluate a Probiotic-Related Skin-Care Product

6.1 Confirm the True Category of the Ingredient

① If a product claims to contain probiotics, determine whether it contains live microorganisms and review the strain identity, viable count, and shelf-life viability data.

② If a product claims to contain prebiotics, determine whether there is evidence that the ingredient can be selectively utilized by target skin microorganisms.

③ If a product claims to contain postbiotics, determine whether it contains inactivated microbial cells or microbial components from a clearly identified source, and whether the specific preparation has demonstrated health benefits in the target population.

① In vitro cell studies may indicate that an ingredient can affect a particular protein, barrier marker, or inflammatory factor, but they cannot directly establish that actual use will improve itching or roughness in humans.

② Reconstructed epidermis and ex vivo skin models more closely resemble the structural organization of human skin than monolayer cell models, but they still cannot fully reproduce the interactions among human sebum, immunity, nerves, and microorganisms.

③ Controlled human studies more closely reflect real-world effects. When evaluating such studies, it is also necessary to determine whether the test product contained only the ingredient of interest or was a complete formulation containing multiple humectants, lipids, and soothing ingredients.

6.3 Examine Outcomes That Correspond to the Intended Need

When the intended goal is to improve dryness and roughness, the following outcomes should receive particular attention:

① Stratum corneum hydration;

② Transepidermal water loss;

③ Degree of scaling and skin-surface roughness;

④ Rate of recovery after barrier damage.

When the intended goal is to improve sensitivity and dryness-associated itching, the following outcomes should receive particular attention:

① Itching, stinging, or burning scores;

② Irritation responses, such as those measured by a lactic acid stinging test;

③ Recovery of the skin barrier after irritation;

④ Changes in symptoms during continuous use.

An observed change in microbial abundance or diversity alone does not necessarily indicate an improvement in skin condition. Microbial outcomes have practical value only when they are accompanied by clearly defined barrier, symptom-based, or clinical outcomes.

6.4 Evaluate the Complete Formulation Rather Than Focusing Only on a Concept Ingredient

For dryness, roughness, and mild dryness-associated itching, the complete formulation is generally more important than a single “probiotic-related” concept ingredient. If a product contains relatively irritating fragrances, acids, or other ingredients that readily cause discomfort, and continued use results in persistent stinging or erythema, the product is not suitable for skin with an impaired barrier or active itching, even if a postbiotic has been included in the formulation.

7 Product Classification Tables for Research on the Skin-Care Microbiome, Microbial Metabolism, the Skin Barrier, and Mechanisms of Dryness and Itching

Table 1. Microbial Nutrient Substrates and Functional Polysaccharides

Table 2. Research Reagents for Microbial Metabolism-Related Compounds, Fermentation-Derived Organic Acids, and Compatible Solutes

Table 3. Bacterial Structural Signals and Reagents for Barrier-Damage and Pruritus Models

Table 4. Research on Stratum Corneum Moisturization, Barrier Lipids, and Repair

Note: The products listed above are primarily intended for scientific and formulation research involving the skin-care microbiome, microbial metabolism, the skin barrier, and mechanisms of dryness and itching. The inclusion of sugars, polysaccharides, metabolites, and related reagents does not indicate that they have been proven to provide prebiotic or postbiotic benefits to the skin. Reagents used in barrier-damage, immune-response, and pruritus models are not ingredients recommended for routine skin-care formulations. Research-reagent, cell-culture, ACS, and AR grades are not equivalent to cosmetic-ingredient grade. For current product names, specifications, intended uses, and quality information, please refer to the relevant product pages and batch-specific documentation on the Aladdin website.

References

[1] Hill C, Guarner F, Reid G, et al. The International Scientific Association for Probiotics and Prebiotics consensus statement on the scope and appropriate use of the term probiotic. Nature Reviews Gastroenterology & Hepatology. 2014;11:506–514. doi:10.1038/nrgastro.2014.66.

[2] Gibson GR, Hutkins R, Sanders ME, et al. Expert consensus document: The International Scientific Association for Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of prebiotics. Nature Reviews Gastroenterology & Hepatology. 2017;14:491–502. doi:10.1038/nrgastro.2017.75.

[3] Salminen S, Collado MC, Endo A, et al. The International Scientific Association of Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of postbiotics. Nature Reviews Gastroenterology & Hepatology. 2021;18:649–667. doi:10.1038/s41575-021-00440-6.

[4] Zheng Y, Hunt RL, Villaruz AE, et al. Commensal Staphylococcus epidermidis contributes to skin barrier homeostasis by generating protective ceramides. Cell Host & Microbe. 2022;30(3):301–313.e9. doi:10.1016/j.chom.2022.01.004.

[5] Sultana R, McBain AJ, O’Neill CA. Strain-dependent augmentation of tight-junction barrier function in human primary epidermal keratinocytes by Lactobacillus and Bifidobacterium lysates. Applied and Environmental Microbiology. 2013;79(16):4887–4894. doi:10.1128/AEM.00982-13.

[6] Jung YO, Jeong H, Cho Y, et al. Lysates of a probiotic, Lactobacillus rhamnosus, can improve skin barrier function in a reconstructed human epidermis model. International Journal of Molecular Sciences. 2019;20(17):4289. doi:10.3390/ijms20174289.

[7] Di Marzio L, Cinque B, De Simone C, Cifone MG. Effect of the lactic acid bacterium Streptococcus thermophilus on ceramide levels in human keratinocytes in vitro and stratum corneum in vivo. Journal of Investigative Dermatology. 1999;113(1):98–106. doi:10.1046/j.1523-1747.1999.00633.x.

[8] Guéniche A, Bastien P, Ovigne JM, et al. Bifidobacterium longum lysate, a new ingredient for reactive skin. Experimental Dermatology. 2010;19(8):e1–e8. doi:10.1111/j.1600-0625.2009.00932.x.

[9] Dinić M, Burgess JL, Lukić J, et al. Postbiotic lactobacilli induce cutaneous antimicrobial response and restore the barrier to inhibit the intracellular invasion of Staphylococcus aureus in vitro and ex vivo. FASEB Journal. 2024;38(14):e23801. doi:10.1096/fj.202400054RR.

[10] Williams MR, Nakatsuji T, Sanford JA, Vrbanac AF, Gallo RL. Staphylococcus aureus induces increased serine protease activity in keratinocytes. Journal of Investigative Dermatology. 2017;137(2):377–384. doi:10.1016/j.jid.2016.10.008.

[11] Feld M, Garcia R, Buddenkotte J, et al. The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves. Journal of Allergy and Clinical Immunology. 2016;138(2):500–508.e24. doi:10.1016/j.jaci.2016.02.020.

[12] Deng L, Costa F, Blake KJ, et al. S. aureus drives itch and scratch-induced skin damage through a V8 protease-PAR1 axis. Cell. 2023;186(24):5375–5393.e25. doi:10.1016/j.cell.2023.10.019.

[13] Di Marzio L, Centi C, Cinque B, et al. Effect of the lactic acid bacterium Streptococcus thermophilus on stratum corneum ceramide levels and signs and symptoms of atopic dermatitis patients. Experimental Dermatology. 2003;12(5):615–620. doi:10.1034/j.1600-0625.2003.00051.x.

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