In clinical practice, wrinkles rarely occur in isolation. They almost always coexist with skin dryness, reduced elasticity, a sensation of tightness, and heightened reactivity. These features reflect impaired barrier function and are accompanied by changes in the skin’s ecology. A 2025 review published in the International Journal of Molecular Sciences argues that the skin microbiome should be viewed as an active contributor to cutaneous aging rather than a secondary bystander [1].

What the authors did and what makes this review distinctive

The authors synthesized experimental, clinical, and molecular evidence into a conceptual axis: microbiome – skin aging – wrinkles. A key strength of the paper is its detailed explanation of how age-related changes in the skin barrier and microbial composition can trigger inflammatory and oxidative cascades that activate matrix metalloproteinases (MMPs)—enzymes responsible for collagen and elastin degradation [1].

Which age-related skin changes can drive a microbiome shift?

With age, skin is characterized by reduced sebum production, lower hydration, and weakened barrier function. Clinically, this presents as xerosis and increased transepidermal water loss (TEWL). These changes create a different microenvironment on the skin surface and within the stratum corneum, promoting a shift in microbial composition [1].
The authors describe a decrease in lipophilic commensals, including Cutibacterium acnes, alongside a relative increase in Corynebacterium and Staphylococcus spp. in older individuals [1]. These shifts are not neutral: they are associated with changes in microbial metabolic activity and in how the microbiome interacts with the skin’s immune system.

Microbiome–MMP connection: the core mechanistic chain

A central idea of the review is a clear explanation of how the microbiome can influence MMP activity.

1. Dysbiosis amplifies the skin's inflammatory tone.
   Age-associated changes in the microbiome are accompanied by activation of innate immune responses in the skin. Specific microbial components and metabolites can stimulate pro-inflammatory signaling pathways, including NF-κB (nuclear factor kappa B) and AP-1 (activator protein 1) [1]. This contributes to chronic, low-grade inflammation.
2. Inflammation and oxidative stress increase MMP expression.
   Activation of NF-κB and AP-1 is directly linked to increased expression of MMP-1 and MMP-9. These enzymes cleave extracellular matrix components: MMP-1 primarily degrades fibrillar collagens I and III, while MMP-9 degrades gelatin and elastin [1].
3. Reactive oxygen species further intensify the effect.
   Dysbiosis and chronic inflammation are associated with increased production of reactive oxygen species (ROS). ROS can further promote MMP activity while simultaneously reducing fibroblast collagen synthesis, shifting the balance toward matrix breakdown [1].

Taken together, the microbiome affects MMPs not through a single direct route, but via inflammation–oxidative signaling cascades well established in the pathophysiology of photoaging and chronological aging.

Why does this results in wrinkle formation

Elevated MMP activity leads to fragmentation of collagen fibers and disruption of the elastin network. The dermis becomes thinner, and its mechanical strength and elasticity decline. These processes underpin the development of both fine lines and deeper wrinkles, particularly under conditions of chronic ultraviolet exposure [1].

The role of barrier lipids and ceramides

The authors also emphasize the importance of the stratum corneum lipid profile. Ceramides play a key role in water retention and barrier integrity. Microbiome disruption may exacerbate ceramide deficiency, increasing TEWL and inflammation. The review cites data showing that a topical intervention with Streptococcus thermophilus was associated with higher ceramide levels in the stratum corneum in older individuals [1, 2]. This matters clinically because improving barrier function may reduce both symptoms and inflammatory stimulation of MMPs.

Microbiome-oriented interventions

The review discusses probiotics and postbiotics as potential tools to modulate inflammation and oxidative stress. One frequently cited clinical example is Lactobacillus plantarum HY7714: a randomized, placebo-controlled study reported improved skin elasticity, reduced TEWL, and decreased wrinkle severity [3]. The proposed mechanism involves lowering inflammatory mediators and suppressing MMP activation [1].
At the same time, the authors note that much of the evidence demonstrates associations rather than direct causality. The effects of probiotics and postbiotics depend on the strain, dose, route of administration, and baseline skin status, limiting the universality of conclusions [1].

How to discuss this with patients 45+

As skin ages, it tends to lose water and lipids, the barrier becomes weaker, and microbial balance can shift. This may sustain chronic inflammation, which accelerates collagen breakdown by activating enzymes. That is why the focus is not only on “treating wrinkles,” but also on stabilizing the barrier and reducing pro-inflammatory drivers. Microbiome-oriented approaches may be part of the strategy, but responses vary and should be assessed through changes in comfort and objective skin physiology.

Conclusion

The review shows that the skin microbiome regulates inflammatory and oxidative processes that are directly linked to MMP activation and collagen and elastin degradation. This supports viewing the microbiome as one factor that can influence the pace of wrinkle formation. Supporting barrier function and carefully modulating microbial balance may serve as adjuncts within a comprehensive strategy for age-related skin concerns [1].

References

1. Challa V., Prajapati S.K., Gangani S. et al. Microbiome–aging–wrinkles axis of skin: molecular insights and microbial interventions. Int J Mol Sci 2025; 26(20): 10022. https://doi.org/10.3390/ijms262010022.
2. Dimarzio L., Cinque B., Cupelli F. et al. Increase of skin-ceramide levels in aged subjects following a short-term topical application of bacterial sphingomyelinase from Streptococcus thermophilus. Int J Immunopathol Pharmacol 2008; 21(1): 137–143.
3. Lee D.E., Huh C.-S., Ra J. et al. Clinical evidence of the effects of Lactobacillus plantarum HY7714 on skin aging. J Microbiol Biotechnol 2015; 25(12): 2160–2168.
4. Li Z., Bai X., Peng T. et al. New insights into the skin microbial communities and skin aging. Front Microbiol 2020; 11: 565549.
5. Teng Y., Huang Y., Danfeng X. et al. The role of probiotics in skin photoaging and related mechanisms. Clin Cosmet Investig Dermatol 2022; 15: 2455–2464.