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1.

001-es BibID:BIBFORM103624
035-os BibID:(WoS)000923633900005 (Scopus)85142716887
Első szerző:Cho, Yeonhee
Cím:Neutrophil extracellular traps contribute to liver damage and increase defective low-density neutrophils in alcoholic hepatitis / Cho Yeonhee, Bukong Terence Ndonyi, Tornai David, Babuta Mrigya, Vlachos Ioannis S., Kanata Eleni, Catalano Donna, Szabo Gyongyi
Dátum:2023
ISSN:0168-8278
Megjegyzések:Background & Aims In alcoholic hepatitis (AH), inflammation and neutrophil counts correlate with poor clinical outcomes. Here, we investigated how neutrophils contribute to liver damage in AH. Methods We isolated blood neutrophils from AH patients to examine neutrophils extracellular traps (NETs) and performed RNA sequencing to explore unique characteristics. Results We found a significant increase of NET production in AH. We also observed a unique low-density neutrophil (LDNs) population in AH patients and alcohol-fed mice that was not present in healthy controls. Transcriptome analysis of peripheral LDNs and high-density neutrophils (HDNs) from AH patients revealed that LDNs exhibit a functionally exhausted phenotype, while HDNs are activated. Indeed, we found that AH HDNs have increased resting reactive oxygen species (ROS) and produce higher ROS upon LPS stimulation than control HDNs, whereas AH LDNs fail to respond to LPS. We show that LDNs are generated from HDNs after alcohol-induced NET release in vitro, and this LDN subset has decreased functionality including reduced phagocytosis. Moreover, LDNs showed reduced homing capacity and clearance by macrophage efferocytosis; therefore, dysfunctional neutrophils could remain in the circulation and liver. Depletion of both HDNs and LDNs in vivo prevented alcohol-induced NET production and liver damage in mice. Granulocyte-colony stimulating factor (G-CSF) treatment also ameliorated alcohol-induced liver injury in mice. Conclusion Neutrophils contribute to liver damage through increased NET formation which increases defective LDNs in AH. Alcohol induces neutrophil phenotype changes; HDNs are activated whereas LDNs are defective. Our findings provide mechanistic insights for therapeutic interventions in AH.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Hepatology. - 78 : 1 (2023), p. 28-44. -
További szerzők:Bukong, Terence Ndonyi Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Babuta, Mrigya Vlachos, Ioannis S. Kanata, Eleni Catalano, Donna Szabó Gyöngyi
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2.

001-es BibID:BIBFORM082950
Első szerző:Lowe, Patrick
Cím:Inhibition of the Inflammasome Signaling Cascade Reduces Alcohol Consumption in Female But Not Male Mice / Patrick P. Lowe, Yeonhee Cho, David Tornai, Sahin Coban, Donna Catalano, Gyongyi Szabo
Dátum:2020
ISSN:0145-6008 1530-0277
Megjegyzések:BACKGROUND: Alcohol use disorder is a significant societal and medical burden that is associated with both organ pathology and addiction. Excessive alcohol use results in neuroinflammation characterized by activation of the inflammasome, a multiprotein complex, and IL-1? increase in the brain. Recent studies suggest that inflammation could contribute to alcohol addiction. Here, we targeted components of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome cascade, which senses and responds to immunologic stimuli, to determine whether NLRP3 inhibition modulates alcohol consumption. METHODS: C57BL/6J male and female mice were provided a 2-bottle choice of alcohol at increasing concentrations (3, 6, 9, and 12%, 4 days each) or water, and some were treated with daily injections of an NLRP3 inhibitor (MCC950), a caspase-1 inhibitor (VX765), IL-1 receptor antagonist (IL-1ra; anakinra), or vehicle injection. RESULTS: Treatment with VX765, MCC950, and IL-1ra significantly reduced alcohol consumption and preference in female mice (p < 0.05). Treatment with MCC950 and IL-1ra reduced alcohol consumption, while IL-1ra reduced alcohol preference in male mice (p < 0.05). VX765 did not affect alcohol consumption or preference in male mice. CONCLUSIONS: These findings highlight gender differences in alcohol preference and demonstrate that inhibition of different steps in inflammasome signaling can reduce alcohol consumption in females. Inhibition of NLRP3 inflammasome activation and the inflammasome-IL-1? cascade opens novel insights into the development of new therapies to address alcohol use disorder in an era of targeted and precision medicine.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Alcohol
Anakinra
NLRP3
Caspase-1
Interleukin-1 Beta
Megjelenés:Alcoholism, Clinical and Experimental Research. - 44 : 2 (2020), p. 567-578. -
További szerzők:Cho, Yeonhee Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Coban, Sahin Catalano, Donna Szabó Gyöngyi
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3.

