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[PMID]: 29386427 [Au] Autor: Tachibana M [Ad] Endereço: Laboratory of Biotechnology and Therapeutics, Graduate School of Pharmaceutical Sciences, Osaka University. [Ti] Título: [The Immunosuppressive Function of Myeloid-derived Suppressor Cells Is Regulated by the HMGB1-TLR4 Axis]. [So] Source: Yakugaku Zasshi;138(2):143-148, 2018. [Is] ISSN: 1347-5231 [Cp] País de publicação: Japan [La] Idioma: jpn [Ab] Resumo: 　Myeloid-derived suppressor cells (MDSCs) accumulate under pathological conditions, including cancer and chronic inflammation, and they suppress various immune responses such as T cell proliferation. Although several inflammatory signals enhance the differentiation and/or function of MDSCs, it is not clear which factors regulate their differentiation and immunosuppressive function. It has been highlighted that damage-associated molecular patterns (DAMPs) play important roles in the induction of inflammation. One of the DAMPs, the high mobility group box 1 (HMGB1), is released from necrotic cells and secreted by macrophages. It has been shown that HMGB1 level is elevated in tumors and tumor-bearing hosts. It has also been reported that HMGB1 transduces intracellular signaling via several receptors, including the receptor for advanced glycation end-products (RAGE) and the toll-like receptor (TLR)4, both of which enhance the differentiation and/or function of MDSCs. However, the effects of HMGB1 on MDSCs remain unclear. In the present study, we examined the effect of HMGB1 on in vitro MDSC differentiation and immunosuppressive functions. Since murine bone marrow (BM) cells can differentiate into MDSCs upon granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation for 4 d in vitro, we cultured murine BM cells in the presence of HMGB1 and GM-CSF. The results demonstrated that HMGB1 enhanced the suppressive activity of in vitro MDSCs, depending on TLR4, whereas lipopolysaccharide (LPS), one of the TLR4 ligands, interfered with this differentiation and immunosuppressive activity of in vitro MDSCs, depending on TLR4. Our findings thus suggest that the HMGB1-TLR4 axis enhances the immunosuppressive function of MDSCs. [Mh] Termos MeSH primário: Células da Medula Óssea/imunologia Proteína HMGB1/fisiologia Imunossupressão Transdução de Sinais/fisiologia Receptor 4 Toll-Like/fisiologia [Mh] Termos MeSH secundário: Alarminas Animais Células da Medula Óssea/citologia Diferenciação Celular Produtos Finais de Glicação Avançada Seres Humanos Inflamação/imunologia Camundongos [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Alarmins); 0 (Glycation End Products, Advanced); 0 (HMGB1 Protein); 0 (Toll-Like Receptor 4) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180228 [Lr] Data última revisão: 180228 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180202 [St] Status: MEDLINE [do] DOI: 10.1248/yakushi.17-00158

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[PMID]: 28746820 [Au] Autor: Rai V; Agrawal DK [Ad] Endereço: Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE 68178, USA. [Ti] Título: The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques. [So] Source: Can J Physiol Pharmacol;95(10):1245-1253, 2017 Oct. [Is] ISSN: 1205-7541 [Cp] País de publicação: Canada [La] Idioma: eng [Ab] Resumo: Atherosclerosis is a chronic inflammatory disease resulting in the formation of the atherosclerotic plaque. Plaque formation starts with the inflammation in fatty streaks and progresses through atheroma, atheromatous plaque, and fibroatheroma leading to development of stable plaque. Hypercholesterolemia, dyslipidemia, and hyperglycemia are the risk factors for atherosclerosis. Inflammation, infection with viruses and bacteria, and dysregulation in the endothelial and vascular smooth muscle cells leads to advanced plaque formation. Death of the cells in the intima due to inflammation results in secretion of damage-associated molecular patterns (DAMPs) such as high mobility group box 1 (HMGB1), receptor for advanced glycation end products (RAGE), alarmins (S100A8, S100A9, S100A12, and