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• W3211854583 abstract "The chemokine CCL2 is a potential biomarker for progression of inflammatory skin disease. In a new article of the Journal of Investigative Dermatology, Shibuya et al. (2021) use murine experimental models to show that CCL2‒CCR2‒dependent IL-1β secretion by local skin cells and skin-infiltrating neutrophils are key drivers of skin irritation. The chemokine CCL2 is a potential biomarker for progression of inflammatory skin disease. In a new article of the Journal of Investigative Dermatology, Shibuya et al. (2021) use murine experimental models to show that CCL2‒CCR2‒dependent IL-1β secretion by local skin cells and skin-infiltrating neutrophils are key drivers of skin irritation. Clinical Implications•Local CCL2‒CCR2 signaling in the skin is central to the development of irritant contact dermatitis.•CCR2-dependent production of IL-1β by skin-resident cells leads to skin irritation by promoting neutrophil infiltration.•Local inhibition of the CCL2‒CCR2 axis may be a potential therapeutic intervention for irritant contact dermatitis. •Local CCL2‒CCR2 signaling in the skin is central to the development of irritant contact dermatitis.•CCR2-dependent production of IL-1β by skin-resident cells leads to skin irritation by promoting neutrophil infiltration.•Local inhibition of the CCL2‒CCR2 axis may be a potential therapeutic intervention for irritant contact dermatitis. Irritant contact dermatitis (ICD) is a common inflammatory skin disease that is caused by irritants, including chemicals, direct friction, and wet work. It is commonly expressed as hand eczema, and as such, it is an increasingly important cause of work-related disease (Reinholz et al., 2021Reinholz M. Kendziora B. Frey S. Oppel E.M. Ruëff F. Clanner-Engelshofen B.M. et al.Increased prevalence of irritant hand eczema in health care workers in a dermatological clinic due to increased hygiene measures during the SARS-CoV-2 pandemic.Eur J Dermatol. 2021; 31: 392-395Crossref PubMed Scopus (4) Google Scholar). The mechanism of ICD is not well-characterized, and this hampers both differentiation from allergic contact dermatitis and initiation of proper treatment. ICD can be treated with topical and systemic corticosteroids, but responses to other therapies such as calcineurin inhibitors and UV are less effective. In chronic cases, ICD can be treated with systemic retinoid alitretinoin (Diepgen et al., 2015Diepgen T.L. Andersen K.E. Chosidow O. Coenraads P.J. Elsner P. English J. et al.Guidelines for diagnosis, prevention and treatment of hand eczema.J Dtsch Dermatol Ges. 2015; 13: e1-e22Crossref PubMed Scopus (58) Google Scholar). However, new treatments for this debilitating disease are greatly needed (Bonnekoh et al., 2021Bonnekoh H. Vera C. Abad-Perez A. Radetzki S. Neuenschwander M. Specker E. et al.Topical inflammasome inhibition with disulfiram prevents irritant contact dermatitis.Clin Transl Allergy. 2021; 11e12045Crossref PubMed Scopus (3) Google Scholar). In a new article of the Journal of Investigative Dermatology, Shibuya et al., 2021Shibuya R. Ishida Y. Hanakawa S. Kataoka T.R. Takeuchi Y. Murata T. et al.CCL2–CCR2 signaling in the skin drives surfactant-induced irritant contact dermatitis through IL-1β–mediated neutrophil accumulation.J Invest Dermatol. 2022; 142: 571-582Abstract Full Text Full Text PDF Scopus (1) Google Scholar identify novel cellular mechanisms that are crucial for the induction of skin irritation through a complementary series of murine knock-out, chimeric, and parabiosis experiments. The authors hypothesized that the CCL2‒CCR2 axis might be important in driving ICD-associated skin inflammation. CCL2 has previously been implicated as a key mediator of inflammation in various organs (Chen et al., 2020Chen H.J. Antonson A.M. Rajasekera T.A. Patterson J.M. Bailey M.T. Gur T.L. Prenatal stress causes intrauterine inflammation and serotonergic dysfunction, and long-term behavioral deficits through microbe- and CCL2-dependent mechanisms.Transl Psychiatry. 