001-es BibID:BIBFORM082949
Első szerző:Saha, Banishree
Cím:Biomarkers of Macrophage Activation and Immune Danger Signals Predict Clinical Outcomes in Alcoholic Hepatitis / Banishree Saha, David Tornai, Karen Kodys, Adeyinka Adejumo, Patrick Lowe, Craig McClain, Mack Mitchell, Arthur McCullough, Srinivasan Dasarathy, Aimee Kroll-Desrosiers, Bruce Barton, Svetlana Radaeva, Gyongyi Szabo
Dátum:2019
ISSN:0270-9139
Megjegyzések:Although mortality due to acute alcoholic hepatitis (AH) correlates with Model for End-Stage Liver Disease (MELD) scores, biomarkers are critically needed to manage this disease. Increases in inflammatory markers and macrophage activation are associated with acute AH and could be potential biomarkers of clinical events and/or mortality. We enrolled 89 clinically diagnosed AH patients in four US academic medical centers. Plasma from AH patients had a significant increase in gut microbial translocation indicators (endotoxin, bacterial 16S ribosomal DNA) and host response indicators (soluble cluster of differentiation 14 [sCD14] and lipopolysaccharide binding protein [LBP]) compared to controls. Patient MELD score and Glasgow Alcoholic Hepatitis score (GAHS) correlated with endotoxin levels. AH patients also had a significant increase in high mobility group protein 1 (HMGB1), a sterile danger signal molecule, and osteopontin (OPN), a multifunctional phosphoprotein involved in neutrophil activation, compared to controls. Increased levels of OPN positively correlated with increasing MELD score, GAHS, and LBP levels. Consistent with these results, AH patients had significantly increased circulating levels of macrophage activation (sCD163 and sCD206) markers compared to healthy controls, and sCD163 and sCD206 significantly and positively correlated with OPN, HMGB1, and LBP levels as well as with MELD score and GAHS. These findings indicate a connection between microbial translocation, immune cell activation, and AH severity. Plasma sCD14, OPN, sCD163, and sCD206 levels were significantly higher in nonsurvivors than survivors. In multivariate regression models, we identified sCD14, sCD163, and OPN as independent predictors of 90-day mortality, infection, and organ failure development, respectively. Conclusion: Our study suggests that sCD14, LBP, OPN, sCD163, and sCD206 are biomarkers to indicate severity and predict clinical outcomes in AH.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
osteopontin
sCD206
sCD163
LBP
HMGB1
sCD14
organ failure
infection
Megjelenés:Hepatology. - 70 : 4 (2019), p. 1134-1149. -
További szerzők:Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Kodys, Karen Adejumo, Adeyinka Lowe, Patrick McClain, Craig Mitchell, Mack McCullough, Arthur Dasarathy, Srinivasan Kroll-Desrosiers, Aimee Barton, Bruce Radaeva, Svetlana Szabó Gyöngyi
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4.