oxidized low-density lipoproteins), and infection with pathogens leads to secretion of pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharides, lipoteichoic acids, and peptidoglycans. DAMPs and PAMPs further activate the inflammatory surface receptors such as TREM-1 and toll-like receptors and downstream signaling kinases and transcription factors leading to increased secretion of pro-inflammatory cytokines such as tumor necrosis factor α, interleukin (IL)-1ß, IL-6, and interferon-γ and matrix metalloproteinases (MMPs). These mediators and cytokines along with MMPs render the plaque vulnerable for rupture leading to ischemic events. In this review, we have discussed the role of DAMPs and PAMPs in association with inflammation-mediated plaque vulnerability. [Mh] Termos MeSH primário: Alarminas/metabolismo Artérias/metabolismo Aterosclerose/metabolismo Mediadores da Inflamação/metabolismo Inflamação/metabolismo Padrões Moleculares Associados a Patógenos/metabolismo Placa Aterosclerótica [Mh] Termos MeSH secundário: Alarminas/imunologia Animais Artérias/imunologia Artérias/patologia Aterosclerose/imunologia Aterosclerose/patologia Seres Humanos Inflamação/imunologia Inflamação/patologia Mediadores da Inflamação/imunologia Padrões Moleculares Associados a Patógenos/imunologia Prognóstico Fatores de Risco Ruptura Espontânea Transdução de Sinais [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Alarmins); 0 (Inflammation Mediators); 0 (Pathogen-Associated Molecular Pattern Molecules) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180205 [Lr] Data última revisão: 180205 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170727 [St] Status: MEDLINE [do] DOI: 10.1139/cjpp-2016-0664

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[PMID]: 28452964 [Au] Autor: Picca A; Lezza AMS; Leeuwenburgh C; Pesce V; Calvani R; Landi F; Bernabei R; Marzetti E [Ad] Endereço: Department of Geriatrics, Neuroscience and Orthopedics, Catholic University of the Sacred Heart School of Medicine, 00168 Rome, Italy. anna.picca1@gmail.com. [Ti] Título: Fueling Inflamm-Aging through Mitochondrial Dysfunction: Mechanisms and Molecular Targets. [So] Source: Int J Mol Sci;18(5), 2017 Apr 28. [Is] ISSN: 1422-0067 [Cp] País de publicação: Switzerland [La] Idioma: eng [Ab] Resumo: Among the complex determinants of aging, mitochondrial dysfunction has been in the spotlight for a long time. As the hub for many cellular functions, the maintenance of an adequate pool of functional mitochondria is crucial for tissue homeostasis. Their unique role in energy supply makes these organelles essential, especially in those tissues strictly dependent on oxidative metabolism. Mitochondrial quality control (MQC) is ensured by pathways related to protein folding and degradation as well as by processes involving the entire organelle, such as biogenesis, dynamics, and mitophagy. Dysfunctional MQC, oxidative stress and inflammation are hallmarks of senescence and chronic degenerative diseases. One of the consequences of age-related failing MQC and oxidative stress is the release of mitochondria-derived damage-associated molecular patterns (DAMPs). Through their bacterial ancestry, these molecules contribute to mounting an inflammatory response by interacting with receptors similar to those involved in pathogen-associated responses. Mitochondrial DAMPs, especially cell-free mitochondrial DNA, have recently become the subject of intensive research because of their possible involvement in conditions associated with inflammation, such as aging and degenerative diseases. Here, we review the contribution of mitochondrial DAMPs to inflammation and discuss some of the mechanisms at the basis of their generation. [Mh] Termos MeSH primário: Envelhecimento Inflamação Mitocôndrias/metabolismo [Mh] Termos MeSH secundário: Alarminas/metabolismo DNA Mitocondrial/metabolismo Seres Humanos Mitocôndrias/genética Degradação Mitocondrial Dinâmica Mitocondrial Estresse Oxidativo [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Alarmins); 0 (DNA, Mitochondrial) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180122 [Lr] Data última revisão: 180122 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170429 [St] Status: MEDLINE