2020; 10: 191Crossref PubMed Scopus (20) Google Scholar; Dimitrijevic et al., 2007Dimitrijevic O.B. Stamatovic S.M. Keep R.F. Andjelkovic A.V. Absence of the chemokine receptor CCR2 protects against cerebral ischemia/reperfusion injury in mice.Stroke. 2007; 38: 1345-1353Crossref PubMed Scopus (265) Google Scholar; Wolf et al., 2019Wolf M. Clay S.M. Zheng S. Pan P. Chan M.F. MMP12 inhibits corneal neovascularization and inflammation through regulation of CCL2.Sci Rep. 2019; 9: 11579Crossref PubMed Scopus (11) Google Scholar) as well as in inflammatory disorders, including atherosclerosis, rheumatoid arthritis, allergic asthma, psoriasis, and atopic dermatitis (AD) (Behfar et al., 2018Behfar S. Hassanshahi G. Nazari A. Khorramdelazad H. A brief look at the role of monocyte chemoattractant protein-1 (CCL2) in the pathophysiology of psoriasis.Cytokine. 2018; 110: 226-231Crossref PubMed Scopus (29) Google Scholar; He et al., 2020He H. Suryawanshi H. Morozov P. Gay-Mimbrera J. Del Duca E. Kim H.J. et al.Single-cell transcriptome analysis of human skin identifies novel fibroblast subpopulation and enrichment of immune subsets in atopic dermatitis.J Allergy Clin Immunol. 2020; 145: 1615-1628Abstract Full Text Full Text PDF PubMed Scopus (89) Google Scholar; Jiang et al., 2019Jiang S. Wang Q. Wang Y. Song X. Zhang Y. Blockade of CCL2/CCR2 signaling pathway prevents inflammatory monocyte recruitment and attenuates OVA-Induced allergic asthma in mice.Immunol Lett. 2019; 214: 30-36Crossref PubMed Scopus (11) Google Scholar). Moreover, CCL2‒CCR2 signaling appears to be involved in wound healing (Whelan et al., 2020Whelan D.S. Caplice N.M. Clover A.J.P. Mesenchymal stromal cell derived CCL2 is required for accelerated wound healing.Sci Rep. 2020; 10: 2642Crossref PubMed Scopus (12) Google Scholar). CCL2 exerts diverse functions on lymphoid and myeloid immune cells, showing immunomodulatory properties beyond chemotaxis (Gschwandtner et al., 2019Gschwandtner M. Derler R. Midwood K.S. More than just attractive: how CCL2 influences myeloid cell behavior beyond chemotaxis.Front Immunol. 2019; 10: 2759Crossref PubMed Scopus (155) Google Scholar). Interestingly, nonimmune cells such as endothelial cells, fibroblasts, and epithelial cells also produce CCL2. CCL2 secretion in the skin appears to recruit inflammatory monocytes, dendritic cells (DCs), and memory T cells. The receptors that bind CCL2 include CCR1, CCR2, and CCR3. CCR2 is the main receptor for CCL2 in inflammation, and it is highly expressed by blood monocytes and skin macrophages (Dyer et al., 2019Dyer D.P. Medina-Ruiz L. Bartolini R. Schuette F. Hughes C.E. Pallas K. et al.Chemokine receptor redundancy and specificity are context dependent.Immunity. 2019; 50 (378–89.e5)Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar). To test the hypothesis that the CCL2‒CCR2 axis might be involved in ICD, Shibuya et al., 2021Shibuya R. Ishida Y. Hanakawa S. Kataoka T.R. Takeuchi Y. Murata T. et al.CCL2–CCR2 signaling in the skin drives surfactant-induced irritant contact dermatitis through IL-1β–mediated neutrophil accumulation.J Invest Dermatol. 2022; 142: 571-582Abstract Full Text Full Text PDF Scopus (1) Google Scholar used both CCL2- and CCR2-deficient mice. Both strains showed attenuated cumulative ICD responses to repeated-dose exposure to the irritant SDS, exhibiting less ear swelling; transepidermal water loss; and recruitment of neutrophils, monocytes, and eosinophils. These results suggested that the CCL2‒CCR2 axis is a key driver of this type of inflammation. To learn whether Ccr2–/– cells responsible for ICD are circulating cells, the authors constructed chimeras with bone marrow (BM) transplanted from wild-type (WT) or Ccr2–/– mice to either WT or Ccr2–/– mice that had their own BM removed by irradiation (Holl, 2013Holl E.K. Generation of bone marrow and fetal liver chimeric mice.Methods Mol Biol. 2013; 1032: 315-321Crossref PubMed Scopus (12) Google Scholar). When CCR2 was lacking in the radioresistant cell compartment, ICD responses were attenuated, and WT BM could not rescue the response. In contrast, when irradiated WT mice were reconstituted with Ccr2–/– BM, fully blown ICD responses developed, including ear swelling and infiltration of neutrophils and eosinophils. Strikingly, in Ccr2–/– BM‒reconstituted WT mice, there was no visible infiltration of monocytes. These results showed that monocytes are redundant to CCR2-dependent induction of SDS-induced ICD. The attenuated accumulation of circulating cells was not due to inadequate BM engraftment because circulating cells in peripheral blood were similar in both WT and Ccr2–/– chimeras. To gain further insights into the mechanism, the authors created parabionts (see Supplementary Figure in the article) in which two mice, one Ccr2–/– (CD45.2+) and one WT (CD45.1+), were surgically joined to share a common blood circulation, as shown by the fact that half of the peripheral blood cells were CD45.1+, and half were CD45.2+. When the ears of the two parabiont mice were treated with SDS, the ICD response was attenuated in Ccr2–/– mice but not in the WT mice, shown by the measurement of ear swelling and the accumulation of monocytes and neutrophils. This proved that the CCR2-mediated effect, resulting in ICD, is dependent on cells that are resident in the skin and not on inflammatory cells that are recruited from blood. The inflammatory response in ICD results from activated innate immune signaling after skin damage caused by external stimuli (Lee et al., 2013Lee H.Y. Stieger M. Yawalkar N. Kakeda M. Cytokines and chemokines in irritant contact dermatitis.Mediators Inflamm. 2013; 2013: 916497Crossref PubMed Scopus (72) Google Scholar). To assess the role of innate immune cells in ICD, Shibuya et al., 2021Shibuya R. Ishida Y. Hanakawa S. Kataoka T.R. Takeuchi Y. Murata T. et al.CCL2–CCR2 signaling in the skin drives surfactant-induced irritant contact dermatitis through IL-1β–mediated neutrophil accumulation.J Invest Dermatol. 2022; 142: 571-582Abstract Full Text Full Text PDF Scopus (1) Google Scholar treated mice with anti-Ly6G (Boivin et al., 2020Boivin G. Faget J. Ancey P.B. Gkasti A. Mussard J. Engblom C. et al.Durable and controlled depletion of neutrophils in mice.Nat Commun. 2020; 11: 2762Crossref PubMed Scopus (56) Google Scholar) to remove neutrophils. This resulted in the amelioration of ICD and impairment not only of neutrophil infiltration but also of the recruitment of eosinophils and monocytes, suggesting that neutrophils are key players in CCR2-mediated ICD. Finally, RNA-sequencing analysis revealed that Ccr2–/– mice have significantly lower expression of neutrophil migration‒associated genes, including Il1β, than WT mice. IL-1β neutralization with antibody also attenuated neutrophil accumulation in WT mice, whereas intradermal injection of IL-1β restored ICD in both WT mice treated with IL-1β antibody and Ccr2–/– mice. This suggests that CCR2-dependent production of IL-1β is critical for the development of ICD. What are the radioresistant cells that this study pinpoints as responsible for IL-1β production and the initiation of ICD? Their exact location and identity are not yet established, but Shibuya et al., 2021Shibuya R. Ishida Y. Hanakawa S. Kataoka T.R. Takeuchi Y. Murata T. et al.CCL2–CCR2 signaling in the skin drives surfactant-induced irritant contact dermatitis through IL-1β–mediated neutrophil accumulation.J Invest Dermatol. 