001-es BibID:BIBFORM071775
Első szerző:Satishchandran, Abhishek
Cím:MicroRNA 122, Regulated by GRLH2, Protects Livers of Mice and Patients From Ethanol-Induced Liver Disease / Abhishek Satishchandran, Aditya Ambade, Sitara Rao, Ying-Chao Hsueh, Arvin Iracheta-Vellve, David Tornai, Patrick Lowe, Benedek Gyongyosi, Jia Li, Donna Catalano, Li Zhong, Karen Kodys, Jun Xie, Shashi Bala, Guangping Gao, Gyongyi Szabo
Dátum:2018
ISSN:0016-5085
Megjegyzések:BACKGROUND & AIMS:Chronic, excessive alcohol consumption leads to alcoholic liver disease (ALD) characterized by steatosis, inflammation, and eventually cirrhosis. The hepatocyte specific microRNA 122 (MIR122) regulates hepatocyte differentiation and metabolism. We investigated whether an alcohol-induced decrease in level of MIR122 contributes to development of ALD.METHODS:We obtained liver samples from 12 patients with ALD and cirrhosis and 9 healthy individuals (controls) and analyzed them by histology and immunohistochemistry. C57Bl/6 mice were placed on a Lieber-DeCarli liquid diet, in which they were fed ethanol for 8 weeks, as a model of ALD, or a control diet. These mice were also given injections of CCl4, to increase liver fibrosis, for 8 weeks. On day 28, mice with ethanol-induced liver disease and advanced fibrosis, and controls, were given injections of recombinant adeno-associated virus 8 vector that expressed the primary miR-122 transcript (pri-MIR122, to overexpress MIR122 in hepatocytes) or vector (control). Two weeks before ethanol feeding, some mice were given injections of a vector that expressed an anti-MIR122, to knock down its expression. Serum and liver tissues were collected; hepatocytes and liver mononuclear cells were analyzed by histology, immunoblots, and confocal microscopy. We performed in silico analyses to identify targets of MIR122 and chromatin immunoprecipitation quantitative polymerase chain reaction analyses in Huh-7 cells.RESULTS:Levels of MIR122 were decreased in liver samples from patients with ALD and mice on the Lieber-DeCarli diet, compared with controls. Transgenic expression of MIR122 in hepatocytes of mice with ethanol-induced liver disease and advanced fibrosis significantly reduced serum levels of alanine aminotransferase (ALT) and liver steatosis and fibrosis, compared with mice given injections of the control vector. Ethanol feeding reduced expression of pri-MIR122 by increasing expression of the spliced form of the transcription factor grainyhead like transcription factor 2 (GRHL2) in liver tissues from mice. Levels of GRHL2 also were increased in liver tissues from patients with ALD, compared with controls; increases correlated with decreases in levels of MIR122 in human liver. Mice given injections of the anti-MIR122 before ethanol feeding had increased steatosis, inflammation, and serum levels of alanine aminotransferase compared with mice given a control vector. Levels of hypoxia-inducible factor 1 alpha (HIF1?) mRNA, a target of MIR122, were increased in liver tissues from patients and mice with ALD, compared with controls. Mice with hepatocyte-specific disruption of Hif1? developed less-severe liver injury following administration of ethanol, injection of anti-MIR122, or both.CONCLUSIONS:Levels of MIR122 decrease in livers from patients with ALD and mice with ethanol-induced liver disease, compared with controls. Transcription of MIR122 is inhibited by GRHL2, which is increased in livers of mice and patients with ALD. Expression of an anti-MIR122 worsened the severity of liver damage following ethanol feeding in mice. MIR122 appears to protect the liver from ethanol-induced damage by reducing levels of HIF1?. These processes might be manipulated to reduce the severity of ALD in patients.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
alkoholos májbetegség
Megjelenés:Gastroenterology. - 154 : 1 (2018), p. 238-252. -
További szerzők:Ambade, Aditya Rao, Sitara Hsueh, Ying-Chao Iracheta-Vellve, Arvin Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Lowe, Patrick Gyöngyösi Benedek Li, Jia Catalano, Donna Zhong, Li Kodys, Karen Xie, Jun Bala, Shashi Gao, Guangping Szabó Gyöngyi
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5.

