Academic literature on the topic 'HBND2'
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Journal articles on the topic "HBND2"
Beadell, Brent A., Andy Chieng, Kevin R. Parducho, Zhipeng Dai, Sam On Ho, Gary Fujii, Yixian Wang, and Edith Porter. "Nano- and Macroscale Imaging of Cholesterol Linoleate and Human Beta Defensin 2-Induced Changes in Pseudomonas aeruginosa Biofilms." Antibiotics 10, no. 11 (October 20, 2021): 1279. http://dx.doi.org/10.3390/antibiotics10111279.
Full textXi, Gang, Melissa A. Solum, Christine Wai, Laura A. Maile, Clifford J. Rosen, and David R. Clemmons. "The Heparin-Binding Domains of IGFBP-2 Mediate Its Inhibitory Effect on Preadipocyte Differentiation and Fat Development in Male Mice." Endocrinology 154, no. 11 (November 1, 2013): 4146–57. http://dx.doi.org/10.1210/en.2013-1236.
Full textRoutsias, John G., Dionysia Marinou, Maria Mavrouli, Athanasios Tsakris, and Vassiliki Pitiriga. "Serum β-Defensin 2, A Novel Biomarker for the Diagnosis of Acute Infections." Diagnostics 13, no. 11 (May 28, 2023): 1885. http://dx.doi.org/10.3390/diagnostics13111885.
Full textHosny, Alaa El-Dien Shawky, Mohammed Abdelhalim Ramadan, Maha Ahmed Shafik, Mahmoud Ahmed Shafeek, and Rania Abdelmonem Khattab. "Expression levels of pro-inflammatory interleukin-8 and certain antimicrobial peptides in concurrent with bacterial conjunctivitis." International Journal of Ophthalmology 14, no. 5 (May 18, 2021): 666–75. http://dx.doi.org/10.18240/ijo.2021.05.05.
Full textYin, Lei, and Beverly A. Dale. "Activation of protective responses in oral epithelial cells by Fusobacterium nucleatum and human β-defensin-2." Journal of Medical Microbiology 56, no. 7 (July 1, 2007): 976–87. http://dx.doi.org/10.1099/jmm.0.47198-0.
Full textHarris, Peggy, Amber Kerstetter-Fogle, Anthony Sloan, Alankrita Raghavan, Harry Hoffman, Jill Barnholtz-Sloan, Marta Couce, Ge Jin, Aaron Weinberg, and Andrew Sloan. "STEM-20. THE ROLE OF HUMAN BETA DEFENSINS IN THE CLONOGENICITY OF GLIOBLASTOMA MULTIFORME." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi25. http://dx.doi.org/10.1093/neuonc/noab196.094.
Full textOuhara, Kazuhisa, Hitoshi Komatsuzawa, Hideki Shiba, Yushi Uchida, Toshihisa Kawai, Koji Sayama, Koji Hashimoto, Martin A. Taubman, Hidemi Kurihara, and Motoyuki Sugai. "Actinobacillus actinomycetemcomitans Outer Membrane Protein 100 Triggers Innate Immunity and Production of β-Defensin and the 18-Kilodalton Cationic Antimicrobial Protein through the Fibronectin-Integrin Pathway in Human Gingival Epithelial Cells." Infection and Immunity 74, no. 9 (September 2006): 5211–20. http://dx.doi.org/10.1128/iai.00056-06.
Full textAntcheva, Nikolinka, Michele Boniotto, Igor Zelezetsky, Sabrina Pacor, Maria Vittoria Verga Falzacappa, Sergio Crovella, and Alessandro Tossi. "Effects of Positively Selected Sequence Variations in Human and Macaca fascicularis β-Defensins 2 on Antimicrobial Activity." Antimicrobial Agents and Chemotherapy 48, no. 2 (February 2004): 685–88. http://dx.doi.org/10.1128/aac.48.2.685-688.2004.
Full textSun, Lingling, Catherine M. Finnegan, Tina Kish-Catalone, Robert Blumenthal, Paolo Garzino-Demo, Gian M. La Terra Maggiore, Sid Berrone, et al. "Human β-Defensins Suppress Human Immunodeficiency Virus Infection: Potential Role in Mucosal Protection." Journal of Virology 79, no. 22 (November 15, 2005): 14318–29. http://dx.doi.org/10.1128/jvi.79.22.14318-14329.2005.
