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Phytomedicines Targeting Antibiotic Resistance through Quorum Sensing and Biofilm Formation Associated with Acne Vulgaris
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Isa A. Lambrechts, Namrita Lall
There is a range of theories about the sequence of these pathogenic factors and their contribution to the progression of acne vulgaris, which have not yet been fully answered. It is believed that follicular hyperkeratinization (the abnormal shedding of the skin) is the first step in the pathogenic pathway, blocking the pilosebaceous unit and leading to excess sebum accumulation. Comedone formation is a combined effect between the overproduction of keratinocytes and a reduction in the shedding of keratocytes due to the skin cells’ inability to separate from one another. Comedones form when keratinocytes block the pilosebaceous unit that results in the accumulation of sebum in the unit. Several factors contribute to hyperkeratinization. These factors include the lack of linoleic acid in the sebum due to hyperseborrhea, resulting in abnormal keratinocyte differentiation. Cytokines such as cytokine interleukin-1 alpha (IL-1α) present in the follicle are believed to induce hyperkeratinization. Furthermore, it was recently discovered that the acne-inducing bacteria Cutibacterium acnes secrete a glycocalyx polymer that is a component of the bacterial biofilm. This secretion is incorporated in the sebum, which increases cohesion between the keratinocytes. This results in a blockage in the pilosebaceous unit and results in the formation of a comedone. It is therefore plausible that the initial step of acne pathogenesis could be the colonization and biofilm formation of C. acnes instead of hyperkeratinization (Dessinioti and Katsambas, 2010; James, Burkhart, and Morrell, 2009; Pawin et al., 2004).
The Immune System in Cutaneous Disease: the Search for a Mouse Model of the Immunopathology of Psoriasis
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
Susan F. Grammer, J. Wayne Streilein
Keratinocytes, T cells, LC, and melanocytes of the epidermis have all been shown to secrete cytokines, however; KC-derived cytokines probably play the major role in dictating the fluid microenvironment of the epidermis and dermis. Most of the cytokines which KC produce are not constitutively secreted but can be induced by irritant chemicals, ultraviolet irradiation, tumor-promoting agents, and trauma. Keratinocytes either secrete or can be induced to secrete interleukin 1 alpha (IL-1α), IL-1β, interferon-alpha (IFNα), IFNβ, IL-3, IL-6, IL-8, GM-CSF, granulocyte colony stimulating factor (G-CSF), macrophage colony stimulating factor (M-CSF), platelet derived growth factor (PDGF), fibroblast growth factor (FGF), tumor necrosis factor-alpha (TNFα), transforming growth factor-alpha (TGFα) and TGFβ. The evidence is rapidly mounting for the existence of a network of interacting cytokines having activating, proliferative, and/or suppressive activity on both immune and nonimmune cells in the skin.7
Skin Equivalents to Measure Phototoxicity
Published in Francis N. Marzulli, Howard I. Maibach, Dermatotoxicology Methods: The Laboratory Worker’s Vade Mecum, 2019
André Rougier, Catherine Cohen, Roland Roguet
Various agents are well known to activate keratinocytes. As an example, both in vivo and in vitro, UV irradiation leads to the expression and release of a broad range of mediators. Among these mediators, interleukin 1 alpha (IL-1α) and prostaglandin E2 (PGE2) have been shown to be increased following UVB and UVA irradiation in vivo (Hawk et al., 1983; Konnikov et al., 1986; Murphy et al., 1988; Oxholm et al., 1988) and in vitro (Ansel et al., 1983; De Leo et al., 1984; Gahring et al., 1984; Cohen et al., 1991).
