Skin and gut microbiota dysbiosis in autoimmune and inflammatory 
skin diseases
Špela Šuler Baglama1 ✉, Katarina Trčko1
1Department of Dermatology and Venereal Diseases, University Medical Centre Maribor, Maribor, Slovenia.
105
2022;31:105-109
doi: 10.15570/actaapa.2022.16
Introduction
The skin and mucosal membranes have a host defense function 
by creating a barrier against noxious external factors. This bar-
rier is complex. Functionally, its components can be subdivided 
into four different levels: a physical, chemical, immune, and mi-
crobial barrier. Because microbes in the microbial barrier can be 
found on the skin surface and on certain mucous membranes, 
they represent the outermost barrier and as such are the first de-
fense against environmental invaders (1, 2). All microorganisms 
that inhabit a specific part of the body, including opportunistic, 
commensal, and pathogenic microorganisms, are united under 
the single term microbiota (2). The human microbiota consists 
mainly of bacteria and viruses, while archaea, fungi, and other 
eukaryotes represent a minor proportion (3). The term microbiome 
is broader and describes the collection of microorganisms and 
their genomes and the environment that the microbes inhabit, 
including the host epithelium, the immune system, and products 
produced by both microbes and the host (4). To better define com-
plex microbial communities of the oral cavity, skin, nostrils, and 
gastrointestinal and urogenital tracts, the Human Microbiome 
Project (HMP) was founded in 2007 (5). When analyzing microbio-
ta and microbiome, one often encounters the terms alpha (α) and 
beta (β) diversity, which represent the diversity of microbes within 
the sample or among the samples investigated, respectively. In re-
cent years, culture-based methods of studying microorganisms 
have been replaced by molecular methods, including polymerase 
chain reaction (PCR), DNA fingerprinting, and especially next-
generation sequencing (NGS), which is becoming increasingly 
sensitive, rapid, and cost-effective. Amplicon sequencing analy-
ses usually target one marker gene; namely, the ubiquitous gene 
for 16S ribosomal ribonucleic acid (rRNA) in bacteria and archaea, 
and the internal transcribed spacer (ITS) region, and the 18S rRNA 
gene in fungi and other single-cell eukaryotes. The 16S rRNA gene 
contains nine variable regions that can be amplified and used for 
taxonomic profiling of the bacteria (and archaea) in the sample 
because they are phylogenetically diverse for a particular genus 
and species. Metagenomic shotgun sequencing, unlike 16S rRNA 
sequencing, fragments and amplifies the entire extracted DNA; 
that is, most or all of the genetic material in the sample. In addi-
tion to taxonomic classification, it makes it possible to study the 
functional potential of the microbes. Even more complex than 
metagenomics is metatranscriptomics, with which, through the 
amplification of microbial messenger RNA, direct information 
about their function can be obtained (6).
Normal skin and gut microbiota
The skin microbiota is taxonomically very diverse, both among 
different hosts and between individual skin regions of the same 
host. Microorganisms can be present in the skin up to the super-
ficial part of the subcutaneous tissue. Whereas the microbiota of 
the epidermis is significantly influenced by environmental fac-
tors, the microbiota of the dermis is more stable and most likely 
universal to all skin regions. The composition of the skin micro-
biota changes during development and depends on the age of the 
subject (7). In newborns, it depends on the method of delivery. It 
stabilizes at about 3 years of age and again goes through hormo-
nally conditioned dramatic changes at puberty, especially due to 
the secretion of sebum. Its third period of evident changes occurs 
with age, when sebum secretion decreases (8). The total number 
of microbes in the skin microbiota is estimated at 1012 (9). The larg-
est share is represented by bacteria (60%), followed by viruses 
(30%) and eukaryotes (10%), whose representatives are mainly 
fungi (10). Part of the skin microbiota are also archaea, which rep-
resent up to 4.2% of all prokaryotes (11). The most dominant bac-
terial phyla of the skin microbiota are Actinobacteria (36–51%), 
Firmicutes (24–34%), Proteobacteria (11–16%), and Bacteroidetes 
(6–9%) (12, 13). Molluscum contagiosum, human papillomavirus, 
and Merkel cell polyomavirus are often part of the skin virome (10).
Abstract
The human body is inhabited by complex communities of microorganisms. Changes in the composition and function of the skin 
and gut microbiota are linked to various skin diseases. The microbiota is an important modulator of the immune system and thus 
maintains homeostasis. Conversely, the immune system can also change the composition of the microorganism community. Thus, 
it is still unknown whether certain skin diseases are caused by primary changes in the local and/or remote microbiota, or whether 
dysbiosis is only a secondary consequence of the dermatoses themselves. Expanding knowledge of skin and gut microbiota dys-
biosis in skin diseases may possibly lead to better understanding of their pathophysiologies and to the discovery of new molecular 
markers for their earlier diagnosis and targeted treatment; for example, using specific microbes to replace missing ones. This nar-
rative review provides an overview of current knowledge about skin and gut microbiota dysbiosis in psoriasis, atopic dermatitis, 
hidradenitis suppurativa, seborrheic dermatitis, acne vulgaris, rosacea, and lichen sclerosus.