Full textZaynullina, O. N., D. V. Pechkurov, Z. R. Khismatullina, and K. R. Mirkhaidarova. "Human beta-defensin 2, secretory immunoglobulin A, and lysozyme in different specimens of children with atopic dermatitis." Voprosy praktičeskoj pediatrii 16, no. 6 (2021): 45–51. http://dx.doi.org/10.20953/1817-7646-2021-6-45-51.
Full textDissertations / Theses on the topic "HBND2"
Yovcheva, Venelina Zlateva [Verfasser], Thomas [Akademischer Betreuer] Hehlgans, and Wulf [Akademischer Betreuer] Schneider. "Die Rolle von hBD2 und hBD3 im entzündlichen und malignen Kontext / Venelina Zlateva Yovcheva. Betreuer: Thomas Hehlgans ; Wulf Schneider." Regensburg : Universitätsbibliothek Regensburg, 2013. http://d-nb.info/1037021355/34.
Full textVargues, Thomas. "Antimicrobial peptides : structure, function and resistance." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4076.
Full textCapewell, Samantha Jessica. "Structural and functional studies of protein targets at the host-pathogen interface." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9636.
Full textWang, Bingjie. "Novel function of human beta-defensin 2 : protecting epidermal barrier against pathogenic proteases." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28756.
Full textCreatti, Luisa. "Studi sulle interazioni tra i peptidi di difesa dell' ospite e cellule dell' immunità." Doctoral thesis, Università degli studi di Trieste, 2010. http://hdl.handle.net/10077/3697.
Full textWe are exposed daily to a myriad of potential pathogens, mainly through dermal contact, ingestion and inhalation. The innate immune system is of crucial importance in preventing pathogens from colonizing and growing to a point where they can cause life-threatening infections. Different types of cationic antimicrobial peptides (AMP), also known as host defense peptides (HDP), are among the innate immune mechanisms involved in this protective activity. -defensins are an important class of antimicrobial peptides that are present in human beings and have been widely reported to display a direct, salt and medium sensitive bactericidal activity, in vitro, against a broad spectrum of bacteria and fungi. Moreover, there is increasing evidence that they may play a significant role in alerting and enhancing other components of innate and adaptive immunity, thus also playing an indirect role in defense against microbes. Human -defensins are induced in vivo at the sites of microbial invasion, where they are thought to provide a bactericidal barrier, and to form chemotactic gradients that contribute to the recruitment of immune cells to the site of infection. Their interaction with the biological membranes of both microbial and host cells, appears to play a central role in both these types of activities. In this thesis, I was interested in characterizing the role of -defensin hBD2 in modulating activities of important immune host cells, such as monocytes, macrophages and immature dendritic cells, and its ability to bind to and/or be internalized within those cells, in relation to a possible immunomodulatory role. Initially, hBD2 was chosen amongst the human -defensins, and the native peptide synthesized, folded and characterized for antimicrobial activity and cytotoxicity. A fluorescent conjugate, as well as several structural analogues were also designed and prepared, and were respectively used to probe internalization and structure/activity relationships for this defensin. Subsequently, the immunomodulatory potential of hBD2 was probed, considering its possible effects in modulating important processes such as chemotaxis, degranulation, phagocytosis and reactive oxygen species (ROS) production of immune cells it comes into contact with. From this investigation, it emerged that hBD2 displays different effects depending on the cell type which comes into contact with it, and the exposure time. In particular, we confirmed the ability of hBD2 to induced chemotaxis of myeloid derived immature dendritic cells (iDC), contributing to recruitment of these cells to site of infection, although, from our studies, the mechanism of action turned out to be rather more complex than that which had been previously been proposed, and our observations may help reconcile apparently conflicting literature reports. Some novel additional properties of hBD2 were then described. In particular, a short exposure of iDC to hBD2 causes a cell type-dependent degranulation process, which could be involved in the tolerogenic/immunogenic roles of these cells, supporting a further immunomodulatory role for the defensin. A longer term exposure to hBD2 seems to augment the ability iDC to recognize bacteria and interact with them, possibly improving their ability to present antigens and activate adaptive