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[PMID]: 29193305 [Au] Autor: Blom K; Elshafie AI; Jönsson UB; Rönnelid J; Håkansson LD; Venge P [Ad] Endereço: Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. [Ti] Título: The genetically determined production of the alarmin eosinophil-derived neurotoxin is reduced in visceral leishmaniasis. [So] Source: APMIS;126(1):85-91, 2018 Jan. [Is] ISSN: 1600-0463 [Cp] País de publicação: Denmark [La] Idioma: eng [Ab] Resumo: Visceral leishmaniasis (VL) is the most severe form of leishmaniasis. Recent findings indicate that dendritic cells have a key role in the defense against the Leishmania parasite and that the activity of this cell may be modified by the eosinophil secretory protein eosinophil-derived neurotoxin (EDN). We hypothesized that the interactions between dendritic cells and EDN might be of importance in the disease development. Cellular content of EDN was analyzed by ELISA. The single-nucleotide polymorphisms at positions 405, 416, and 1122 in the EDN gene were analyzed by real-time PCR with TaqMan reagents. The study cohorts comprised 239 Sudanese subjects (65 healthy controls and 174 with VL) and 300 healthy Swedish controls. The eosinophil content of EDN was lower in VL as compared with controls (p < 0.0001). The EDN405 (G>C) genotype distribution was similar among Swedish and Sudanese controls, whereas VL subjects had a higher prevalence of the EDN405-GG genotype (p < 0.0001). The content of EDN in the eosinophils was closely linked to the EDN405 polymorphism (p = 0.0002). Our findings suggest that the predisposition to acquire VL is related to the genetic polymorphism of the EDN gene and the reduced production by the eosinophil of this gene product. [Mh] Termos MeSH primário: Alarminas/genética Neurotoxina Derivada de Eosinófilo/genética Leishmaniose Visceral/genética [Mh] Termos MeSH secundário: Células Dendríticas/imunologia Predisposição Genética para Doença Genótipo Seres Humanos Leishmaniose Visceral/imunologia Polimorfismo de Nucleotídeo Único Receptor 2 Toll-Like/fisiologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Alarmins); 0 (TLR2 protein, human); 0 (Toll-Like Receptor 2); EC 3.1.- (Eosinophil-Derived Neurotoxin) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180108 [Lr] Data última revisão: 180108 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171202 [St] Status: MEDLINE [do] DOI: 10.1111/apm.12780

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[PMID]: 28911261 [Au] Autor: Klee NS; McCarthy CG; Martinez-Quinones P; Webb RC [Ad] Endereço: Department of Physiology, Medical College of Georgia at Augusta University, 1120 15th Street, Augusta, GA 30912, USA. [Ti] Título: Out of the frying pan and into the fire: damage-associated molecular patterns and cardiovascular toxicity following cancer therapy. [So] Source: Ther Adv Cardiovasc Dis;11(11):297-317, 2017 Nov. [Is] ISSN: 1753-9455 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Cardio-oncology is a new and rapidly expanding field that merges cancer and cardiovascular disease. Cardiovascular disease is an omnipresent side effect of cancer therapy; in fact, it is the second leading cause of death in cancer survivors after recurrent cancer. It has been well documented that many cancer chemotherapeutic agents cause cardiovascular toxicity. Nonetheless, the underlying cause of cancer therapy-induced cardiovascular toxicity is largely unknown. In this review, we discuss the potential role of damage-associated molecular patterns (DAMPs) as an underlying contributor to cancer therapy-induced cardiovascular toxicity. With an increasing number of cancer patients, as well as extended life expectancy, understanding the mechanisms underlying cancer therapy-induced cardiovascular disease is of the utmost importance to ensure that cancer is the only disease burden that cancer survivors have to endure. [Mh] Termos MeSH primário: Alarminas/metabolismo