Naturally derived bioactive compounds as precision modulators of immune and inflammatory mechanisms in psoriatic conditions

Abstract

Psoriasis represents a chronic autoimmune skin condition defined by various clinical forms, including inverse, erythrodermic, pustular, guttate, plaque types. While current therapies, including topical treatments but also systemic through conventional synthetic drugs and biologics, have improved symptom management, no treatment completely cures the disease, and numerous options are linked to considerable adverse effects, including immunosuppression and carcinogenic risks. Therefore, there is growing interest in bioactive compounds from natural sources due to their potential to reduce inflammation and oxidative stress in psoriasis with fewer adverse effects. The present narrative review aimed to address the limitations of current psoriasis therapies by exploring the therapeutic potential of bioactive compounds in the classes of flavonoids, terpenoids, omega-3 fatty acids, and alkaloids assessed through complex experimental models, focusing on their immunomodulatory and anti-inflammatory properties. Recent studies highlight the efficacy of natural bioactive compounds in reducing psoriasis symptoms, either as standalone treatments or in combination with conventional therapies. While these compounds show promise in alleviating psoriasis-related inflammation, further research is needed to optimize their therapeutic use, understand their mechanisms of action, and assess long-term safety. Future studies should focus on clinical trials to establish standardized protocols for incorporating bioactive compounds into psoriasis management and explore their potential role in personalized treatment strategies. Continued research is essential to develop more effective, safer, and affordable therapeutic options for psoriasis patients.

Keywords: Anti-inflammation; Autoimmune disease; Diet; Natural bioactive compounds; Psoriasis.

Fig. 1

Classification of psoriasis clinical forms

Fig. 2

Methodological approaches regarding the selection of the analyzed literature

Fig. 3

Disparities in publication output across keyword searches highlighting the insufficient focus on addressing psoriasis with naturally derived bioactive substances

Fig. 4

Interrelationships in biological pathways and genetic implications in the pathogenesis of psoriasis. The bolded structures (i.e., IL12B, TYK2, IL23R, and IL23A) are proteins currently addressed by psoriasis treatments, while the arrows indicate the interaction between the depicted immunological pathways. CARD14 caspase recruitment domain family member 14, ERAP1 endoplasmic reticulum aminopeptidase 1, GWAS genome-wide association studies, HLA-C human leukocyte antigen C, IKK IκB kinase, IL-17 Interleukin 17, IL-23 Interleukin 23, IL12B Interleukin 12 subunit beta, IL23A Interleukin 23 subunit alpha, IL23R Interleukin 23 receptor, IRF4 Interferon Regulatory Factor 4, NFKBIZ NF-kB inhibitor zeta, NF-kB nuclear factor kappa-light-chain-enhancer of activated B cells, p50 NF-kB subunit p50, p65 NF-kB subunit p65/c-Rel, REL regulator of nuclear factor kappa B, STAT3 signal transducer and activator of transcription 3, TNFAIP3 TNF alpha-induced protein 3, TNFSF15 tumor necrosis factor superfamily member 15, TLRs toll-like receptors, TYK2 tyrosine kinase 2, Th17 T helper 17 cells, TRAF3IP2 TNF receptor-associated factor 3 interacting protein 2

Fig. 5

Inflammation mechanisms in psoriasis. IFN interferon, pDC plasmacytoid dendritic cell, IL interleukin, LL-37 cathelicidin (human antimicrobial peptide)

Fig. 6

Chemical structures of key natural polyphenols in psoriasis

Fig. 7

Chemical structures of key terpenoids and alkaloids in psoriasis