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Pharmaceuticals and Nutraceuticals from Fish and Their Activities
Published in Ramasamy Santhanam, Santhanam Ramesh, Subramanian Nivedhitha, Subbiah Balasundari, Pharmaceuticals and Nutraceuticals from Fish and Fish Wastes, 2022
Ramasamy Santhanam, Santhanam Ramesh, Subramanian Nivedhitha, Subbiah Balasundari
Cole et al. (1997) reported that the purified peptide pleurocidin derived from the skin mucous secretions of this species showed antibacterial activity on certain bacterial species and the MIC values are given below.
Defining in vitro topical antimicrobial and antibiofilm activity of epoxy-tigliane structures against oral pathogens
Published in Journal of Oral Microbiology, 2023
Wenya Xue, Manon F. Pritchard, Saira Khan, Lydia C. Powell, Joana Stokniene, Jingxiang Wu, Nicholas Claydon, Paul Reddell, David W. Thomas, Katja E. Hill
In peri-implantitis, extracellular matrix (ECM) remodeling will occur following surgical debridement [32]. EBC-1013, being a PKC activator (and potentially other C1 domain-containing proteins), exhibits immunomodulatory activity [15]. Interestingly, in diabetic skin wounds, EBC-1013 was able to induce a local inflammatory response, with Tnf, Il1b, Il6, Il36g, and Cxcl2 induction and polymorphonuclear leukocyte (PMNL) recruitment, as well as reorganization and remodeling of the extracellular matrix, and wound re-epithelialization. The immunostimulatory activity of EBC-1013 contrasts with the immunomodulatory activities of peptides such as pleurocidin [33], and essential oils (already in use in dentistry) [34], which inhibit inflammatory responses by suppressing the production of important mediators of pro-inflammatory pathways [35–37]. Innate immune induction by EBC-1013 induced healing in 6/7 diabetic wounds, compared to only 1/7 of untreated wounds. The induction of a rapidly resolving local innate immune response, combined with rapid remodeling at the implant/host interface, may contribute to the removal of biofilm persister cells from the sites of debridement.
Antimicrobial peptide GH12 targets Streptococcus mutans to arrest caries development in rats
Published in Journal of Oral Microbiology, 2019
Yufei Wang, Yuhao Zeng, Yuanjing Wang, Haoran Li, Sihan Yu, Wentao Jiang, Yingxue Li, Linglin Zhang
Over the last decade, a significant advancement in studies on control of oral pathogens by antimicrobial peptides (AMPs) has been made [13]. To date, natural AMPs and synthetic analogous have shown potent efficacy in inhibiting S. mutans, such as Pleurocidin, human beta-defensin-3 C15 peptide and synthetic octadecapeptide derived from α-amylase [14–17]. In addition, due to AMPs’ preferential attack on cell membranes and the ability of individual AMPs to interact with multiple targets [18], bacterial resistance to AMPs is relatively less prone to develop. Given these facts, AMPs are promising alternative solutions for dental caries.
Programmed cell death in human pathogenic fungi – a possible therapeutic target
Published in Expert Opinion on Therapeutic Targets, 2018
Éva Leiter, László Csernoch, István Pócsi
Numerous antimicrobial proteins are discovered as apoptosis inducers without yet-unidentified targets. For example, the plant-derived peptide Adenanthera pavonina ApDef1 through a cell-cycle-dependent process and via interaction of a component of the plasma membrane induced ROS accumulation, cell membrane permeabilization, caspase activation, and chromatin condensation in S. cerevisiae [92]. Cecropin A produced by the giant silk moth Hyalophora cecropia inhibited the growth of C. albicans via programmed cell death [93]. This 37-mer peptide increased the cytosolic and mitochondrial Ca2+ level, induced K+ efflux, PS externalization, elevation of intracellular ROS level by reducing the NADPH and GSH levels, dissipated the mitochondrial membrane potential, triggered cytochrome c release from mitochondria, activated caspases, and induced nuclear and DNA fragmentation [93]. Melittin – isolated from the European honeybee, Apis mellifera – is an antimicrobial peptide which elicited apoptosis through intracellular ROS elevation, PS externalization, mitochondrial membrane dissipation, mitochondrial Ca2+ elevation, cytochrome c release, metacaspase activation, and eventually DNA and nuclear fragmentation in C. albicans [94,95]. Psacotheasin – produced by the larvae of the yellow-spotted long-horned beetle Psacothea hilaris – increased intracellular ROS, PS externalization, disruption of the mitochondrial membrane potential, metacaspase activation, and finally DNA condensation and fragmentation [96]. Another insect-derived antimicrobial peptide papiliocin – discovered in the swallowtail butterfly Papilio xuthus – exerts its anticandidal activity via apoptosis by intracellular ROS elevation, flip-flop of PS, activation of metacaspases, DNA fragmentation, and nuclear condensation [97]. Scolopendin 1 from adult centipede, Scolopendra subspinipes mutilans induced intracellular ROS accumulation, mitochondrial Ca2+ increase, cytochrome c release, and eventually caspase activation [98]. Another antimicrobial peptide, arenicin-1 derived from the marine polychaeta lugworm, Arenicola marina exhibited apoptotic effects by increasing ROS, PS externalization, depolarization of the plasma membrane and mitochondrial membrane, activation of metacaspase, DNA fragmentation, and nuclear condensation [99]. Pleurocidin isolated from winter flounder Pleuronectes americanus exerted its anticandidal activity similarly to arenicin-1, namely via apoptotic pathway including ROS accumulation, PS externalization, mitochondrial membrane depolarization, metacaspase activation, and DNA fragmentation as well as nuclear condensation [100]. Periplanetasin-2 from the American cockroach Periplaneta americana induced mitochondrial depolarization and Ca2+ accumulation in C. albicans, which finally evoked apoptosis via caspase activation [101]. Coprisin isolated from the dung beetle, Copris tripartitus is a 43 aa defensin-like peptide triggered programmed cell death via PS externalization, ROS generation, mitochondrial membrane dissipation, cytochrome c release, metacaspase activation, and finally DNA fragmentation in C. albicans [102].