Cytotoxicity, oxidative stress, and inflammatory response of smokeless tobacco extracts and cytotoxicity of combustible cigarette whole smoke in a 3D oral organotypic buccal cell model
Published in Toxicology Mechanisms and Methods, 2022
Post-exposure basolateral media was removed following each time point and stored at −80 °C until cytokine analysis. Cytokines were evaluated by Luminex® xMAP® technology (cat. # HCYTOMAG-60K MILLIPLEX MAP, EMD Millipore, Burlington, MA) as per manufacturer’s protocols using a Bio-Rad Luminex 100 Bio-Plex. The cytokines evaluated were interferon gamma-induced protein 10 (IP-10), interleukin 8 (IL-8), and interleukin 1 alpha (IL-1α). A mixture of 10 ng/mL tumor necrosis factor-alpha (TNF-α) and 10 ng/mL of interleukin 1 beta (IL-1β) was added to the basolateral media and exposed to the tissues for the same duration as the CRPs. Before analysis, samples were thawed at room temperature and subsequently maintained at room temperature during processing. All samples were centrifuged before pipetting onto the assay plate. Each sample was analyzed in duplicate.
Pharmacologic agents directed at the treatment of pain associated with maladaptive neuronal plasticity
Published in Expert Opinion on Pharmacotherapy, 2022
Joseph V. Pergolizzi, Giustino Varrassi, Peter Magnusson, Frank Breve, Robert B. Raffa, Paul J. Christo, Maninder Chopra, Antonella Paladini, Jo Ann LeQuang, Kailyn Mitchell, Flaminia Coluzzi
The most abundant of the glial cells of the central nervous system, astrocytes are closely associated with neuroinflammation [21], which the body manages with neuro-immune hemostasis [13]. Astrocytes are morphologically complex cells that also play a crucial role in synaptogenesis, synapse maturation, and function [9]. In the mouse, one astrocyte can cover over 100,000 synapses; in the human, it is one million [22]. Following injury or insult, astrocytes become reactive and undergo morphological changes as well as altered gene expression. Depending on the injurious event, an astrocyte can become a neurotoxic type A1 reactive astrocyte or a neuroprotective A2 type reactive astrocyte [9]. Pro-inflammatory mediators, such as tumor necrosis factor alpha (TNF-α) or interleukin 1 alpha (IL-1α), creates A1 reactive astrocytes which, in turn, advance neurodegeneration and neurotoxicity and preclude synaptogenesis [9].
Is individual genetic susceptibility a link between silica exposure and development or severity of silicosis? A systematic review
Published in Inhalation Toxicology, 2020
Kaio Cezar Rodrigues Salum, Marcos Cesar Santos Castro, Ângela Santos Ferreira Nani, Fabiana Barzotto Kohlrausch
The release of the pro-inflammatory cytokines of the interleukin-1 (IL-1) family is the main driver of crystal-induced pathology (Herseth et al. 2008; Rabolli et al. 2014). The IL-1 family includes the structurally related proteins interleukin 1 alpha (IL-1α), interleukin 1 beta (IL-1β), and interleukin 1 receptor antagonist (IL-1RN). IL-1 appears to be the most important cytokine involved in silicosis, since the expression of other inflammatory molecules, including IL-6, IL-8, and TNF-α, is reduced when IL-1 is blocked (Herseth et al. 2008). Additionally, the blockage of IL-1α largely prevents silica-induced inflammation (Rabolli et al. 2014), and the blockage of IL-1β reduces the fibrotic response (Guo et al. 2013). However, besides the clear importance of these proteins in inflammation and fibrosis, Single Nucleotide Polymorphisms (SNPs) in IL1A, such as +4845 G/T (Ala114Ser) (Yucesoy et al. 2001a, 2001b) and −889 C > T (Wu et al. 2008a; Salum et al. 2020), and in IL1B, such as +3954 C/T (Yucesoy et al. 2001a, 2001b; Wu et al. 2008a; Helmig et al. 2012; Salum et al. 2020), −511 T/C (Yucesoy et al. 2001a, 2001b; Wu et al. 2008a; Helmig et al. 2012), −31 C/T (Wu et al. 2008b), −580 C/T (rs1143627) and the EX5 + 14C/T (Weng et al. 2015) were not associated with silicosis in Caucasians and in the Chinese and Brazilian populations.