001-es BibID:BIBFORM102659
035-os BibID:(Scopus)85134156844 (WOS)000826112000001
Első szerző:Szabó Gyöngyi
Cím:Response from Authors of HEP-21-2131.R1 / Gyongyi Szabo, Mack Mitchell, Craig J. McClain, Srinivasan Dasarathy, Bruce Barton, Arthur J. McCullough, Laura E. Nagy, Aimee Kroll-Desrosiers, David Tornai, Hyesung Alice Min, Svetlana Radaeva, Lisa Casey, Jennifer Cuthbert
Dátum:2022
ISSN:0270-9139
Tárgyszavak:Orvostudományok Klinikai orvostudományok hozzászólás
folyóiratcikk
Megjelenés:Hepatology. - 76 : 5 (2022), p. E114-E115. -
További szerzők:Mitchell, Mack McClain, Craig Dasarathy, Srinivasan Barton, Bruce McCullough, Arthur Nagy Laura E. Kroll-Desrosiers, Aimee Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Min, Hyesung Alice Radaeva, Svetlana Casey, Lisa Cuthbert, Jennifer
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Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM101156
035-os BibID:(Scopus)85128889535 (WOS)000804710000001
Első szerző:Szabó Gyöngyi
Cím:IL-1 receptor antagonist plus pentoxifylline and zinc for severe alcohol-associated hepatitis / Gyöngyi Szabó, Mack Mitchell, Craig J. McClain, Srinivasan Dasarathy, Bruce Barton, Arthur McCullough, Laura E. Nagy, Aimee Kroll-Desrosiers, David Tornai, Hyesung Alice Min, Svetlana Radaeva, M. E. Blair Holbein, Lisa Casey, Jennifer Cuthbert
Dátum:2022
ISSN:0270-9139
Megjegyzések:Background & aims: Patients with severe alcohol-associated hepatitis (AH) have high mortality. Corticosteroids improve survival only for 30 days. We targeted inflammation, cellular injury and gut leakiness in a randomized clinical trial comparing combination therapy to corticosteroids on 180-day survival. Approach & results: Subjects with a clinical diagnosis of severe AH (MELD>20, MDF>32) were randomized to receive methylprednisolone (28 days) (PRED) or a combination of anakinra (14 days) plus pentoxifylline (28 days) plus zinc (180 days) (COMB). The primary endpoint was survival at 180 days. The study was designed in 2013, initiated in October 2014 and completed in March 2018. Five hundred (500) patients were screened to randomize 104 subjects with a clinical diagnosis of AH with a Model for End Stage Liver Disease (MELD) score > 20. Fifty-three (53) patients were randomized into the COMB and fifty (50) to the PRED treatment; one dropped out of the study before randomization. The mean age was 45.3?10.4 years. 60.6% were males, 92.3% white, mean MELD 25.7?3.9. Kaplan-Meier survival estimate at 180-day was 67.9% in COMB and 56% in PRED (HR=0.69; p=0.3001). Survival curves separated by 90 days (COMB: 69.8%; PRED: 58.0%; HR=0.69, p=0.28). Survival at 28 days was similar between the COMB (83.4%) and PRED groups (81.2%) (HR=0.91, p=0.85). There were no unexpected serious adverse events and the incidence of infection was comparable between groups. MELD 20-25 and MELD >26 strata showed non-significant treatment effects in favor of COMB. Conclusions: A combination of anakinra, pentoxifylline plus zinc provides similar survival benefits compared to corticosteroid therapy in severe AH.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Interleukin-1 antagonist
MELD
inflammation
interleukin-1
liver failure
Megjelenés:Hepatology. - 76 : 4 (2022), p. 1058-1068. -
További szerzők:Mitchell, Mack McClain, Craig Dasarathy, Srinivasan Barton, Bruce McCullough, Arthur Nagy Laura E. Kroll-Desrosiers, Aimee Tornai Dávid (1989-) (hepatológia, biomarker kutatás) Min, Hyesung Alice Radaeva, Svetlana Holbein, M. E. Blair Casey, Lisa Cuthbert, Jennifer
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM115266
035-os BibID:(cikkazonosító)e0296
Első szerző:Tornai Dávid (hepatológia, biomarker kutatás)
Cím:A novel score of IL-13 and age predicts 90-day mortality in severe alcohol-associated hepatitis : a multicenter plasma biomarker analysis / David Tornai, Mack Mitchell, Craig J. McClain, Srinivasan Dasarathy, Arthur McCullough, Svetlana Radaeva, Aimee Kroll-Desrosiers, JungAe Lee, Bruce Barton, Gyongyi Szabo
Dátum:2023
ISSN:2471-254X
