Periodic Reporting for period 1 - NEUROSKIN (Modulating skin innervation to treat cutaneous inflammation)
Período documentado: 2019-05-01 hasta 2020-10-31
Skin diseases are the most common human illnesses, with a third of the world population affected at any given time. The need for treatment is usually lifelong and is aimed at achieving remission. So far, there is no therapy that can provide hope of a cure for psoriasis and other inflammatory skin conditions. NEUROSKIN project aims to determine how different skin innervations affect psoriasis, representing the largest class of skin conditions mediated by inflammation. Stress represents a strong aggravating factor for psoriasis in both adults and children, regardless of the nature of the stressor. Yet the mechanism by which stress affects the disease is not known.
The research utilised a transgenic mouse model that enables optogenetic control of local peripheral innervations using light. Thus, by performing a basic screen of the involvement of the various neuronal subsets on disease initiation and progression, we collected data that can enhance our mechanistic understanding of this disease ethology. Such understanding is especially important as we anticipate that different stages of the disease may be differentially affected by neuronal activity.
Even at this early stage of the research, NEUROSKIN was able to provide a matrix of potential therapeutic targets based on a proteomic screen that we performed.
Collectively, this project had three main achievements: 1. Setting up the experimental system of using light to manipulate local neuronal innervations. 2. Identify new potential targets, specifically those induced by the parasympathetic innervations. 3. Identify an unexpected effect on skin cancer model of B16, which requires further investigation.
Further research is required to develop each component that emerged from this study, which of successful, reach far beyond our original aim to manipulate skin inflammatory conditions.
The research utilised a transgenic mouse model that enables optogenetic control of local peripheral innervations using light. Thus, by performing a basic screen of the involvement of the various neuronal subsets on disease initiation and progression, we collected data that can enhance our mechanistic understanding of this disease ethology. Such understanding is especially important as we anticipate that different stages of the disease may be differentially affected by neuronal activity.
Even at this early stage of the research, NEUROSKIN was able to provide a matrix of potential therapeutic targets based on a proteomic screen that we performed.
Collectively, this project had three main achievements: 1. Setting up the experimental system of using light to manipulate local neuronal innervations. 2. Identify new potential targets, specifically those induced by the parasympathetic innervations. 3. Identify an unexpected effect on skin cancer model of B16, which requires further investigation.
Further research is required to develop each component that emerged from this study, which of successful, reach far beyond our original aim to manipulate skin inflammatory conditions.