Dysbiosis

Dysbiosis refers to a qualitative or quantitative change in the composition and/or function of a microbial community (microbiome) that disrupts the normally stable interaction between the microbiota, the host organism, and the local tissue environment. Dysbiosis may be characterized by the loss of protective microorganisms or the proliferation of potentially harmful microorganisms, by reduced microbial diversity, or by altered microbial metabolic activity.

The term dysbiosis primarily refers to the microbiota of the gut, skin, oral cavity, respiratory tract, and urogenital tract. The functionally balanced state is referred to as eubiosis (Iebba V et al. 2016).

Dysbiosis can manifest as:

• the loss of protective or immunoregulatory microorganisms
• an increase in facultative pathogenic microorganisms or pathobionts
• a decrease in microbial diversity
• a shift in the relative abundance of individual microorganisms
• changes in microbial metabolites, such as short-chain fatty acids
• impaired barrier function, colonization resistance, and immune homeostasis
• However, dysbiosis does not necessarily constitute an infection. In contrast to a classic infection, the focus is often not on a single pathogen but rather on an ecological and functional shift in the entire microbiome.

Clinical Examples:

• Intestine: Loss of diversity, decrease in butyrate-producing bacteria, increase in pro-inflammatory proteobacteria. Possible consequences include chronic inflammatory bowel diseases; see also intestinal microbiome.
• Intestine after antibiotics: Loss of colonization resistance with expansion of Clostridioides difficile. Possible consequences include antibiotic-associated diarrhea and pseudomembranous colitis.
• Vagina: Decrease in Lactobacillus species; increase in mixed anaerobic flora such as Gardnerella and Prevotella. A possible consequence is bacterial vaginosis or a clinically significant Candida infection.
• Oral cavity: Shift toward proteolytic, anaerobic bacteria, including Porphyromonas gingivalis; a possible consequence is periodontitis.
  • Gut-skin axis: The mechanisms by which the gut microbiome influences skin health remain unclear (Borrego-Ruiz A et al. 2024, Mahmud MR et al. 2022). There are gaps in our understanding of the gut-skin axis and the question of how microbial interactions contribute to skin diseases (e.g., psoriasis, atopic dermatitis, acne vulgaris, rosacea, alopecia areata, and hidradenitis suppurativa), as well as how the microbiome can be effectively modulated for therapeutic purposes (Parhizkar E et al. 2025).
  • Skin in atopic dermatitis: reduced bacterial diversity and expansion of Staphylococcus aureus, particularly during flare-ups. Possible consequences include barrier dysfunction with activation or initiation of cutaneous inflammation.
  • Skin in acne: a shift in certain strains of Cutibacterium acnes and their functional properties. Possible consequences include the onset or exacerbation of acne.
  • Scalp: altered balance of Malassezia species, sebum, and the cutaneous immune response. Possible consequences include seborrhea, seborrheic dermatitis, or atopic scalp and neck dermatitis.
• See also: Gut-Brain Axis.

1. Iebba V et al. (2016) Eubiosis and dysbiosis: the two sides of the microbiota. New Microbiol 39:1-12.
2. Borrego-Ruiz A et al. (2024) Nutritional and Microbial Strategies for Treating Acne, Alopecia, and Atopic Dermatitis. Nutrients 16:3559.
3. Budden KF et al. (2017) Emerging pathogenic links between the microbiota and the gut-lung axis. Nat Rev Microbiol 15:55–63.
4. Mahmud MR et al. (2022) Impact of the gut microbiome on skin health: the gut-skin axis viewed through the lens of therapeutics and skin diseases. Gut Microbes 14:2096995.
5. Parhizkar E et al. (2025) Probiotics and gut microbiota modulation: implications for skin health and disease management. Arch Microbiol 207(3):68.