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Berlin Brandenburg

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  • 1
    Language: English
    In: Alcoholism, clinical and experimental research, March 2011, Vol.35(3), pp.392-9
    Description: Tissue injury owing to acute and chronic alcohol consumption has extensive medical consequences, with the level and duration of alcohol exposure affecting both the magnitude of injury and the time frame to recovery. While the understanding of many of the molecular processes disrupted by alcohol has advanced, mechanisms of alcohol-induced tissue injury remain a subject of intensive research. Alcohol has multiple targets, as it affects diverse cellular and molecular processes. Some mechanisms of tissue damage as a result of alcohol may be common to many tissue types, while others are likely to be tissue specific. Here, we present a discussion of the alcohol-induced molecular and cellular disruptions associated with injury or recovery from injury in bone, muscle, skin, and gastric mucosa. In every case, the goal of characterizing the sites of alcohol action is to devise potential measures for protection, prevention, or therapeutic intervention.
    Keywords: Alcohol Drinking -- Adverse Effects ; Ethanol -- Toxicity ; Wound Healing -- Physiology
    ISSN: 01456008
    E-ISSN: 1530-0277
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  • 2
    In: Alcoholism: Clinical and Experimental Research, May 2014, Vol.38(5), pp.1347-1355
    Description: To purchase or authenticate to the full-text of this article, please visit this link: http://onlinelibrary.wiley.com/doi/10.1111/acer.12369/abstract Byline: Brenda J. Curtis, Sara Hlavin, Aleah L. Brubaker, Elizabeth J. Kovacs, Katherine A. Radek Keywords: Antimicrobial Peptides; Proteases; Wound Healing; Macrophages; Cathelicidin; Inflammation Background Exacerbation of cutaneous wound infections and delayed wound closure are frequent complications seen in alcohol exposed subjects who sustain injuries. We previously reported that acute alcohol exposure alters the early dermal inflammatory phase of wound healing and also several parameters of the proliferative wound healing phase in wounds from ethanol (EtOH)-treated mice for several days or weeks after EtOH exposure. Hence, it is likely that the cumulative defects arising in the early phases of the wound healing process directly contribute to the increased complications observed in intoxicated patients at the time of injury. Methods C57BL/6 mice were given intraperitoneal EtOH (2.2 g/kg body weight) or vehicle (saline) EtOH using our episodic binge EtOH exposure protocol (3 days EtOH, 4 days off, 3 days EtOH) to yield a blood alcohol concentration (BAC) of 300 mg/dl at the time of wounding. Mice were subjected to six 3 mm full-thickness dorsal wounds and immediately treated topically with 10 I1/4l of sterile saline (control) or diluted Staphylococcus aureus corresponding to 1 x 10.sub.4 CFU/wound. Wounds were harvested at 24 hours post injury to evaluate wound area, neutrophil and macrophage accumulation, and the protein levels of cytokines, interleukin-6 (IL-6), IL-1[beta], and IL-10, and chemokines, macrophage inflammatory protein-2 (MIP-2) and MIP-1[alpha], monocyte chemotactic protein-1 (MCP-1), and keratinocyte-derived chemokine (KC). The abundance and localization of cathelicidin-related antimicrobial peptide (CRAMP) and the kallikrein epidermal proteases (KLK5 and KLK7) were also determined. Results Compared to control mice, EtOH-treated mice exhibited delayed wound closure, decreased macrophage accumulation, and impaired production of MIP-1[alpha]. Furthermore, skin from EtOH-treated mice demonstrated a reduction in the abundance of epidermal CRAMP and KLK7. Conclusions These findings suggest that EtOH exposure hinders several distinct components of the innate immune response, including phagocyte recruitment and chemokine/cytokine and AMP production. Together, these effects likely contribute to delayed wound closure and enhanced infection severity observed in intoxicated patients. Article Note: These authors contributed equally.
