scholarly journals Novel peptide therapeutics for treatment of infections

2009 ◽  
Vol 58 (8) ◽  
pp. 977-987 ◽  
Author(s):  
P. C. F. Oyston ◽  
M. A. Fox ◽  
S. J. Richards ◽  
G. C. Clark
Keyword(s):  
Antimicrobial Peptides ◽  
Therapeutic Agents ◽  
Innate Immune ◽  
Antimicrobial Compounds ◽  
Peptide Therapeutics ◽  
Cationic Antimicrobial Peptides ◽  
Immune Effector ◽  
New Approaches ◽  
Innate Immune Effector ◽  
Topical Applications

As antibiotic resistance increases worldwide, there is an increasing pressure to develop novel classes of antimicrobial compounds to fight infectious disease. Peptide therapeutics represent a novel class of therapeutic agents. Some, such as cationic antimicrobial peptides and peptidoglycan recognition proteins, have been identified from studies of innate immune effector mechanisms, while others are completely novel compounds generated in biological systems. Currently, only selected cationic antimicrobial peptides have been licensed, and only for topical applications. However, research using new approaches to identify novel antimicrobial peptide therapeutics, and new approaches to delivery and improving stability, will result in an increased range of peptide therapeutics available in the clinic for broader applications.

Cationic Antimicrobial Peptides for Tuberculosis: A Mini-Review

2019 ◽  
Vol 20 (9) ◽  
pp. 885-892
Author(s):  
Sara Silva ◽  
Nuno Vale
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Amino Acid ◽  
Antimicrobial Peptides ◽  
Resistance Mechanisms ◽  
Therapeutic Agents ◽  
Pharmacological Properties ◽  
Therapeutic Activity ◽  
Alternative Strategies ◽  
Cationic Antimicrobial Peptides ◽  
Specific Amino Acid

Cationic antimicrobial peptides (CAMPs) can be considered as new potential therapeutic agents for Tuberculosis treatment with a specific amino acid sequence. New studies can be developed in the future to improve the pharmacological properties of CAMPs and also understand possible resistance mechanisms. This review discusses the principal properties of natural and/or synthetic CAMPs, and how these new peptides have a significant specificity for Mycobacterium tuberculosis. Also, we propose some alternative strategies to enhance the therapeutic activity of these CAMPs that include coadministration with nanoparticles and/or classic drugs.

scholarly journals Masking of β(1-3)-Glucan in the Cell Wall of Candida albicans from Detection by Innate Immune Cells Depends on Phosphatidylserine

2014 ◽  
Vol 82 (10) ◽  
pp. 4405-4413 ◽  
Author(s):  
Sarah E. Davis ◽  
Alex Hopke ◽  
Steven C. Minkin ◽  
Anthony E. Montedonico ◽  
Robert T. Wheeler ◽  
...  
Keyword(s):  
Cell Wall ◽  
Candida Albicans ◽  
De Novo ◽  
Invasive Disease ◽  
Innate Immune ◽  
Dependent Manner ◽  
Content Type ◽  
Immune Effector ◽  
Host Interactions ◽  
Innate Immune Effector

ABSTRACTThe virulence ofCandida albicansin a mouse model of invasive candidiasis is dependent on the phospholipids phosphatidylserine (PS) and phosphatidylethanolamine (PE). Disruption of the PS synthase geneCHO1(i.e.,cho1Δ/Δ) eliminates PS and blocks thede novopathway for PE biosynthesis. In addition, thecho1Δ/Δ mutant's ability to cause invasive disease is severely compromised. Thecho1Δ/Δ mutant also exhibits cell wall defects, and in this study, it was determined that loss of PS results in decreased masking of cell wall β(1-3)-glucan from the immune system. In wild-typeC. albicans, the outer mannan layer of the wall masks the inner layer of β(1-3)-glucan from exposure and detection by innate immune effector molecules like the C-type signaling lectin Dectin-1, which is found on macrophages, neutrophils, and dendritic cells. Thecho1Δ/Δ mutant exhibits increases in exposure of β(1-3)-glucan, which leads to greater binding by Dectin-1 in both yeast and hyphal forms. The unmasking of β(1-3)-glucan also results in increased elicitation of TNF-α from macrophages in a Dectin-1-dependent manner. The role of phospholipids in fungal pathogenesis is an emerging field, and this is the first study showing that loss of PS inC. albicansresults in decreased masking of β(1-3)-glucan, which may contribute to our understanding of fungus-host interactions.