Megjegyzések:Background: Severe alcoholic hepatitis (AH) has a high short-term mortality rate. The Model for End-Stage Liver Disease (MELD) assesses disease severity and mortality, however, it is not specific for AH. We screened plasma samples from severe AH patients for biomarkers of multiple pathological processes and identified predictors of short-term mortality. Methods: Plasma was collected at baseline from 85 severe AH patients (MELD?20, MDF?32) enrolled in the DASH clinical trial (investigating IL-1receptor antagonist+pentoxifylline+zinc vs. methylprednisolone+placebo). Samples were analyzed for 43 biomarkers and the markers' association with 28 and 90-day mortality was assessed. Results: Thirty-one (36.5%) patients died during the 90-day follow-up with similar ratios in the treatment groups. Eight biomarkers showed association with mortality. Interleukin-6, IL-22, IFN-?2, sTNF-R1, lipocalin-2 and ?-fetoprotein levels were associated with 28-day, while IL-6, IL-13 and endotoxin levels with 90-day mortality. In multivariable Cox regression, encephalopathy, lipocalin-2 and ?-fetoprotein levels were independent predictors of 28-day mortality and IL-6, IL-13, INR levels and age were independent predictors of 90-day mortality. The combination of IL-13 and age had superior performance predicting 90-day mortality compared to MELD in the total cohort and the individual treatment groups. Conclusions: We identified predictors of short-term mortality in a cohort exclusively involving severe AH patients. We created a composite score of IL-13 and age that predicts 90-day mortality regardless of treatment type with a performance superior to MELD in severe AH.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
anakinra
interleukin
short-term mortality
composite score
prognosis
Megjelenés:Hepatology Communications. - 7 : 12 (2023), p. 1-13. -
További szerzők:Mitchell, Mack McClain, Craig Dasarathy, Srinivasan McCullough, Arthur Radaeva, Svetlana Kroll-Desrosiers, Aimee Lee, JungAe Barton, Bruce Szabó Gyöngyi
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8.

001-es BibID:BIBFORM102219
Első szerző:Tornai Dávid (hepatológia, biomarker kutatás)
Cím:A novel composite score of biomarkers and age predicts mortality in severe alcoholic hepatitis patients / Tornai Dávid, Mack C. Mitchell, Craig J. McClain, Srinivasan Dasarathy, Arthur J. McCullough, Svetlana Radaeva, Aimee Kroll-Desrosiers, Bruce Barton, Szabó Gyöngyi
Dátum:2019
ISSN:0270-9139
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Hepatology. - 70 : Suppl. 1 (2019), p. 835A. -
További szerzők:Mitchell, Mack C. McClain, Craig Dasarathy, Srinivasan McCullough, Arthur Radaeva, Svetlana Kroll-Desrosiers, Aimee Barton, Bruce Szabó Gyöngyi
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Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM088181
Első szerző:Tornai Dávid (hepatológia, biomarker kutatás)
Cím:Emerging medical therapies for severe alcoholic hepatitis / David Tornai, Gyongyi Szabo
Dátum:2020
ISSN:2287-2728 2287-285X
Megjegyzések:Severe alcoholic hepatitis (AH) is an acute and often devastating form of alcohol-associated liver disease. Clinically, AH is characterized by elevated bilirubin, model for end stage liver disease scores >20, and nonspecific symptoms that are caused by underlying inflammation, hepatocyte injury, and impaired intestinal barrier function. Compromised immune defense in AH contributes to infections, sepsis and organ failure. To date, corticosteroids are the only recommended treatment for severe AH, however it does not provide survival benefits beyond 1 month. Recent preclinical and early clinical studies in AH aided understanding of the disease and presented opportunities for new therapeutic options targeting inflammation, oxidative stress, liver regeneration and modification of intestinal microbiota. In this comprehensive review, we discuss promising preclinical results and ongoing clinical trials evaluating novel therapeutic agents for the treatment of severe AH.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Fibrosis
Gastrointestinal microbiome
Hepatocytes
Oxidative stress
Fatty liver
Alcohol
Megjelenés:Clinical and molecular hepatology. - 26 : 4 (2020), p. 686-696. -
További szerzők:Szabó Gyöngyi
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Intézményi repozitóriumban (DEA) tárolt változat
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10.