    Keywords: Antimicrobial Peptides ; Proteases ; Wound Healing ; Macrophages ; Cathelicidin ; Inflammation
    ISSN: 0145-6008
    E-ISSN: 1530-0277
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  • 3
    In: Critical Care Medicine, 2014, Vol.42(6), pp.e420-e431
    Description: OBJECTIVES:: Our objective was to characterize the mechanisms by which local burn injury compromises epithelial barrier function in burn margin, containing the elements necessary for healing of the burn site, and in distal unburned skin, which serves as potential donor tissue. DESIGN:: Experimental mouse scald burn injury. SETTING:: University Research Laboratory. SUBJECTS:: C57/Bl6 Male mice, 8–12 weeks old. INTERVENTIONS:: To confirm that dehydration was not contributing to our observed barrier defects, in some experiments mice received 1 mL of saline fluid immediately after burn, while a subgroup received an additional 0.5 mL at 4 hours and 1 mL at 24 hours following burn. We then assessed skin pH and transepidermal water loss every 12 hours on the burn wounds for 72 hours postburn. MEASUREMENTS AND MAIN RESULTS:: Burn margin exhibited increased epidermal barrier permeability indicated by higher pH, greater transepidermal water loss, and reduced lipid synthesis enzyme expression and structural protein production up to 96 hours postburn. By contrast, antimicrobial peptide production and protease activity were elevated in burn margin. Skin extracts from burn margin did not exhibit changes in the ability to inhibit bacterial growth. However, distal unburned skin from burned mice also demonstrated an impaired response to barrier disruption, indicated by elevated transepidermal water loss and reduced lipid synthesis enzyme and structural protein expression up to 96 hours postburn. Furthermore, skin extracts from distal unburned skin exhibited greater protease activity and a reduced capacity to inhibit bacterial growth of several skin pathogens. Finally, we established that antimicrobial peptide levels were also altered in the lung and bladder, which are common sites of secondary infection in burn-injured patients. CONCLUSIONS:: These findings reveal several undefined deficiencies in epithelial barrier function at the burn margin, potential donor skin sites, and organs susceptible to secondary infection. These functional and biochemical data provide novel insights into the mechanisms for graft failure and secondary infection after burn injury.
    Keywords: Medicine;
    ISSN: 0090-3493
    E-ISSN: 15300293
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  • 4
    Language: English
    In: Life Sciences, 27 November 2012, Vol.91(21-22), pp.1070-1076
    Description: To characterize how nicotinic acetylcholine receptors (nAChRs) influence epidermal barrier function and recovery following prolonged stress or direct nAChR activation or antagonism. Mice were subjected to psychological stress or treated topically with nAChR agonist or antagonist for 3 days. We assessed barrier permeability and recovery by measuring transepidermal water loss (TEWL) before and after barrier disruption. In parallel, we analyzed the production and localization of several epidermal cornified envelope proteins in mouse skin and in human EpiDerm™ organotypic constructs stimulated with a nAChR agonist (nicotine) and/or a nAChR selective antagonist (α-bungarotoxin). We determined that psychological stress in mice impairs barrier permeability function and recovery, an effect that is reversed by application of the α7 selective nAChR antagonist, α-bungarotoxin (Bung). In the absence of stress, both topical nicotine or Bung treatment alone impaired barrier permeability. We further observed that stress, topical nicotine, or topical Bung treatment in mice influenced the abundance and/or localization of filaggrin, loricrin, and involucrin. Similar alterations in these three major cornified envelope proteins were observed in human EpiDerm™ cultures. Perceived psychological stress and nicotine usage can both initiate or exacerbate several dermatoses by altering the cutaneous permeability barrier. Modulation of nAChRs by topical agonists or antagonists may be used to improve epidermal barrier function in skin diseases associated with defects in epidermal barrier permeability.