2022; 142: 571-582Abstract Full Text Full Text PDF Scopus (1) Google Scholar showed that the majority of IL-1β–expressing skin cells stain positive for vimentin. Vimentin was initially discovered in fibroblasts (Geisler et al., 1983Geisler N. Plessmann U. Weber K. Amino acid sequence characterization of mammalian vimentin, the mesenchymal intermediate filament protein.FEBS Lett. 1983; 163: 22-24Crossref PubMed Scopus (29) Google Scholar) but has now been detected in various immature cells, including mesenchymal stem cells (MSCs). In human skin, vimentin is expressed in fibroblasts, endothelial cells of blood vessels, in smooth vascular musculature, in melanocytes, in macrophages, and in T cells (Uhlén et al., 2015Uhlén M. Fagerberg L. Hallström B.M. Lindskog C. Oksvold P. Mardinoglu A. et al.Proteomics. Tissue-based map of the human proteome.Science. 2015; 347: 1260419Crossref PubMed Scopus (6164) Google Scholar). MSCs migrate to sites of inflammation, and they have recently gained considerable attention in the context of skin inflammation. MSCs have a potent immunoregulatory capacity (Castro-Manrreza and Montesinos, 2015Castro-Manrreza M.E. Montesinos J.J. Immunoregulation by mesenchymal stem cells: biological aspects and clinical applications.J Immunol Res. 2015; 2015: 394917Crossref PubMed Scopus (262) Google Scholar), and they promote wound healing in a CCL2-dependent manner (Whelan et al., 2020Whelan D.S. Caplice N.M. Clover A.J.P. Mesenchymal stromal cell derived CCL2 is required for accelerated wound healing.Sci Rep. 2020; 10: 2642Crossref PubMed Scopus (12) Google Scholar). MSCs can be isolated from both epidermal and dermal layers of the skin (Castro-Manrreza et al., 2019Castro-Manrreza M.E. Bonifaz L. Castro-Escamilla O. Monroy-García A. Cortés-Morales A. Hernández-Estévez E. et al.Mesenchymal stromal cells from the epidermis and dermis of psoriasis patients: morphology, immunophenotype, differentiation patterns, and regulation of T cell proliferation.Stem Cells Int. 2019; 2019: 4541797Crossref PubMed Scopus (12) Google Scholar), and they have been observed in psoriasis (Liu et al., 2014Liu R. Wang Y. Zhao X. Yang Y. Zhang K. Lymphocyte inhibition is compromised in mesenchymal stem cells from psoriatic skin.Eur J Dermatol. 2014; 24: 560-567Crossref PubMed Scopus (35) Google Scholar), but whether they contribute to this disease remains to be established. A considerable obstacle in MSC-related investigations is the lack of definite markers, requiring the utilization of a number of criteria to identify MSCs with certainty. Shibuya et al., 2021Shibuya R. Ishida Y. Hanakawa S. Kataoka T.R. Takeuchi Y. Murata T. et al.CCL2–CCR2 signaling in the skin drives surfactant-induced irritant contact dermatitis through IL-1β–mediated neutrophil accumulation.J Invest Dermatol. 2022; 142: 571-582Abstract Full Text Full Text PDF Scopus (1) Google Scholar show that many of the CCL2-positive cells in SDS-irritated skin are positive for vimentin, suggesting the involvement of fibroblasts; endothelial cells; smooth muscle cells; or perhaps other skin residential cells, such as MSCs, as sources of this pivotal chemokine. An inflammatory role for fibroblasts has recently been proposed by He et al., 2020He H. Suryawanshi H. Morozov P. Gay-Mimbrera J. Del Duca E. Kim H.J. et al.Single-cell transcriptome analysis of human skin identifies novel fibroblast subpopulation and enrichment of immune subsets in atopic dermatitis.J Allergy Clin Immunol. 2020; 145: 1615-1628Abstract Full Text Full Text PDF PubMed Scopus (89) Google Scholar, who explored the skin transcriptome in AD at the single-cell level. Their study revealed a novel subset of fibroblasts expressing both CCL2 and CCL19 that interacted closely with DCs and macrophages. Previous studies have shown that binding of CCL2 to CCR2 triggers nuclear translocation of NF-KB, which is crucial for DC maturation and migration from the skin to draining lymph nodes for antigen presentation to T cells (Jimenez et al., 2010Jimenez F. Quinones M.P. Martinez H.G. Estrada C.A. Clark K. Garavito E. et al.CCR2 plays a critical role in dendritic cell maturation: possible role of CCL2 and NF-kappa B.J Immunol. 