Keywords: microbiota, dysbiosis, skin, autoimmune, inflammatory
Acta Dermatovenerologica 
Alpina, Pannonica et Adriatica
Acta Dermatovenerol APA
Received: 30 August 2022 | Returned for modification: 1 September 2022 | Accepted: 5 September 2022
✉ Corresponding author: spela.baglama@gmail.com
106
Acta Dermatovenerol APA | 2022;31:105-109Š. Šuler Baglama et al.
Of the fungi, the genus Malassezia is the most predominant. In ad-
dition to sex, age, and geographical area, the diversity and com-
position of the microbial population depends on physiological 
characteristics of the skin, such as temperature, pH, exposure to 
ultraviolet rays, humidity, and the amount of sebum secreted. On 
the basis of these physiological factors, different skin areas can be 
classified into three topographical categories, including dry areas 
(e.g., underarms), which are mainly colonized by Betaproteobac-
teria, moist areas (e.g. the groin and popliteal areas), where the 
genera Staphylococcus and Corynebacterium predominate, and, 
finally, sebaceal areas (e.g., the face), with a predominance of the 
lipophilic genus Cutibacterium, followed by Staphylococcus and 
Corynebacterium (12–14). Figure 1 shows topographical skin re-
gions with their characteristic bacterial species.
The highest number of microbes is found in the gut. Bacteria 
again represent the largest proportion of gut microbiota. Their to-
tal abundance is estimated from 107 in the stomach to up to 1014 
per gram of content in the colon. The main bacteria inhabiting the 
small intestine are from the phyla Firmicutes and Proteobacteria. 
Anaerobes predominate in the large intestine, with the majority of 
bacteria belonging to the phyla Firmicutes, Bacteroidetes, Actino-
bacteria, Verrucomicrobia (Akkermansia), and Proteobacteria (15).
Skin and gut dysbiosis in autoimmune and inflammatory 
skin diseases
Skin and gut dysbiosis associated with various autoimmune and 
inflammatory skin diseases is presented in Table 1.
Interplay between microbiota dysbiosis and host immune 
system
The microbiota is an important modulator of the immune system 
and, vice versa, the immune system can also influence changes 
in the composition of the microbial community, which is called 
dysbiosis or disruption of the microbial balance. It results in the 
absence of usual microbes and the presence of microbes with 
unfavorable effects. With the loss of beneficial functions of com-
mensal microorganisms or due to harmful functions of pathogen-
ic microorganisms, activation of the immune system can occur, 
thereby possibly causing or aggravating diseases. However, it is 
still unknown whether changes in the local and/or remote mi-
crobiota are the primary event in the development of certain skin 
diseases, or whether dysbiosis is only a secondary consequence of 
the dermatoses themselves (1). The recent discovery of dysbiosis 
already present on clinically unaffected predilection sites of hi-
dradenitis suppurativa that resembled the microbiota of lesions 
of hidradenitis suppurativa suggests a primary role of dysbiosis 
in the initiation of inflammation and lesion formation and argues 
against secondary dysbiosis (38).
When pathogenic microbes come into contact with the human 
body through the epithelium, they are detected by pattern recogni-
tion receptors (PRRs) on macrophages (39). PRRs include toll-like 
receptors (TLRs) and NOD-like receptors (NLRs) for the detection 
of bacterial peptidoglycans and viral and fungal proteins (8). Upon 
detection of pathogenic microorganisms, PRRs trigger the secretion 
of first-line pro-inflammatory cytokines, mainly interleukin (IL)-1 
and IL-18. IL-1 is a strong inducer of the release of antimicrobial 
peptides (AMPs) from keratinocytes (40). In addition, microbes 
can influence the growth of other microbes through the secretion 
of bacteriocins, auto-induced peptides, and phenol-soluble mod-
ulins, and by releasing signaling inhibitory molecules. Some of 
these bacterial products, for example, reduce the virulence of the 
pathogen and increase the immune response against it. In addition 
to the release of bacterial products, commensal microbes prevent 
the development of dysbiosis with an effect on mucosal-associated 
invariant T cells (MAITs) (8). Likewise, commensals regulate com-
plement components and can stimulate neutrophil and cytokine 
production (7). Moreover, microbial metabolites can induce epige-
netic modifications (41). AMPs, together with other inflammatory 
cytokines characteristic of specific inflammatory dermatoses, trig-
ger the differentiation of T lymphocytes, which further stimulate 
the release of inflammatory mediators that stimulate the formation 
of chemokines and, last but not least, AMPs, which creates a “vi-
cious cycle” of inflammation (40). Table 2 presents the potential 
role of excess and deficient microbes in the pathogenesis of auto-
immune and inflammatory skin diseases.
