The Role of Propionibacterium acnes in the Pathogenesis of Sarcoidosis and Ulcerative Colitis: How This Connection May Inspire Novel Management of These Conditions.

A lesser-acknowledged role of Propionibacterium acnes is its effect on the development of sarcoidosis. This literature review not only further explores this association but also that of Propionibacterium acnes and other inflammatory conditions, such as ulcerative colitis and pyoderma gangrenosum, acne, ulcerative colitis syndrome (PAC syndrome). This article reviews the effect that isotretinoin, a commonly used treatment of acne, has on the pathogenesis of ulcerative colitis, and the immune dysregulation and genetic susceptibility of individuals prone to developing acne, sarcoidosis, and ulcerative colitis. Literature for this article review was obtained from PubMed by utilizing both regular keywords and medical subject heading (MeSH) subheadings for data gathering. Regular keywords were: Propionibacterium acnes, sarcoidosis, ulcerative colitis, and isotretinoin. MeSH subheadings used were: Propionibacterium acnes/immunology, Propionibacterium acnes/pathogenicity, Propionibacterium acnes/genetics, sarcoidosis/immunology, and sarcoidosis/genetics. Following the application of inclusion and exclusion criteria, a total of 5172 publications were obtained. A total of 5086 publications were removed due to a lack of relevancy to outcomes of interest. The remaining 86 publications from all the regular and MeSH keywords were selected due to relevancy to outcomes of interest. Following this, a refined manual search was done, with the removal of duplicates, and 33 publications from PubMed were selected for review. Following a review of these records, Propionibacterium acnes was repeatedly concluded to be a causative agent of sarcoidosis. Variable results for the association between Propionibacterium acnes and ulcerative colitis were found. Most studies showed no significant association between the use of isotretinoin and the development of ulcerative colitis. A strong overlapping role of genetic susceptibility and immune dysregulation in the pathogeneses of sarcoidosis, ulcerative colitis, and Propionibacterium acnes was found.

Neuroprotective and Neurodegenerative Aspects of Coffee and Its Active Ingredients in View of Scientific Literature.

Coffee and its components have several neuroprotective properties that lower the risk of cognitive decline and other neurodegenerative diseases. This study reviews the mechanisms by which coffee and its respective compounds affect the brain and its pathologies. Many epidemiological studies in this literature review have shown coffee to reduce the risk of developing dementia, stroke, and Alzheimer's disease. It may also have a positive impact on the disease course of amyotrophic lateral sclerosis, Parkinson's disease, and depression. The optimal benefits achieved from coffee in these pathologies rely on higher daily doses. Most of its effects are attributed to caffeine by the antagonism of adenosine receptors in the central nervous system; however, other coffee constituents like chlorogenic acids have also shown much promise in therapeutic value. Existing research considers coffee to have great potential, but additional studies are still needed to clarify the mechanisms and actual causal relationships in certain neuropathologies.

Mechanisms of Beta-Blocker Induced Psoriasis, and Psoriasis De Novo at the Cellular Level.

Beta-blockers are a commonly prescribed medication, but the increase in use goes hand in hand with increasing side effects; one of particular interest lately has been its dermatological reactions. Although rare, beta-blockers can exacerbate pre-existing psoriasis and also cause de novo psoriasis in patients naïve to the disease. The mechanism by which this occurs is still unclear, although numerous articles have been published throughout the years as to how this unusual effect takes place. The most common mechanism suggests that beta-blockers cause intracellular changes in calcium, affecting both keratinocyte proliferation and granulocyte function via decreased cyclic adenosine monophosphate (cAMP) levels. Several inflammatory mediators are known to play a role, as well as reduced expression and desensitization of the beta-adrenergic receptor itself. We discuss these posed pathways in-depth and how each contributes to the worsening or formation of new psoriasis. With this knowledge, future physicians may be more mindful of this side effect should it occur, and why they occur, to better manage our patients on this widely used medication.