Antineoplásicos/efeitos adversos Doenças Cardiovasculares/induzido quimicamente Sistema Cardiovascular/efeitos dos fármacos Sistema Cardiovascular/efeitos da radiação Neoplasias/terapia Lesões por Radiação/etiologia [Mh] Termos MeSH secundário: Animais Cardiotoxicidade Doenças Cardiovasculares/metabolismo Doenças Cardiovasculares/patologia Doenças Cardiovasculares/fisiopatologia Sistema Cardiovascular/metabolismo Sistema Cardiovascular/patologia Morte Celular/efeitos dos fármacos Morte Celular/efeitos da radiação Seres Humanos Lesões por Radiação/metabolismo Lesões por Radiação/patologia Lesões por Radiação/fisiopatologia Radioterapia/efeitos adversos Medição de Risco Fatores de Risco Transdução de Sinais/efeitos dos fármacos Transdução de Sinais/efeitos da radiação [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Alarmins); 0 (Antineoplastic Agents) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171030 [Lr] Data última revisão: 171030 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170916 [St] Status: MEDLINE [do] DOI: 10.1177/1753944717729141

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[PMID]: 28608409 [Au] Autor: Murakami T; Homma Y; Matsuyama R; Mori R; Miyake K; Tanaka Y; Den K; Nagashima Y; Nakazawa M; Hiroshima Y; Ueda M; Tanaka K; Hoffman RM; Bouvet M; Endo I [Ad] Endereço: Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan. [Ti] Título: Neoadjuvant chemoradiotherapy of pancreatic cancer induces a favorable immunogenic tumor microenvironment associated with increased major histocompatibility complex class I-related chain A/B expression. [So] Source: J Surg Oncol;116(3):416-426, 2017 Sep. [Is] ISSN: 1096-9098 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: Damage-associated molecular patterns (DAMPs) are related to immune responses in malignant tumors including tumor-infiltrating lymphocytes (TILs). The aim of the present study was to determine the relationship between expression of components of DAMPs and TILs in pancreatic cancer patients who underwent neoadjuvant chemoradiotherapy (NACRT) versus those who did not. METHODS: NACRT was administered to 51 patients with borderline-resectable pancreatic cancer and not to 33 patients with resectable pancreatic cancer. Resected specimens were analyzed for the presence of DAMPs, major histocompatibility complex class I-related chain A/B (MICA/B), and CD8 TILs, CD4 TILs, and forkhead box P3 positive (Foxp3 ) TILs. The Treg/TIL ratio was obtained by dividing the number of Foxp3 TILs, a surrogate for regulatory T cells, by the sum of CD8 and CD4 TILs. RESULTS: Overexpression of calreticulin, Hsp70, and MICA/B were all significantly correlated with NACRT administration. In the NACRT group, high MICA/B expression was associated with a low Treg/TIL ratio, indicating a favorable immunogenic tumor microenvironment. Patients with a lower Treg/TIL ratio had longer survival. CONCLUSIONS: Overexpression of MICA/B, a component of DAMPs induced by NACRT, may play an important role in acquiring a favorable immune response for pancreatic cancer which contributes to longer survival, suggesting the potential of immunotherapy of this recalcitrant disease, especially for patients with overexpression of DAMPs. [Mh] Termos MeSH primário: Quimiorradioterapia Antígenos de Histocompatibilidade Classe I/metabolismo Terapia Neoadjuvante Neoplasias Pancreáticas/metabolismo Neoplasias Pancreáticas/terapia [Mh] Termos MeSH secundário: Idoso Alarminas/metabolismo Feminino Seres Humanos Linfócitos do Interstício Tumoral/fisiologia Masculino Meia-Idade Estudos Retrospectivos Microambiente Tumoral [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Alarmins); 0 (Histocompatibility Antigens Class I); 0 (MHC class I-related chain A); 0 (MICB antigen) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170908 [Lr] Data última revisão: 170908 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170614 [St] Status: MEDLINE [do] DOI: 10.1002/jso.24681