Figure 1 | Skin topographical microenvironments based on the physiology of 
the skin site with the top five abundant bacterial species (Byrd et al., 2018). 
Created by BioRender.
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Acta Dermatovenerol APA | 2022;31:105-109 Skin and gut microbiota dysbiosis
AD = atopic dermatitis, HS = hidradenitis suppurativa, IBD = inflammatory bowel disease, NA = not available, NB = narrow band, UV = ultraviolet.
Table 1 | Skin and gut dysbiosis associated with various autoimmune and inflammatory skin diseases.
Skin microbiota changes compared to healthy controls Gut microbiota changes compared to healthy controls
Skin disease Excess microbes Deficient microbes Reduced dysbiosis after treatment Excess microbes Deficient microbes
Reduced dysbiosis 
after treatment
Psoriasis Firmicutes, 
Corynebacterium, 
Staphylococcus,
and Streptococcus (16)
Actinobacteria, 
Cutibacterium (16)
With NB UVB, 
cyclosporin A, retinoic 
acid, fumarates, 
methotrexate, 
adalimumab, 
ustekinumab (17, 18)
Firmicutes, 
Actinobacteria, 
Verrucomicrobia, 
Faecalibacterium, 
Bacteroides, 
Bifidobacterium, 
Megamonas, and 
Roseburia (19)
Bacteroidetes, 
Euryarchaeota, 
Proteobacteria, 
Prevotella,
Alistipes, and 
Eubacterium (19)
With secukinumab; 
no significant change 
with ustekinumab 
(20)
Atopic 
dermatitis
Staphylococcus 
aureus (correlates 
with intensity of 
AD), Staphylococcus 
epidermidis, 
Staphylococcus 
haemolyticus; 
more diverse non-
Malassezia spp. 
(Aspergillus, Candida 
albicans, Cryptococcus 
diffluens) (21)
Streptococci, 
Cutibacterium, 
Acinetobacter, 
Corynebacterium, 
and Prevotella; 
Malassezia spp.
(21)
With dupilumab, 
conventional 
therapy (topical 
corticosteroids), and 
dilute bleach baths 
(21–23)
Bifidobacterium 
pseudocatenulatum, 
Faecalibacterium 
prausnitzii, 
Clostridium, and 
Escherichia coli (24)
Akkermansia, 
Bifidobacterium, 
Enterococcus, 
Bacteroides, and 
Ruminococcus (24)
NA
Hidradenitis 
suppurativa
Coagulase-negative 
staphylococci, 
Porphyromonas, 
Prevotella, and 
Staphylococcus aureus 
(25); in HS tunnels 
Corynebacterium and 
Acinetobacter (26)
NA NA Conflicting results (25) NA
Seborrheic 
dermatitis / 
dandruff
Malassezia, 
Ascomycota, 
Bisidiomycota, 
Mycosphaerella, 
Candida, 
Filobasidium, 
Staphylococcus and 
Streptococcus (27)
Cutibacterium 
(lower expression 
in lesions, higher 
expression in healthy 
skin of patients), 
Ganoderma, Exidia, 
Pilatoporus, and 
Engyodontium (27)
With peroral 
itraconazole (28)
NA NA
Acne vulgaris Difference in the diversity of 
Cutibacterium acnes strains; 
Staphylococcus epidermidis (29)
Increased abundance 
of antibiotic resistant 
Cutibacterium acnes 
and other skin 
commensal bacteria 
(e.g., Staphylococcus 
epidermidis) after 
various antibiotic 
therapies; changes of 
microbiota following 
treatment with peroral 
lymecyclin and 
sarecycline (29)
Bacteroidetes (30) Firmicutes, 
Clostridium, 
Clostridiales, 
Lachnospiraceae, 
and 
Ruminococcaceae 
(30)
NA
Rosacea Demodex
folliculorum, 
Firmicutes, 
Staphylococcus, 
Streptococcus
(31, 32)
Actinobacteria, 
Cutibacterium (31)
Topical 1% 
metronidazole in 
cream did not affect 
microbiota change, 
whereas peroral 
doxycycline did
(33, 34)
Acidaminococcus 
and Megasphaera 
(35)
Peptococcaceae, 
Methanobrevibacter, 
Slackia, 
Coprobacillus, 
Citrobacter, and 
Desulfovibrio (35)
NA
Lichen 
sclerosus
Porphyromonas, 
Parvimonas, 
Peptoniphilus, 
Prevotella, 
Dialister, and 
Peptostreptococcus 
(prepubertal girls) 
(36); Fusobacterium 
(balanopreputial sac) 
(37)
Corynebacterium 
(prepubertal girls) 
(36); Finegoldia 
(balanopreputial sac) 
(37)
NA Dialister, 
Clostridiales, 
Paraprevotella, and 
Escherichia coli (36)
Phascolarctobacte-
rium (36)
NA
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Acta Dermatovenerol APA | 2022;31:105-109Š. Šuler Baglama et al.
