Immune Markers in Psoriasis

Psoriasis is a chronic inflammatory skin disorder with high immunological background caused by a complex interplay between an altered immune system, genetic factors, autoantigens, lifestyle, and environmental factors. Extensive literature in recent years highlighted the crucial role played by the immune system in the pathogenesis of this pathology. Although it is unequivocally accepted that psoriasis is a T-cell mediated autoimmune condition, both innate and specific immune cells are highly involved in the pathogenesis of psoriasis. The aberrant interactions between immune cells and resident hyper-proliferative keratinocytes are mediated by immune and non-immune related molecules which lead to amplification of the local immune responses, that maintain the chronic inflammatory status. In this chapter, we will highlight the immune molecules resident in the psoriatic tissue or appending to the blood circulation that can indicate the prognosis of this systemic autoimmune disease. Moreover, we will focus on immune cells resident or circulating ones that can pinpoint the clinical evolution of the psoriatic disease. All these data can be developed in immune markers patterns that aid psoriasis diagnosis and/or future (immune)therapies

Immune Portrayal of a New Therapy Targeting Microbiota in an Animal Model of Psoriasis

Background: Despite all the available treatments, psoriasis remains incurable; therefore, finding personalized therapies is a continuous challenge. Psoriasis is linked to a gut microbiota imbalance, highlighting the importance of the gut–skin axis and its inflammatory mediators. Restoring this imbalance can open new perspectives in psoriasis therapy. We investigated the effect of purified IgY raised against pathological human bacteria antibiotic-resistant in induced murine psoriatic dermatitis (PSO). Methods: To evaluate the immune portrayal in an imiquimod experimental model, before and after IgY treatment, xMAP array and flow cytometry were used. Results: There were significant changes in IL-1α,β, IL-5, IL-6, IL-9, IL-10, IL-12 (p70), IL-13, IL-15, IL-17a, IFN-γ, TNF-α, IP-10/CXCL10, MCP-1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, MIG/CXCL9, and KC/CXCL1 serum levels. T (CD3ε+), B (CD19+) and NK (NK1.1+) cells were also quantified. In our model, TNF-α, IL-6, and IL-1β cytokines and CXCL1 chemokine have extremely high circulatory levels in the PSO group. Upon experimental therapy, the cytokine serum values were not different between IgY-treated groups and spontaneously remitted PSO. Conclusions: Using the murine model of psoriatic dermatitis, we show that the orally purified IgY treatment can lead to an improvement in skin lesion healing along with the normalization of cellular and humoral immune parameters

Oxidative Stress: A Possible Trigger for Pelvic Organ Prolapse

Pelvic organ prolapse is a frequent health problem in women, encountered worldwide, its physiopathology being still incompletely understood. The integrity of the pelvic-supportive structures is a key element that prevents the prolapse of the pelvic organs. Numerous researchers have underlined the role of connective tissue molecular changes in the pathogenesis of pelvic organ prolapse and have raised the attention upon oxidative stress as an important element involved in its appearance. The advancements made over the years in terms of molecular biology have allowed researchers to investigate how the constituent elements of the pelvic-supportive structures react in conditions of oxidative stress. The purpose of this paper is to underline the importance of oxidative stress in the pathogenesis of pelvic organ prolapse, as well as to highlight the main oxidative stress molecular changes that appear at the level of the pelvic-supportive structures. Sustained mechanical stress is proven to be a key factor in the appearance of pelvic organ prolapse, correlating with increased levels of free radicals production and mitochondrial-induced fibroblasts apoptosis, the rate of cellular apoptosis depending on the intensity of the mechanical stress, and the period of time the mechanical stress is applied. Oxidative stress hinders normal cellular signaling pathways, as well as different important cellular components like proteins, lipids, and cellular DNA, therefore significantly interfering with the process of collagen and elastin synthesis