immune responses. An equivalent treatment of macrophages resulted in a significant increase in their phagocytic activity and release of ROS, thus allowing these immune cells to better respond against a bacterial invasion. All these activities were evidenced in vitro at relatively low (micromolar) and sub-cytotoxic concentrations, which are compatible with the likely hBD2 concentration at sites of infection. Moreover, contrary to the direct bactericidal activity, these activities were not found to be salt or medium sensitive, but occur in conditions closely resembling the physiological ones. The activities of hBD2 were also compared to those of the structural analogues to study whether specific structural features of this defensin are required for its activity on immune cells. Results were somewhat puzzling because the evolutionarily conserved defensin scaffold seems to be quite important for exerting some biological function, such as the antimicrobial activity and phagocytosis, but not others, such as chemotaxis. This observation and the time and cell-type dependent activity may point to the concurrent existence of multiple modes of action. In the last part of this thesis, I describe the interaction of fluorescently labelled hBD2 with immune cells, with the aim of determining whether a cellular internalization could play a part for its biological effects. hBD2 was able to interact in a cell specific manner with different types of immune cells, upon short term exposure, leading to differentiated binding and cellular uptake, in a process devoid of cytotoxic or permeabilizing consequences. Macrophages were the most efficient in peptide internalization, whereas iDC seemed to be more avid for peptide surface binding than peptide internalization. The mechanism by which this occurs is as yet unknown, but our preliminary flow-cytometric data indicated that uptake of the defensin was an energy-dependent and temperature-sensitive process, which depends on actin fibers and can reasonably be supposed to involve lipid rafts, and/or clathrin-mediated endocytosis. Moreover, confocal microscopy of macrophages treated with labelled peptide showed that it may interact with specific patches on the membrane and, on binding, the peptide rapidly re-localized in the cytoplasm of cells with a characteristic punctate distribution. Taken together, these data could suggest that the peptide selectively binds to specific sites on membrane, such as lipid rafts, and that endocytosis could be a general mechanism of hBD2 internalization. These observations may thus indicate that hBD2 is capable of modulating activities of host cells not only by interacting with the membrane and surface receptors, but also with cytoplasmic targets. Noi siamo costantemente esposti a una miriade di potenziali patogeni, principalmente attraverso il contatto, l’ingestione e l’inalazione. Il sistema immunitario innato è di importanza cruciale nel prevenire la colonizzazione e la proliferazione dei patogeni che possono causare infezioni pericolose per la sopravvivenza. Tra i diversi meccanismi del sistema immunitario innato coinvolti in questa azione protettiva si contano diversi tipi di peptidi antimicrobici di natura cationica (AMP), anche noti come peptidi di difesa dell’ospite (HDP). Le -defensine sono un’importante classe di peptidi antimicrobici presenti anche nell’uomo che hanno dimostrato di possedere in vitro un’azione battericida diretta sensibile alla concentrazione salina nei confronti di un largo spettro di batteri e funghi. Inoltre è stato dimostrato che esse giocano un ruolo significativo nell’allertare e potenziare altri componenti dell’immunità innata e adattativa, esercitando così anche un’azione indiretta nella difesa contro i patogeni. Le -defensine umane vengono indotte in vivo nei siti dove si verifica un’invasione batterica, formando così una barriera battericida e creando un gradiente chemiotattico che contribuisce a reclutare cellule immunitarie nel sito d’infezione. La loro interazione con le membrane biologiche, sia dei microbi che delle cellule dell’ospite, sembra essere centrale in entrambe le attività. In questa tesi l’interesse principale è caratterizzare il ruolo della -defensina hBD2 nel modulare l’attività di importanti cellule immunitarie, quali monociti, macrofagi e cellule dendritiche immature, e la sua abilità di legarsi a tali cellule e/o di essere internalizzata da esse. Inizialmente, tra le -defensine umane è stata scelta hBD2 e il peptide naturale è stato sintetizzato, “foldato” e caratterizzato per l’attività antimicrobica e la citotossicità. Un coniugato fluorescente e molti analoghi strutturali sono stati inoltre progettati e sintetizzati e sono stati utilizzati, rispettivamente, per indagare