The pathogenesis of psoriasis, an immune-mediated inflammatory skin disorder, is not entirely understandable. But, various studies demonstrated the strong correlation between gastrointestinal health and skin, particularly microbiome interaction with the immune system, which affects the pathophysiology of inflammatory situations[1, 4, 7, 8]. In this regard, dietary factors, mainly, probiotics with significant modifying effect on the gut microbiome and thereby influence the inflammatory state, must be considered in therapeutic protocols. However, there is limited evidence on probiotic supplementation in psoriasis treatment; accordingly, this study designed to specify the probable therapeutic effects of probiotic supplementation in psoriatic patients. This study demonstrated that probiotics supplementation for eight weeks in psoriatic patients had a beneficial impact on improving QOL scores, disease severity, reduction of LDL, and total cholesterol levels, and attenuating inflammation cytokines/oxidative stress biomarkers.
Previous studies reported a positive linear correlation between the severity of psoriasis disease and its negative impact on the patient’s life (health-related Quality of Life), workplace, and loss of productivity [6, 10, 15]. In this study, we defined that probiotic supplementation improved QOL scores in patients with psoriasis. Similarly, several probiotics supplementation studies in other diseases and situations have shown improvement in QoL scores of probiotic consumers [16, 17]. The mechanisms behind this effect remain uncertain. It seems that modulation of the bacterial species in the gut via oral probiotics was associated with psychological status through gut microbiota–brain interaction and neuroactive potential of gut microbiota. The gut microbiome generates molecules with neuro-active functions as well as particles that influence human cells to produce neuroactive agents, So the psychiatric state and a sense of wellness could be affected by the gut microbiome . Recently, it is documented that Butyrate-producing Faecalibacterium and Coprococcus bacteria were consistently associated with a higher quality of life indicators. Moreover, microbial synthesis substances have a potential rolein dopamine metabolite 3,4-dihydroxy phenylacetic acid, and a possible part of microbial γ-aminobutyric acid production are correlated positively with mental quality of life .
Our data reveal that eight weeks’ supplementation with probiotics improved the clinical outcomes of the psoriasis disease, which assessed by standardized index, PASI. Similarly, other studies [3, 20, 21] support this finding of the potential improvement effect of probiotic supplementation on psoriasis, and consequently, altering the gut microbiome. The gut–skin axis contributes to the involving mechanisms behind this effect. The generated neurotransmitters (dopamine, serotonin, GABA, and acetylcholine) by the intestinal microbiome cross the intestinal epithelium into the bloodstream to regulate skin functions, alter barrier function, hair growth and melatonin synthesis in the skin [1, 3]. Moreover, it affects the production of short-chain fatty acids (SCFAs), in particular, butyrate It binds to G-protein-coupled receptors expressed on keratinocytes and endothelial and immune cells and inhibits inflammation through regulating the histone deacetylases activity, modulating the inflammatory NFκB signaling pathway, and promoting Treg accumulation in the skin [3, 20, 21]. Accordingly, it seems that modifying the gut microbiota by probiotics supplementation could be an important therapeutic option in psoriasis (Figure. 3).
Nowadays, the relationship between psoriasis and an increased incidence of cardiovascular diseases is well established . Several studies confirmed that patients with psoriasis have a higher risk of developing severe cardiovascular events, such as stroke and myocardial infarction (MI) [10, 23]. The chronic inflammation which occurs in psoriasis accelerates involved systemic mechanisms in other chronic inflammatory diseases, including atherosclerosis [24, 25]. Regarding, systemic inflammation is considered the leading cause of CVD risk in psoriasis; our study aimed to evaluate the effect of eight-weeks of probiotic supplementation on the inflammatory status of psoriatic patients. We found that this intervention led to decrees MDA, IL-6, and hs-CRP levels in patients with psoriasis. Up to now, there are a few studies that investigate the role of probiotics supplementation in psoriasis. However, there is some evidence that probiotics may exert beneficial immunoregulatory effects by reducing inflammation [20, 26]. One study showed that oral administration of Lactobacillus pentosus GMNL-77 (as a probiotic), in a mouse model of psoriasis, reduced tumor necrosis factor-α and IL-23–IL-17 axis cytokines, which was associated with significant decreased erythematous scaling lesions and epidermal thickening in comparison to untreated control mice . Another study showed that Lactobacillus rhamnosus suppressed the expression of TNF‑α, IL‑6, and proinflammatory cytokines in the IL‑23/IL‑17 cytokine axis . Our findings are in agreement with the previous study on severe pustular psoriasis cases; that did not respond to steroids, dapsone, and methotrexate. However, after beginning probiotic supplementation (Lactobacillus sporogenes) three times per day, the psoriatic patients showed significant clinical improvement within two weeks with almost complete remission after four weeks . In a placebo-controlled study of psoriasis patients, Bifidobacterium Infantis supplementation for eight weeks led to significantly decreased plasma levels of inflammatory C-reactive protein and TNF‑α in comparison with the placebo group . The authors proposed that in response to probiotic supplementation, levels of the beneficial microbial inhabitant of the large intestine increased. These species are much less abundant in the gut of psoriatic patients than in healthy ones. Butyrate, an SCFA that provides energy for colonocytes, reduces oxidative stress, and exerts anti-inflammatory action by triggering regulatory T cells, thereby conferring immune tolerance beyond the GI system [1, 3, 24, 28].