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[PMID]: 28596295 [Au] Autor: Pouwels SD; Faiz A; den Boef LE; Gras R; van den Berge M; Boezen HM; Korstanje R; Ten Hacken NHT; van Oosterhout AJM; Heijink IH; Nawijn MC [Ad] Endereço: Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; s.d.pouwels@umcg.nl. [Ti] Título: Genetic variance is associated with susceptibility for cigarette smoke-induced DAMP release in mice. [So] Source: Am J Physiol Lung Cell Mol Physiol;313(3):L559-L580, 2017 Sep 01. [Is] ISSN: 1522-1504 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Chronic obstructive pulmonary disease (COPD) is characterized by unresolved neutrophilic airway inflammation and is caused by chronic exposure to toxic gases, such as cigarette smoke (CS), in genetically susceptible individuals. Recent data indicate a role for damage-associated molecular patterns (DAMPs) in COPD. Here, we investigated the genetics of CS-induced DAMP release in 28 inbred mouse strains. Subsequently, in lung tissue from a subset of strains, the expression of the identified candidate genes was analyzed. We tested whether small interfering RNA-dependent knockdown of candidate genes altered the susceptibility of the human A549 cell line to CS-induced cell death and DAMP release. Furthermore, we tested whether these genes were differentially regulated by CS exposure in bronchial brushings obtained from individuals with a family history indicative of either the presence or absence of susceptibility for COPD. We observed that, of the four DAMPs tested, double-stranded DNA (dsDNA) showed the highest correlation with neutrophilic airway inflammation. Genetic analyses identified 11 candidate genes governing either CS-induced or basal dsDNA release in mice. Two candidate genes ( and ) showed differential expression in lung tissue on CS exposure between susceptible and nonsusceptible mouse strains. Knockdown of and in A549 cells altered susceptibility to CS extract-induced cell death and DAMP release. In bronchial brushings, CS-induced expression of and was significantly different between individuals susceptible or nonsusceptible for COPD. Our study shows that genetic variance in a mouse model is associated with CS-induced DAMP release, and that this might contribute to susceptibility for COPD. [Mh] Termos MeSH primário: Alarminas/metabolismo Estudos de Associação Genética Predisposição Genética para Doença Variação Genética Fumar/efeitos adversos [Mh] Termos MeSH secundário: Animais Líquido da Lavagem Broncoalveolar Linhagem Celular DNA/metabolismo Regulação para Baixo/genética Epitélio/metabolismo Feminino Haplótipos/genética Seres Humanos Contagem de Leucócitos Camundongos Polimorfismo de Nucleotídeo Único/genética Doença Pulmonar Obstrutiva Crônica/genética Doença Pulmonar Obstrutiva Crônica/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Alarmins); 9007-49-2 (DNA) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170918 [Lr] Data última revisão: 170918 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170610 [St] Status: MEDLINE [do] DOI: 10.1152/ajplung.00466.2016

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[PMID]: 28521686 [Au] Autor: Samara P; Karachaliou CE; Ioannou K; Papaioannou NE; Voutsas IF; Zikos C; Pirmettis I; Papadopoulos M; Kalbacher H; Livaniou E; Tsitsilonis OE; Voelter W [Ad] Endereço: Section of Animal & Human Physiology, Department of Biology, National and Kapodistrian University of Athens, Panepistimiopolis, Athens 15784, Greece. [Ti] Título: Prothymosin Alpha: An Alarmin and More... [So] Source: Curr Med Chem;24(17):1747-1760, 2017. [Is] ISSN: 1875-533X [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: BACKGROUND/OBJECTIVE: Prothymosin alpha (proTα) is a ubiquitous polypeptide first isolated by Haritos in 1984, whose role still remains partly elusive. We know that proTα acts both, intracellularly, as an anti-apoptotic and proliferation mediator, and extracellularly, as a biologic response modifier mediating immune responses similarly to molecules termed as "alarmins". Our research team pioneered the elucidation of the mechanisms underlying the observed activities of proTα. RESULTS: We were the first to demonstrate that proTα levels increase during