l’eventuale internalizzazione e per fare studi di relazione fra struttura e attività. Successivamente è stato analizzato il potenziale immunomodulatorio di hBD2, considerando i suoi possibili effetti nel regolare importanti processi delle cellule immunitarie con cui il peptide viene in contatto, quali ad esempio la chemiotassi, la degranulazione, la fagocitosi e la produzione di specie reattive dell’ossigeno (ROS). Da questa analisi è emerso che hBD2 esercita diverse azioni a seconda del tipo cellulare con cui viene a contatto e del tempo di esposizione delle cellule alla defensina. In particolare, è stata confermata l’abilità di hBD2 a indurre la chemiotassi di cellule dendritiche immature (iDC), contribuendo a reclutare tali cellule al sito d’infezione. Negli studi condotti è però emerso che il meccanismo d’azione potrebbe essere più complesso di quanto proposto fino ad ora; tuttavia le osservazioni proposte in questa tesi appaiono in grado di conciliare i dati contrastanti riportati in letteratura. Sono inoltre emerse alcune nuove proprietà per hBD2. In particolare, un breve tempo di esposizione delle iDC alla defensina causa un processo di degranulazione che risulta dipendente dal tipo cellulare e che potrebbe essere coinvolto nel ruolo immunogenico/tolerogenico di queste cellule, supportando un ruolo immunomodulatorio per hBD2. Un’esposizione per tempi più lunghi a hBD2 sembra incrementare l’abilità delle iDC di riconoscere i batteri e interagire con loro, probabilmente aumentando la loro capacità di presentare gli antigeni e attivare le risposte immunitarie. Un trattamento equivalente sui macrofagi risulta invece in un aumento significativo della loro attività fagocitaria e della produzione di ROS, permettendo così a queste cellule di rispondere meglio ad un’invasione batterica. Tutte queste attività sono state evidenziate in vitro a concentrazioni relativamente basse (micromolari) e sub-citotossiche, compatibili con quelle che hBD2 raggiunge ai siti d’infezione. Inoltre, contrariamente all’attività battericida diretta, l’attività immunomodulatoria non è risultata sensibile alla concentrazione salina, ma si esplica in condizioni simili a quelle fisiologiche. L’attività di hBD2 è stata anche paragonata a quella di analoghi strutturali per studiare quali siano le caratteristiche di questa defensina che sono richieste per le attività sulle cellule immunitarie. I risultati sono per certi versi inspiegabili in quanto la struttura evolutivamente conservata delle defensine sembra essere importante per alcune attività biologiche, come l’attività antimicrobica diretta o la fagocitosi, mentre non lo è in altre, come la chemiotassi. Questa osservazione e la dipendenza dell’attività da tempo di esposizione e dal tipo cellulare considerato potrebbero indicare che esistono diversi meccanismi d’azione. Nell’ultima parte della tesi vengono descritti gli studi effettuati con il coniugato fluorescente di hBD2 con l’obiettivo di determinare se l’internalizzazione del peptide può giocare un ruolo nella sua attività biologica nei confronti delle cellule immunitarie. È emerso che hBD2 è capace di interagire in modo specifico già dopo una breve esposizione con i diversi tipi di cellule immunitarie considerati in questa tesi. Si è evidenziata una diversa capacità di legame e di internalizzazione a seconda del tipo cellulare, ma il processo è risultato sempre non accompagnato da effetti citotossici o permeabilizzazione delle cellule. In particolare, i macrofagi sono risultati i più efficienti nell’internalizzare del peptide, mentre le iDC sembrano più avide nel legare il peptide sulla superficie che nell’internalizzazione. Il meccanismo attraverso cui avvengono legame e internalizzazione è ancora ignoto, ma i nostri dati al citofluorimetro indicano che l’uptake della defensina è un processo che dipendente dall’energia e dalla temperatura, che è legato alla polimerizzazione delle fibre di actina e probabilmente coinvolge un processo di endocitosi mediata dai lipid rafts e/o dalla clatrina. Inoltre, la microscopia confocale di macrofagi trattati con il peptide fluorescente ha mostrato che esso interagisce con specifiche zone della membrana e, dopo il legame, si localizza rapidamente nel citoplasma della cellula con una caratteristica distribuzione puntata. Nell’insieme, questi dati suggeriscono che il peptide si leghi selettivamente a zone specifiche della membrana, come ad esempio i lipid rafts, e che l’endocitosi potrebbe essere un meccanismo generale per l’internalizzazione di hBD2. Tutti queste osservazioni suggeriscono quindi che hBD2 è capace di modulare le attività delle cellule dell’ospite non solo interagendo con le membrane o i recettori di superficie, ma anche con target citoplasmatici.