Manipulation of dysbiosis as a therapeutic approach in the 
treatment of skin diseases
Manipulation of the microbiota with the goal of reducing dysbio-
sis has potential for new therapeutic approaches to the prevention 
and treatment of autoimmune and inflammatory diseases. Strat-
egies to achieve gut microbiota eubiosis are well known and in-
clude the use of probiotics, prebiotics, synbiotics, fecal microbiota 
transplants, and antimicrobial interventions (49). A systematic 
review of the effectiveness of probiotics for psoriasis based on ran-
domized controlled trials has shown that probiotics can improve 
the Psoriasis Area and Severity Index (PASI); however, the differ-
ence between patients and a placebo group on meta-analysis was 
not statistically significant (50). In contrast, a systematic review of 
randomized controlled trials of supplementation with probiotics 
in adults with atopic dermatitis has confirmed their beneficial ef-
fect on outcomes, both in reducing the severity of the disease and 
in improving quality of life. A mixture of Lactobacillus salivarius 
(LS01) and Bifidobacterium (BR03) appeared to be the best supple-
ment for adult atopic dermatitis (51). Similarly, infants and children 
with atopic dermatitis treated with oral probiotics have significant 
differences in SCORing Atopic Dermatitis (SCORAD) compared to 
controls (52). Interestingly, a meta-analysis has shown that treat-
ment with probiotics during both the prenatal and postnatal pe-
riods reduced the incidence of atopic dermatitis in infants and 
children (53). In contrast to gut microbiota manipulation, methods 
of human skin microbiota manipulation are developed to a lesser 
degree and include skin microbiota transplantation, antimicrobial 
therapy, prebiotics, probiotics, and postbiotics (54). Autologous 
transplantation of coagulase-negative Staphylococcus was tried 
in a randomized, double-blind, placebo-controlled clinical trial 
on patients with atopic dermatitis and led to a reduction of skin 
colonization with Staphylococcus aureus as well as to significant 
clinical improvement as assessed by the local Eczema Area and 
Severity Index (EASI) score (55).
Conclusions
Skin and gut microbiota are promising for research on the patho-
genesis of autoimmune and inflammatory skin diseases. With 
the development of new molecular methods, there is increasing 
evidence of a link between dysbiosis and the immune system, and 
thus indirectly with the development of various diseases. In addi-
tion to bacterial dysbiosis, viruses and fungi also show potential 
for research into the pathogenesis of autoimmune and inflamma-
tory skin diseases. Further research is needed to better understand 
the dialogue between microbes and the immune system.
Acknowledgement
The authors thank Prof. dr. Maja Rupnik for her advice on writing 
the manuscript.
Table 2 | Potential role of microbes in the pathogenesis of autoimmune and inflammatory skin diseases.
Microbe(s): disease Potential role of microbe(s) in pathogenesis of disease (reference)
Staphylococcus aureus: psoriasis Induction of IL-17-mediated inflammation (42)
Corynebacterium: psoriasis Negatively regulates interferon signaling (43)
Bacteroides: psoriasis Produces polysaccharide A, which activates Treg cells (19)
Prevotella: psoriasis Improves intestinal mucosal integrity, reduces inflammatory markers in cecum (19)
Staphylococcus aureus: AD Its peptidoglycan induces development of Th2 cells (44)
Cutibacterium acnes: AD Strong inducer of Th1 immune response (45)
Porphyromonas, Prevotella: HS Increase secretion of AMPs; Prevotella also stimulates Th17 and secretion of IL-23 and IL-1 (46, 47)
Acne-associated Propionibacterium acnes 
strains: acne vulgaris
Induce inflammatory responses in keratinocytes, sebocytes, and peripheral blood mononuclear 
cells (29) 
Staphylococcus epidermidis: acne vulgaris Possibly inhibits Propionibacterium acnes through various mechanisms (29)
Clostridium: acne vulgaris Produces butyrate and inhibits inflammation (30)
Demodex folliculorum: rosacea Activates TLR2, which then stimulates activity of kallikrein 5 (48)
AD = atopic dermatitis, AMPs = antimicrobial peptides, HS = hidradenitis suppurativa, IL = interleukin, Th = T helper, TLR = toll-like receptors, Treg = regulatory 
T cells.
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