scholarly journals Neutrophil Extracellular Traps Serve as Key Effector Molecules in the Protection Against Phialophora verrucosa

2021 ◽  
Vol 186 (3) ◽  
pp. 367-375
Author(s):  
Qin Liu ◽  
Wenjuan Yi ◽  
Si Jiang ◽  
Jiquan Song ◽  
Pin Liang
Keyword(s):  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Immune Effector ◽  
Phialophora Verrucosa ◽  
Extracellular Traps ◽  
Sytox Green ◽  
Innate Immune Effector ◽  
Pathogen Control ◽  
Extracellular Structures

AbstractPhialophora verrucosa (P. verrucosa) is a pathogen that can cause chromoblastomycosis and phaeohyphomycosis. Recent evidence suggests that neutrophils can produce neutrophil extracellular traps (NETs) that can protect against invasive pathogens. As such, we herein explored the in vitro functional importance of P. verrucosa-induced NET formation. By assessing the co-localization of neutrophil elastase and DNA, we were able to confirm the formation of classical NETs entrapping P. verrucosa specimens. Sytox Green was then used to stain these NETs following neutrophil infection with P. verrucosa in order to quantify the formation of these extracellular structures. NET formation was induced upon neutrophil exposure to both live, UV-inactivated, and dead P. verrucosa fungi. The ability of these NETs to kill fungal hyphae and conidia was demonstrated through MTT and pouring plate assays, respectively. Overall, our results confirmed that P. verrucosa was able to trigger the production of NETs, suggesting that these extracellular structures may represent an important innate immune effector mechanism controlling physiological responses to P. verrucosa infection, thereby aiding in pathogen control during the acute phases of infection.

scholarly journals Gelatinase B/Matrix Metalloproteinase-9 as Innate Immune Effector Molecule in Achalasia

2018 ◽  
Vol 9 (11) ◽  
pp. e208 ◽  
Author(s):  
Janette Furuzawa-Carballeda ◽  
Lise Boon ◽  
Gonzalo Torres-Villalobos ◽  
Fernanda Romero-Hernández ◽  
Estefania Ugarte-Berzal ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Innate Immune ◽  
Gelatinase B ◽  
Immune Effector ◽  
Effector Molecule ◽  
Innate Immune Effector ◽  
Metalloproteinase 9

scholarly journals Actin polymerization as a key innate immune effector mechanism to controlSalmonellainfection

2014 ◽  
Vol 111 (49) ◽  
pp. 17588-17593 ◽  
Author(s):  
Si Ming Man ◽  
Andrew Ekpenyong ◽  
Panagiotis Tourlomousis ◽  
Sarra Achouri ◽  
Eugenia Cammarota ◽  
...  
Keyword(s):  
Actin Polymerization ◽  
Innate Immune ◽  
Immune Effector ◽  
Effector Mechanism ◽  
Innate Immune Effector

scholarly journals The innate immune effector ISG12a promotes cancer immunity by suppressing the canonical Wnt/β-catenin signaling pathway

2020 ◽  
Vol 17 (11) ◽  
pp. 1163-1179
Author(s):  
Rilin Deng ◽  
Chaohui Zuo ◽  
Yongqi Li ◽  
Binbin Xue ◽  
Zhen Xun ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Innate Immune ◽  
Immune Effector ◽  
Cancer Immunity ◽  
Innate Immune Effector ◽  
Canonical Wnt
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