XXI Ciclo
1981
Huang, Kun-Che, and 黃堃哲. "HBD2-Overexpression decreases BMSC Proinflammatory Cytokine Expression of BMSC after Porphyromonas gingivalis Lipopolysaccharide Stimulation." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/2ghv7x.
Full text國立陽明大學
口腔生物研究所
106
Periodontitis is a common oral inflammatory disease caused by bacterial infection which leads to destruction of periodontal tissues. Successful periodontal regenerative therapy requires reduction of bacteria-related pathogenic factors and promotion of tissue regeneration. Porphyromonas gingivalis (Pg) is a major pathogen of periodontitis. Pg lipopolysaccharide (LPS) induces the production of proinflammatory cytokines, such as interleukin (IL)-1β (IL-1β), IL-6, and IL-8, and plays an important role in Pg’s pathogenic mechanism. Human β-defensin 2 (hBD2) is an important antimicrobial peptide of innate immune system. Previous studies indicated that hBD2 is effective against Pg. The positive charge of hBD2 potentially can neutralize the negative-charged LPS. Stem cell therapy is an effective treatment strategy for regenerative therapies including the regeneration of periodontal defects. Application of hBD2-overexpressing bone marrow stem cell (hBD2/BMSC) in treatment of bacteria-contaminated bone defect shows excellent antimicrobial and bone regenerative effects. Thus, hBD2/BMSC shows great potential in periodontal regenerative therapies. It has been reported that LPS induces production of proinflammatory cytokines in bone marrow stem cells. However, the effects of Pg-LPS on hBD2/BMSC may be different. We hypothesized that hBD2 produced by hBD2/BMSC can neutralize Pg-LPS and reduce the expression of proinflammatory cytokines from cells stimulated by Pg-LPS. The purpose of this study was to determine the Pg-LPS-induced proinflammatory cytokine expression of hBD2/BMSC. Human bone marrow stem cells (3A6) overexpressing red fluorescent protein (RFP) or hBD2, namely RFP/3A6 and hBD2/3A6, were produced by lentiviral infection method. The red fluorescence of RFP/3A6 was verified under fluorescent microscope. The secreted hBD2 from hBD2/3A6 was quantified by enzyme-linked immunosorbent assay (ELISA). Various concentrations of Pg-LPS (0, 0.1, 1 μg/ml) were used to treat RFP/3A6 and hBD2/3A6. The induced expression of proinflammatory cytokines (IL-1β、IL-6, and IL-8) of RFP/3A6 and hBD2/3A6 was determined by quantitative PCR and compared. The results indicated that the secretion of hBD2 can be increased through repeated lentiviral infection strategy. Pg-LPS stimulation dose-dependently increase the expression of proinflammatory cytokines (IL-1β、IL-6, and IL-8) of RFP/3A6 and hBD2/3A6. The trend of expression increase is significantly smaller in hBD2/3A6 when compared with RFP/3A6. When treated with Pg-LPS (0.1 or 1 μg/ml)),hBD2/3A6 showed lower expression of proinflammatory cytokines (IL-1β、IL-6, and IL-8) than RFP/3A6. In conclusion, the overexpression of hBD2 of BMSCs can lower the Pg-LPS-induced expression of proinflammatory cytokines. The phenomenon may reduce the local inflammation during periodontal regenerative therapy and benefit the periodontal regeneration
Book chapters on the topic "HBND2"
Enna, S. J., and David B. Bylund. "HBD2." In xPharm: The Comprehensive Pharmacology Reference, 1. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.61878-1.
Full textConference papers on the topic "HBND2"
Armbruster, N., B. Jensen, D. Mailänder-Sánchez, S. Kjaerulf, K. Sidelmann Brinch, B. Andersen, EF Stange, N. Malek, P. Nordkild, and J. Wehkamp. "Rekombinantes orales humanes beta-Defensin 2 (hBD2) verbessert signifikant die experimentell induzierte Colitis in vivo." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604801.
Full textMailänder-Sánchez, D., N. Armbruster, S. Kjaerulf, K. Sidelmann Brinch, B. Andersen, EF Stange, NP Malek, P. Nordkild, and J. Wehkamp. "Rekombinantes subkutanes humanes beta-Defensin 2 (hBD2) lindert die experimentell induzierte Colitis in verschiedenen Mausmodellen in vivo." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604800.
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