    Keywords: Nicotinic Receptors ; Barrier Permeability ; Epidermal Proteins ; Acetylcholine ; Sciences (General) ; Biology
    ISSN: 0024-3205
    E-ISSN: 1879-0631
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  • 5
    Language: English
    In: International Immunopharmacology, November 2015, Vol.29(1), pp.63-70
    Description: The cholinergic anti-inflammatory pathway spans several macro- and micro-environments to control inflammation α7 nicotinic acetylcholine receptors (nAChRs). Physiologic inflammation is necessary for normal wound repair and is triggered, in part, Toll-like receptors (TLRs). Here, we demonstrate that keratinocyte nAChR activation dampens TLR2-mediated migration and pro-inflammatory cytokine and antimicrobial peptide (AMP) production, which is restored by a α7-selective nAChR antagonist. The mechanism of this response occurs by blocking the NF-κB and Erk1/2 pathway during early and late wound healing. In a mouse model of wound infection, topical nAChR activation reduces wound AMP and TLR2 production to augment bacterial survival in wild-type mice. These findings suggest that aberrant α7 nAChR activation may impair normal wound healing responses, and that pharmacologic administration of topical nAChR antagonists may improve wound healing outcomes in wounds necessitating a more robust inflammatory response.
    Keywords: Keratinocytes ; Nicotinic Receptors ; Toll-Like Receptor-2 ; Antimicrobial Peptides ; Wound Healing ; Infection ; Biology ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 1567-5769
    E-ISSN: 1878-1705
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  • 6
    Language: English
    In: PLoS One, CA: Public Library of Science
    Description: This article explores the interrelationship between the urinary microbiota and host antimicrobial peptides as mechanisms for urinary tract infection risk.
    Keywords: Resident Bacterial Communities ; Host Antimicrobial Peptides ; Urinary Tract Infection
    ISSN: 19326203
    E-ISSN: 19326203
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  • 7
    Language: English
    In: PLoS ONE, 01 January 2013, Vol.8(1), p.e54646
    Description: Despite two centuries of reports linking alcohol consumption with enhanced susceptibility to bacterial infections and in particular gut-derived bacteria, there have been no studies or model systems to assess the impact of long-term alcohol exposure on the ability of the epithelial barrier to withstand bacterial infection. It is well established that acute alcohol exposure leads to reduction in tight and adherens junctions, which in turn leads to increases in epithelial cellular permeability to bacterial products, leading to endotoxemia and a variety of deleterious effects in both rodents and human. We hypothesized that reduced fortification at junctional structures should also reduce the epithelial barrier's capacity to maintain its integrity in the face of bacterial challenge thus rendering epithelial cells more vulnerable to infection. In this study, we established a cell-culture based model system for long-term alcohol exposure to assess the impact of chronic alcohol exposure on the ability of Caco-2 intestinal epithelial cells to withstand infection when facing pathogenic bacteria under the intact or wounded conditions. We report that daily treatment with 0.2% ethanol for two months rendered Caco-2 cells far more susceptible to wound damage and cytotoxicity caused by most but not all bacterial pathogens tested in our studies. Consistent with acute alcohol exposure, long-term ethanol exposure also adversely impacted tight junction structures, but in contrast, it did not affect the adherens junction. Finally, alcohol-treated cells partially regained their ability to withstand infection when ethanol treatment was ceased for two weeks, indicating that alcohol's deleterious effects on cells may be reversible.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 8
    In: Critical Care Medicine, 2017, Vol.45(6), pp.e543-e551
    Description: OBJECTIVES:: Characterization of urinary bacterial microbiome and antimicrobial peptides after burn injury to identify potential mechanisms leading to urinary tract infections and associated morbidities in burn patients. DESIGN:: Retrospective cohort study using human urine from control and burn subjects. SETTING:: University research laboratory. PATIENTS:: Burn patients. INTERVENTIONS:: None. MEASUREMENTS AND MAIN RESULTS:: Urine samples from catheterized burn patients were collected hourly for up to 40 hours. Control urine was collected from “healthy” volunteers. The urinary bacterial microbiome and antimicrobial peptide levels and activity were compared with patient outcomes. We observed a significant increase in urinary microbial diversity in burn patients versus controls, which positively correlated with a larger percent burn and with the development of urinary tract infection and sepsis postadmission, regardless of age or gender. Urinary psoriasin and β-defensin antimicrobial peptide levels were significantly reduced in burn patients at 1 and 40 hours postadmission. We observed a shift in antimicrobial peptide hydrophobicity and activity between control and burn patients when urinary fractions were tested against Escherichia coli and Enterococcus faecalis urinary tract infection isolates. Furthermore, the antimicrobial peptide activity in burn patients was more effective against E. coli than E. faecalis. Urinary tract infection–positive burn patients with altered urinary antimicrobial peptide activity developed either an E. faecalis or Pseudomonas aeruginosa urinary tract infection, suggesting a role for urinary antimicrobial peptides in susceptibility to select uropathogens. CONCLUSIONS:: Our data reveal potential links for urinary tract infection development and several morbidities in burn patients through alterations in the urinary microbiome and antimicrobial peptides. Overall, this study supports the concept that early assessment of urinary antimicrobial peptide responses and the bacterial microbiome may be used to predict susceptibility to urinary tract infections and sepsis in burn patients.
