What is it?
Psoriasis is one of the more common inflammatory, non-infectious skin diseases. It is characterized by bumpy, red, often scaly patches (lesions) resulting from accelerated skin cell formation – up to 10x the normal rate. There are five main types of psoriasis, characterized by the different manifestations and spread of these lesions. The most prevalent form of psoriasis, making up 85-90% of all cases, is psoriasis vulgaris – also known as plaque psoriasis, due to the formation of plaques (raised inflamed skin covered in white scaly skin). These lesions can appear anywhere but are more frequently located on the scalp, elbows, knees, and lower back.
What causes it?
Psoriasis is an autoimmune disease, meaning it results from abnormal activity of the body’s immune system – in this case over-reacting and attacking its own skin cells. As often is the case with skin diseases, the exact cause of psoriasis is not fully understood, though genetic and environmental components hold crucial roles in its development. Environmental triggers can include infection, stress, and temperature changes.
As psoriasis involves abnormal rates of keratinocyte (keratin-producing skin cells) proliferation, treatments aim to remove scales and stop these skin cells from growing so quickly, through use of topical ointments and medications.
Psoriasis and the gut microbiome
The bidirectional link between the health of the gut and the skin is increasingly being explored. Changes in our gut bacteria have been shown to affect skin homeostasis (its stable state) and influence its immune response. Psoriasis is one such condition for which this link has been demonstrated.
Research has shown that bacterial DNA originating from the gut has been detected in plasma of psoriasis patients, demonstrating how the gut disseminates its microbes and metabolites from the gut to other issues, such as the skin affecting its physiology and immune response. A characteristic of psoriasis is increased vascularization (blood vessel formation) which allows the accumulation of inflammatory immune cells.
One type of immune cells, Th17 cells, are abundant in both the skin and intestine and have been shown to contribute directly to the development of several inflammatory disorders – including psoriasis, with Th17 cells a known target in research for psoriatic therapies.
An association between psoriasis and inflammation of the gut has also been observed; 7-11% of patients with inflammatory bowel disease (IBD) are also diagnosed with psoriasis. Further, the same pattern of dysbiosis (microbial imbalance) has been described in both IBD and psoriasis patients, regardless of whether the conditions are co-occurring. This dysbiosis has been shown to include a depletion in healthy bacteria, such as Lactobacillus spp., Bifidobacterium spp., and F. prausnitzii, as well as colonization of certain pathogenic bacteria, including E.coli and Salmonella sp. Additionally, evidence has shown that colonization of S. aureus, Malassezia, and C. albicans in the skin, gut, or both, exacerbates psoriasis.
As such, the gut microbiome can be targeted when treating this condition. In fact, promising developments in therapeutic research have shown potential benefits of using probiotics to restore microbiome functionality in the gut to prevent or treat psoriasis.
Alesa et al, 2019 – The role of gut microbiome in the pathogenesis of psoriasis and the therapeutic effects of probiotics
Rungjang et al, 2020 – Skin and Gut Microbiota in Psoriasis: A Systematic Review
Psoriasis and the skin
A link between commensal streptococci (a genus of bacteria) in the nasopharynx (the upper part of the throat behind the nose) and psoriasis was first investigated as far back as the earlier 20th century, when scientists began connecting microorganisms to skin diseases.
Since then it has been shown, that immune cells – including Th17 cells, as above – are involved in the development of psoriasis.
So… while we know the link between T cells to psoriasis, what is the missing link between streptococcal infection and psoriasis?
Particular M proteins, antigens produced by specific streptococci, may be the answer. These proteins, found on several streptococci bacteria, were linked to psoriasis after it was noted the worsening of chronic plaque psoriasis – the most common presentation of psoriasis – was associated with these M protein-producing bacteria.
It was hypothesized that these M proteins were mimicking sub-units of human keratin (structural material found in the outer layer of skin, the epidermis) to induce psoriatic T cell activation. Indeed, following investigation, similarities in configuration were found between the conserved component of several M proteins and sub-units of keratin. Other antigens from streptococcal bacteria influence T cell activation, triggering psoriasis.
Differences in bacterial diversity and community distribution have been associated with psoriasis. Studies have shown an increase in diversity from healthy skin, to unaffected, and lesional psoriatic skin, with psoriasis shown as the major contributor to this pattern of diversity. Indeed, comparisons between healthy and psoriatic microbiomes have highlighted a loss in microbial stability and decrease in immunoregulatory bacteria. This reduction opens up an opportunity for higher colonization of pathogens, such as Staphylococcus aureus, which could exacerbate cutaneous inflammation via Th17 cells.
These significant differences in microbial community structure between healthy individuals and psoriatic patients suggest that psoriasis induces physiological changes and that microbial differences may be of diagnostic relevance.
Beyond bacteria, certain fungi such as Malassezia have been associated with psoriasis. The formation of psoriatic lesions was observed when Malassezia ovalis fragments were applied to the unaffected skin of patients suffering from psoriasis in an experiment dating back to the ‘80s. This association has also been shown when deposits of Malassezia originating from the scalp were made to non-psoriatic skin of psoriasis patients (read more about the role of Malassezia in dandruff). The resulting psoriatic lesions formed were responsive to an oral antifungal treatment, further highlighting this connection. An increased concentration of Malassezia yeast in lesional skin has also been associated with exacerbations of psoriasis.
Malassezia’s role in psoriasis is likely due to its ability to upregulate the expression (i.e. increase the response) of particular molecules which promote immune cell migration, inducing an immune response, and cause abnormal proliferation of keratin-producing skin cells – causing lesions.
Alekseyenko et al, 2013 – Community differentiation of the cutaneous microbiota in psoriasis
Benhadou et al, 2018 – Psoriasis and Microbiota: A Systematic Review
Chang et al, 2018 – Alteration of the cutaneous microbiome in psoriasis and potentl role in Th17 polarization
When we examine the role of the skin microbiome in relation to psoriasis, as so often is the case, we cannot say for certain whether microbes are the cause or result of the disease. However, associations of certain bacteria provide potential markers for diagnosis and, with certain fungi, provide potential targets for treatments.