normal and abnormal cell proliferation. We showed that proTα acts pleiotropically, inducing immunomodulatory effects on immune cell populations. We revealed that the immunoreactive region of proTα is the carboxyterminal decapeptide proTα(100-109) and both molecules stimulate innate immune responses, signaling through Toll-like receptors (TLRs), specifically TLR-4. We reported that proTα and proTα(100-109) bind on the surface of human neutrophils on sites involving TLR-4, and cell activation is complemented by cytoplasmic calcium ion influx. Further, we showed that proTα and proTα(100-109) act as adjuvants upstream of lymphocyte stimulation and, in the presence of antigen, promote the expansion of antigen-reactive effectors. Most recently, we reported that proTα(100-109) may accumulate in experimentally inflamed sites and can serve as a surrogate biomarker in severe bacterial infections, proposing that extracellular release of proTα or proTα(100- 109) alerts the immune system during conditions of danger. CONCLUSION: We, therefore, suggest that proTα, and likely proTα(100-109), act as alarmins, being important immune mediators as well as biomarkers, and could eventually become targets for new therapeutic/diagnostic approaches in immune-related diseases like cancer, inflammation, and sepsis. [Mh] Termos MeSH primário: Alarminas/metabolismo Precursores de Proteínas/metabolismo Timosina/análogos & derivados [Mh] Termos MeSH secundário: Alarminas/química Doenças Autoimunes/metabolismo Doenças Autoimunes/patologia Seres Humanos Imunidade Inata/efeitos dos fármacos Células Matadoras Naturais/citologia Neoplasias/tratamento farmacológico Neoplasias/metabolismo Neoplasias/patologia Precursores de Proteínas/química Precursores de Proteínas/uso terapêutico Sepse/metabolismo Sepse/patologia Linfócitos T/citologia Linfócitos T/efeitos dos fármacos Linfócitos T/metabolismo Timosina/química Timosina/metabolismo Timosina/uso terapêutico Receptores Toll-Like/química Receptores Toll-Like/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Alarmins); 0 (Protein Precursors); 0 (Toll-Like Receptors); 0 (prothymosin alpha); 61512-21-8 (Thymosin) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170908 [Lr] Data última revisão: 170908 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170520 [St] Status: MEDLINE [do] DOI: 10.2174/0929867324666170518110033

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[PMID]: 28404746 [Au] Autor: Handly LN; Wollman R [Ad] Endereço: Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, CA 90095. [Ti] Título: Wound-induced Ca wave propagates through a simple release and diffusion mechanism. [So] Source: Mol Biol Cell;28(11):1457-1466, 2017 Jun 01. [Is] ISSN: 1939-4586 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Damage-associated molecular patterns (DAMPs) are critical mediators of information concerning tissue damage from damaged cells to neighboring healthy cells. ATP acts as an effective DAMP when released into extracellular space from damaged cells. Extracellular ATP receptors monitor tissue damage and activate a Ca wave in the surrounding healthy cells. How the Ca wave propagates through cells after a wound is unclear. Ca wave activation can occur extracellularly via external receptors or intracellularly through GAP junctions. Three potential mechanisms to propagate the Ca wave are source and sink, amplifying wave, and release and diffusion. Both source and sink and amplifying wave regulate ATP levels using hydrolysis or secretion, respectively, whereas release and diffusion relies on dilution. Here we systematically test these hypotheses using a microfluidics assay to mechanically wound an epithelial monolayer in combination with direct manipulation of ATP hydrolysis and release. We show that a release and diffusion model sufficiently explains Ca -wave propagation after an epithelial wound. A release and diffusion model combines the benefits of fast activation at short length scales with a self-limiting response to prevent unnecessary inflammatory responses harmful to the organism. [Mh] Termos MeSH