    Keywords: Medicine;
    ISSN: 0090-3493
    E-ISSN: 15300293
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  • 9
    In: Alcoholism: Clinical and Experimental Research, June 2007, Vol.31(6), pp.1045-1052
    Description: Clinical studies demonstrate that intoxicated patients exhibit an increased incidence of wound healing complications. Previous studies in a murine excisional wound model revealed that acute ethanol exposure impairs the wound healing response, causing decreased angiogenesis and a significant reduction in wound collagen content. Using the same murine model of excisional wounding, we examined the effect of a single dose of ethanol on the overall collagen content and collagen type I and type III mRNA expression, transforming growth factor‐ (TGF‐) production, and levels of several components of the extracellular matrix proteolytic cascade. Wounds from ethanol‐treated mice exhibited a significant decrease in collagen and in the production of collagen type I mRNA compared with saline controls. Exposure to ethanol also caused significant increase in wound TGF‐ by day 2 after injury (1.69 ± 0.29 vs 12.34 ± 3.97 pg/g protein, 〈0.01). In addition, wounds from mice exposed to ethanol had significantly increased levels of active urokinase plasminogen activator at day 7, (205.10 ± 48.79 vs 642.70 ± 159.80 pg/g protein, 〈0.001). The level of matrix metalloproteinase‐8, a collagen type I proteinase, was 2.2‐fold higher in wounds of ethanol‐treated mice compared with control at day 7 (〈0.05). These studies demonstrate that a single dose of ethanol decreases collagen production, increases the production of TGF‐ and increases levels of matrix degrading enzymes. This alteration in protease balance may partially explain the impaired wound healing that follows acute alcohol intoxication.
    Keywords: Extracellular Matrix ; Ethanol ; Wound Healing
    ISSN: 0145-6008
    E-ISSN: 1530-0277
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  • 10
    In: Journal of Burn Care & Research, 2012, Vol.33(3), pp.299-310
    Description: Thousands of patients suffer from burn injuries each year, yet few therapies have been developed to accelerate the wound healing process. Most fibroblast growth factors (FGFs) have been extensively evaluated but only a few have been found to participate in the wound healing process. In particular, FGF-10 is robustly increased in the wound microenvironment after injury and has demonstrated some ability to promote wound healing in vitro and in vivo. Glycosaminoglycans are linear carbohydrates that participate in wound repair by influencing cytokine/growth factor localization and interaction with cognate receptors. Dermatan sulfate (DS) is the most abundant glycosaminoglycan in human wound fluid and has been postulated to be directly involved in the healing process. Recently, the combination of FGF-10 and DS demonstrated the potential to accelerate wound healing via increased keratinocyte proliferation and migration. Based on these preliminary studies, DS may serve as a cofactor for FGF-10, and together they are likely to expedite the healing process by stimulating keratinocyte activity. As a specific subtype of wounds, the overall healing process of burn injuries does not significantly differ from other types of wounds, where optimal repair results in matrix regeneration and complete reepithelialization. At present, standard burn treatment primarily involves topical application of antimicrobial agents, while no routine therapies target acceleration of reepithelialization, the key to wound closure. Thus, this novel therapeutic combination could be used in conjunction with some of the current therapies, but it would have the unique ability to initiate wound healing by stimulating keratinocyte epithelialization.
    Keywords: Burns -- Drug Therapy ; Dermatan Sulfate -- Therapeutic Use ; Fibroblast Growth Factor 10 -- Therapeutic Use ; Wound Healing -- Drug Effects;
    ISSN: 1559-047X
    E-ISSN: 15590488
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