001-es BibID:BIBFORM082948
Első szerző:Tornai Dávid (hepatológia, biomarker kutatás)
Cím:Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice / David Tornai, Istvan Furi, Zu T. Shen, Alexander B. Sigalov, Sahin Coban, Gyongyi Szabo
Dátum:2019
ISSN:2471-254X
Megjegyzések:Alcoholic liver disease (ALD) is characterized by macrophage and neutrophil leukocyte recruitment and activation in the liver. Damage- and pathogen-associated molecular patterns contribute to a self-perpetuating proinflammatory state in ALD. Triggering receptor expressed on myeloid cells 1 (TREM-1) is a surface receptor that amplifies inflammation induced by toll-like receptors (TLRs) and is expressed on neutrophils and monocytes/macrophages. We hypothesized that TREM-1 signaling contributes to proinflammatory pathway activation in ALD. Using an in vivo ALD model in mice, we tested the effects of ligand-independent TREM-1 inhibitory peptides that were formulated into human high-density lipoprotein (HDL)-mimicking complexes GF9-HDL and GA/E31-HDL. As revealed in vitro, macrophages endocytosed these rationally designed complexes through scavenger receptors. A 5-week alcohol feeding with the Lieber-DeCarli diet in mice resulted in increased serum alanine aminotransferase (ALT), liver steatosis, and increased proinflammatory cytokines in the liver. TREM-1 messenger RNA (mRNA) expression was significantly increased in alcohol-fed mice, and TREM-1 inhibitors significantly reduced this increase. TREM-1 inhibition significantly attenuated alcohol-induced spleen tyrosine kinase (SYK) activation, an early event in both TLR4 and TREM-1 signaling. The TREM-1 inhibitors significantly inhibited macrophage (epidermal growth factor-like module-containing mucin-like hormone receptor-like 1 [F4/80], clusters of differentiation [CD]68) and neutrophil (lymphocyte antigen 6 complex, locus G [Ly6G] and myeloperoxidase [MPO]) markers and proinflammatory cytokines (monocyte chemoattractant protein 1 [MCP-1], tumor necrosis factor ? [TNF-?], interleukin-1? [IL-1?], macrophage inflammatory protein 1? [MIP-1?]) at the mRNA level compared to the HDL vehicle. Administration of TREM-1 inhibitors ameliorated liver steatosis and early fibrosis markers (?-smooth muscle actin [?SMA] and procollagen1? [Pro-Col1?]) at the mRNA level in alcohol-fed mice. However, the HDL vehicle also reduced serum ALT and some cytokine protein levels in alcohol-fed mice, indicating HDL-related effects. Conclusion: HDL-delivered novel TREM-1 peptide inhibitors ameliorate early phases of inflammation and neutrophil and macrophage recruitment and activation in the liver and attenuate hepatocyte damage and liver steatosis. TREM-1 inhibition represents a promising therapeutic approach for further investigations in ALD.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Hepatology Communications. - 3 : 1 (2019), p. 99-115. -
További szerzők:Furi István Shen, Zu T. Sigalov, Alexander B. Coban, Sahin Szabó Gyöngyi
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