primário: Alarminas/metabolismo Sinalização do Cálcio/fisiologia [Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo Cálcio/metabolismo Células Cultivadas Difusão Células Epiteliais/metabolismo Células Epiteliais/fisiologia Espaço Extracelular/metabolismo Junções Comunicantes/metabolismo Seres Humanos Microfluídica/estatística & dados numéricos Modelos Biológicos Transdução de Sinais [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Alarmins); 8L70Q75FXE (Adenosine Triphosphate); SY7Q814VUP (Calcium) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171113 [Lr] Data última revisão: 171113 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170414 [St] Status: MEDLINE [do] DOI: 10.1091/mbc.E16-10-0695

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[PMID]: 28394332 [Au] Autor: Shichita T; Ito M; Morita R; Komai K; Noguchi Y; Ooboshi H; Koshida R; Takahashi S; Kodama T; Yoshimura A [Ad] Endereço: Department of Microbiology and Immunology, School of Medicine, Keio University, Tokyo, Japan. [Ti] Título: MAFB prevents excess inflammation after ischemic stroke by accelerating clearance of damage signals through MSR1. [So] Source: Nat Med;23(6):723-732, 2017 Jun. [Is] ISSN: 1546-170X [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Damage-associated molecular patterns (DAMPs) trigger sterile inflammation after tissue injury, but the mechanisms underlying the resolution of inflammation remain unclear. In this study, we demonstrate that common DAMPs, such as high-mobility-group box 1 (HMGB1), peroxiredoxins (PRXs), and S100A8 and S100A9, were internalized through the class A scavenger receptors MSR1 and MARCO in vitro. In ischemic murine brain, DAMP internalization was largely mediated by MSR1. An elevation of MSR1 levels in infiltrating myeloid cells observed 3 d after experimental stroke was dependent on the transcription factor Mafb. Combined deficiency for Msr1 and Marco, or for Mafb alone, in infiltrating myeloid cells caused impaired clearance of DAMPs, more severe inflammation, and exacerbated neuronal injury in a murine model of ischemic stroke. The retinoic acid receptor (RAR) agonist Am80 increased the expression of Mafb, thereby enhancing MSR1 expression. Am80 exhibited therapeutic efficacy when administered, even at 24 h after the onset of experimental stroke. Our findings uncover cellular mechanisms contributing to DAMP clearance in resolution of the sterile inflammation triggered by tissue injury. [Mh] Termos MeSH primário: Alarminas/imunologia Encéfalo/imunologia Infarto da Artéria Cerebral Média/imunologia Fator de Transcrição MafB/imunologia Células Mieloides/imunologia Receptores Imunológicos/imunologia Receptores Depuradores Classe A/imunologia [Mh] Termos MeSH secundário: Animais Benzoatos/farmacologia Encéfalo/efeitos dos fármacos Isquemia Encefálica/imunologia Sistemas CRISPR-Cas Calgranulina A/imunologia Calgranulina B/imunologia Imunoprecipitação da Cromatina Proteína HMGB1/imunologia Inflamação Fator de Transcrição MafB/efeitos dos fármacos Fator de Transcrição MafB/genética Camundongos Células Mieloides/metabolismo Peroxirredoxinas/imunologia Receptores Imunológicos/genética Receptores do Ácido Retinoico/agonistas Receptores Depuradores Classe A/efeitos dos fármacos Receptores Depuradores Classe A/genética Acidente Vascular Cerebral/imunologia Tetra-Hidronaftalenos/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Alarmins); 0 (Benzoates); 0 (Calgranulin A); 0 (Calgranulin B); 0 (HMGB1 Protein); 0 (HMGB1 protein, mouse); 0 (MafB Transcription Factor); 0 (Mafb protein, mouse); 0 (Marco protein, mouse); 0 (Msr1 protein, mouse); 0 (Receptors, Immunologic); 0 (Receptors, Retinoic Acid); 0 (S100A9 protein, mouse); 0 (S100a8 protein, mouse); 0 (Scavenger Receptors, Class A); 0 (Tetrahydronaphthalenes); 08V52GZ3H9 (tamibarotene); EC 1.11.1.15 (Peroxiredoxins) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170829 [Lr] Data última revisão: 170829 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170411 [St] Status: MEDLINE [do] DOI: 10.1038/nm.4312

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