The role of keratinocytes in inflammation

Sterol‐standardized phytopharmaceutical from ground cherry: Corticoid‐like properties on human keratinocytes and fibroblasts and its effects in a randomized double‐blind placebo‐controlled clinical trial

“…Besides monocytes, inflammatory phase involves an extravasation of inflammatory cells into the wound area, including neutrophils that removes particles and bacteria, and generates several pro‐inflammatory cytokines, such as IL‐1α, IL‐1β, IL‐6, and TNF‐α, which can stimulate monocytes to differentiate into M1 macrophages. Keratinocytes activation by pro‐inflammatory cytokines from macrophages and neutrophils promotes release of the first signals, known as alarmins, including heat shock proteins, antimicrobial peptides and cytokines such as IL‐1α, initiating an immune response . These mediators, via Toll‐like receptors, mainly IL‐1 receptor, activate nuclear factor kappa‐B (NF‐κB) in immune cells such as dendritic cells, neutrophils, macrophages, and T‐cells to transcript pro‐inflammatory IL‐1 family cytokines, IL‐6, TNF‐α, chemokine IL‐8 or COX‐2.…”

“…These mediators, via Toll‐like receptors, mainly IL‐1 receptor, activate nuclear factor kappa‐B (NF‐κB) in immune cells such as dendritic cells, neutrophils, macrophages, and T‐cells to transcript pro‐inflammatory IL‐1 family cytokines, IL‐6, TNF‐α, chemokine IL‐8 or COX‐2. Among these mediators, TNF‐α, IL‐1α, and IL‐6 can provide positive feedback to NF‐κB and amplify the inflammatory response . Indeed, IL‐1α from activated keratinocytes stimulates IL‐6 gene expression IL‐6 .…”

Ashwagandha root extract exerts anti‑inflammatory effects in HaCaT cells by inhibiting the MAPK/NF‑κB pathways and by regulating cytokines

“…The epidermis, which is comprised mainly of keratinocytes, is classified into multiple layers, the stratum corneum, granular layer, spinous layer and basal layer, based on the differentiation stage of the keratinocytes (1). Keratinocytes are known to have an important role in inflammation (2). Indeed, many inflammation-related skin diseases, such as allergic contact dermatitis, psoriasis and atopic dermatitis, are highly associated with the function of keratinocytes and cytokines (3).…”

“…Indeed, many inflammation-related skin diseases, such as allergic contact dermatitis, psoriasis and atopic dermatitis, are highly associated with the function of keratinocytes and cytokines (3). Keratinocytes are also a major source of inflammatory mediators, including members of the tumor necrosis factor (TNF)-α and interleukin (IL) families (2). Overproduction of pro-inflammatory mediators may lead to an abnormal inflammatory response.…”

>i<In vivo>/i< effects of DNA lesions in Nucleotide Excision Repair deficient mice

“…The main hypothesis regarding this health improvement involves the decrease of proinflammatory SASP and subsequent decrease of basal, non-pathogenic induced (sterile) inflammation, as inflammation as a process has been implicated in several different aging-associated disorders, including cancer, cardiovascular and neurodegenerative diseases, as well as a decrease in lifespan(118).Inflammation, much like cell senescence, is a concept that has recently been expanded upon(119). It is generally defined as a response of the innate immune system to stimulation by invading pathogens or endogenous damage signals involving several different cell types, such as immune, vascular, and tissue specific immuno-competent cells, such as Langerhans cells and keratinocytes in skin tissue(120,121), and astrocytes and microglia in the brain(122).Though it is classically and most often associated with defense against pathogens and/or tissue damage and repair, new data and insights have revealed a more multifaceted concept with interactions to other systems, such as metabolism and nucleic acid damage. Both lesions in DNA and RNA have been shown to elicit some pro-inflammatory cell and molecular responses through different mechanisms, such as activation of IL-1α (123), of the protein complex known as the inflammasome (124), the transcription factor NF-κB (125) and toll-like receptors (126), with these non-pathogen related (sterile) inflammation mechanisms being novel concepts, with its underlying structures and effects currently being established.…”