Melanocytes and Skin Immunity

Hong, Yuxiao; Song, Bing; Chen, Hong‐Duo; Gao, Xinghua

doi:10.1038/jidsymp.2015.14

Cited by 36 publications

(31 citation statements)

References 30 publications

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“…Previous studies have suggested that melanocytes could play an active role in fighting pathogens. 84 , 85 Our data support this hypothesis by showing that melanocyte-derived supernatants and cell lysates increase the resistance to infection in our amphibian model. Interestingly, only extracts derived from actively proliferating melanocytes induce this increase, while quiescent, melanin-secreting, and more differentiated melanocytes have no significant effect.…”

Section: Discussionsupporting

confidence: 82%

Bioelectric regulation of innate immune system function in regenerating and intact Xenopus laevis

2017

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Two key inputs that regulate regeneration are the function of the immune system, and spatial gradients of transmembrane potential (V mem). Endogenous bioelectric signaling in somatic tissues during regenerative patterning is beginning to be understood, but its role in the context of immune response has never been investigated. Here, we show that V mem levels modulate innate immunity activity in Xenopus laevis embryos. We developed an assay in which X. laevis embryos are infected with a uropathogenic microorganism, in the presence or absence of reagents that modify V mem, prior to the ontogenesis of the adaptive immune system. General depolarization of the organism’s V mem by pharmacological or molecular genetic (ion channel misexpression) methods increased resistance to infection, while hyperpolarization made the embryos more susceptible to death by infection. Hyperpolarized specimens harbored a higher load of infectious microorganisms when compared to controls. We identified two mechanisms by which V mem mediates immune function: serotonergic signaling involving melanocytes and an increase in the number of primitive myeloid cells. Bioinformatics analysis of genes whose transcription is altered by depolarization revealed a number of immune system targets consistent with mammalian data. Remarkably, amputation of the tail bud potentiates systemic resistance to infection by increasing the number of peripheral myeloid cells, revealing an interplay of regenerative response, innate immunity, and bioelectric regulation. Our study identifies bioelectricity as a new mechanism by which innate immune response can be regulated in the context of infection or regeneration. V mem modulation using drugs already approved for human use could be exploited to improve resistance to infections in clinical settings.

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Section: Discussionsupporting

confidence: 82%

Bioelectric regulation of innate immune system function in regenerating and intact Xenopus laevis

2017

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“…Melanization produces intermediate toxic compounds which exhibit strong antimicrobial activities. Additionally, melanin—the end-product—may have the capacity to trap, inhibit, and even kill invading pathogens [75]. Due to their location within stratified epithelia, Langerhans cells (LCs) are part of the first line of defense against pathogens present in the environment.…”

Section: Barrier Sites In the Human Bodymentioning

confidence: 99%

Candida albicans at Host Barrier Sites: Pattern Recognition Receptors and Beyond

Swidergall

2019

Pathogens

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Over the last decades, fungal infections have emerged as a growing threat to human health. Although the human body is at potential risk, various body sites host several commensal fungal species, including Candida albicans. In healthy individuals, C. albicans colonizes different mucosal surfaces without causing harm, while under diverse circumstances the fungus can proliferate and cause disease. In this context, the understanding of host–C. albicans interactions in health and during infection may lead to novel therapeutic approaches. Importantly, host cells express pattern recognition receptors (PRRs), which sense conserved fungal structures and orchestrate innate immune responses. Herein, important findings on the topic of the recognition of C. albicans at host barrier sites are discussed. This review briefly summarizes the importance and functions of myeloid PRRs, reviews the fungal recognition and biology of stromal cells, and highlights important C. albicans virulence attributes during site-specific proliferation and invasion.

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Section: Introductionmentioning

confidence: 99%

“…Melanin is a polymeric pigment synthesized within melanosomes by melanocytes, cells derived from the neural crest, and it confers a host of protective biological benefits ranging from UV photoprotection [1] to free-radical chelation [2] and immune regulation [3]. The synthesis of melanin within melanosomes is primarily regulated by [3]. The synthesis of melanin within melanosomes is primarily regulated by the rate-limiting enzyme tyrosinase which catalyzes the conversion of L-Tyrosine to L-Dihydroxyphenylalanine (L-DOPA) and undergoes further oxidation to the quinone, L-dopaquinone, which is then polymerized to melanin [4].…”

Section: Introductionmentioning

confidence: 99%

Comparative Study of Curcumin and Its Hydrogenated Metabolites, Tetrahydrocurcumin, Hexahydrocurcumin, and Octahydrocurcumin, on Melanogenesis in B16F10 and MNT-1 Cells

Goenka

Simon

2021

Cosmetics

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Curcumin, a bioactive from Curcuma longa, has been shown to possess anti-melanogenic activity previously; however, the effects of its hydrogenated metabolites (HMs)—Tetrahydrocurcumin (THC), Hexahydrocurcumin (HHC), and Octahydrocurcumin (OHC)—on melanogenesis have not been sufficiently explored. We have studied and compared three HMs (THC, HHC, and OHC) with the parent compound, curcumin (PC), on melanin synthesis in B16F10 mouse and MNT-1 human melanoma cells. Our results demonstrated that all the HMs were nontoxic over the concentration range 5–40 µM, while PC was nontoxic at 5 µM but induced toxicity at 20 and 40 µM in B16F10 cells. All three HMs enhanced melanin synthesis, while PC (5 µM) inhibited it. THC (40 µM) significantly stimulated melanin synthesis to a greater degree than HHC and OHC in both B16F10 and MNT-1 cells; the order of melanogenesis stimulation was THC = OHC > HHC in B16F10 mouse cells, while it was THC > HHC > OHC in MNT-1 cells. HMs stimulated melanogenesis by pathways not involving tyrosinase, as neither the intracellular tyrosinase activity nor the protein levels of tyrosinase were affected. In addition, mushroom tyrosinase activity, using L-Dihydroxyphenylalanine (L-DOPA) as the substrate, showed no direct effects of HMs. In summary, our results demonstrate that the HMs enhanced melanogenesis, which establishes that the hydrogenation of the heptadiene moiety of curcumin leads to a loss of its anti-melanogenic activity and instead results in the stimulation of melanogenesis. This stimulation is not further enhanced upon hydrogenation of the β-diketone, which was noted in MNT-1 cells, although the correlation to the number of keto groups differed in B16F10 cells where HHC was the weakest stimulator of melanogenesis. Collectively, THC with both keto groups intact is the best stimulator. Moreover, our results also validate that the electrophilicity of curcumin is necessary for its anti-melanogenic activity, as the non-electrophilic HMs did not inhibit melanogenesis. Furthermore, our results suggest that THC might hold promise as a stimulator of melanogenesis for treatment of hypopigmentation disorders and anti-graying therapies. Future studies to probe the molecular signaling mechanisms and test whether the pro-melanogenic activity of HMs is retained in primary human melanocytes are warranted.

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Melanocytes and Skin Immunity

Cited by 36 publications

References 30 publications

Bioelectric regulation of innate immune system function in regenerating and intact Xenopus laevis

Bioelectric regulation of innate immune system function in regenerating and intact Xenopus laevis

Candida albicans at Host Barrier Sites: Pattern Recognition Receptors and Beyond

Comparative Study of Curcumin and Its Hydrogenated Metabolites, Tetrahydrocurcumin, Hexahydrocurcumin, and Octahydrocurcumin, on Melanogenesis in B16F10 and MNT-1 Cells

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