2010; 184: 5571-5581Crossref PubMed Scopus (70) Google Scholar). Nevertheless, the identity of the skin-resident, radioresistant cell that responds to CCL2 and produces IL-1β remains a mystery. In the skin, the main cell types that express CCR2 are tissue-resident leukocytes. In contrast to most leukocytes, many of these tissue-resident leukocytes are highly radioresistant, including macrophages and DCs with fetal origin (Bogunovic et al., 2006Bogunovic M. Ginhoux F. Wagers A. Loubeau M. Isola L.M. Lubrano L. et al.Identification of a radio-resistant and cycling dermal dendritic cell population in mice and men.J Exp Med. 2006; 203: 2627-2638Crossref PubMed Scopus (115) Google Scholar) or mast cells (Soule et al., 2007Soule B.P. Brown J.M. Kushnir-Sukhov N.M. Simone N.L. Mitchell J.B. Metcalfe D.D. Effects of gamma radiation on FcepsilonRI and TLR-mediated mast cell activation.J Immunol. 2007; 179: 3276-3286Crossref PubMed Scopus (33) Google Scholar). Importantly, CCL2‒CCR2 signaling activates both DC and macrophages, and it triggers mast cell degranulation (Campbell et al., 1999Campbell E.M. Charo I.F. Kunkel S.L. Strieter R.M. Boring L. Gosling J. et al.Monocyte chemoattractant protein-1 mediates cockroach allergen-induced bronchial hyperreactivity in normal but not CCR2-/- mice: the role of mast cells.J Immunol. 1999; 163: 2160-2167PubMed Google Scholar). Thus, it is possible that the responsible cell type is a tissue-resident macrophage, an Langerhans cell, or a mast cell or a combination thereof (Figure 1). In aggregate, the results of Shibuya et al., 2021Shibuya R. Ishida Y. Hanakawa S. Kataoka T.R. Takeuchi Y. Murata T. et al.CCL2–CCR2 signaling in the skin drives surfactant-induced irritant contact dermatitis through IL-1β–mediated neutrophil accumulation.J Invest Dermatol. 2022; 142: 571-582Abstract Full Text Full Text PDF Scopus (1) Google Scholar and others suggest a key role for skin-resident cells in driving skin irritation, involving intricate cell to cell communication involving the CCL2‒CCR2 axis. The study by Shibuya et al., 2021Shibuya R. Ishida Y. Hanakawa S. Kataoka T.R. Takeuchi Y. Murata T. et al.CCL2–CCR2 signaling in the skin drives surfactant-induced irritant contact dermatitis through IL-1β–mediated neutrophil accumulation.J Invest Dermatol. 2022; 142: 571-582Abstract Full Text Full Text PDF Scopus (1) Google Scholar uniquely pinpoints the local production of IL-1β and the recruitment of neutrophils as key initiators of skin irritation. Surprisingly, the study shows that monocytes play a minor role in the context, although many other studies have identified this cell subset as a major player in conditions such as psoriasis (Behfar et al., 2018Behfar S. Hassanshahi G. Nazari A. Khorramdelazad H. A brief look at the role of monocyte chemoattractant protein-1 (CCL2) in the pathophysiology of psoriasis.Cytokine. 2018; 110: 226-231Crossref PubMed Scopus (29) Google Scholar) or wound healing (Whelan et al., 2020Whelan D.S. Caplice N.M. Clover A.J.P. Mesenchymal stromal cell derived CCL2 is required for accelerated wound healing.Sci Rep. 2020; 10: 2642Crossref PubMed Scopus (12) Google Scholar). The exact role and nature of the mechanisms that lead to IL-1β production and the cellular source of IL-1β remain unknown. In future studies, it will be important to determine whether this phenomenon is generalizable to all types of irritant reactions irrespective of the causative agent and importantly to human ICD." @default.
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• W3211854583 title "New Key Players in Irritant Contact Dermatitis: Residential Skin Cells and Neutrophils Drive Inflammation" @default.
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