LL-37; The Human Epithelial Antimicrobial Peptide and Innate Immunity System

2015 ◽  
Vol 1 (4) ◽  
pp. 76
Author(s):  
Seyadeh Zahra Sajjadiyan ◽  
Sarah Mohammadinejad ◽  
Leila Hassani
Keyword(s):  
Innate Immunity ◽  
Antimicrobial Peptide

The novel antimicrobial peptide β3-defensin is produced by the amnion: A possible role of the fetal membranes in innate immunity of the amniotic cavity

2004 ◽  
Vol 191 (5) ◽  
pp. 1678-1687 ◽  
Author(s):  
Irina A. Buhimschi ◽  
Maher Jabr ◽  
Catalin S. Buhimschi ◽  
Anelia P. Petkova ◽  
Carl P. Weiner ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Antimicrobial Peptide ◽  
Fetal Membranes ◽  
The Novel ◽  
Amniotic Cavity

scholarly journals Antimicrobial peptides signal need for sleep from peripheral wounds to the nervous system

2020 ◽  
Author(s):  
Marina Sinner ◽  
Florentin Masurat ◽  
Jonathan Ewbank ◽  
Nathalie Pujol ◽  
Henrik Bringmann
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Nervous System ◽  
Antimicrobial Peptides ◽  
Antimicrobial Peptide ◽  
Long Range ◽  
Innate Immune Response ◽  
Innate Immune ◽  
List Type ◽  
Active Neuron

AbstractWounding triggers a protective innate immune response that includes the production of antimicrobial peptides and increased sleep. Little is known, however, about how peripheral wounds signal need for sleep to the nervous system. We found that during C. elegans larval molting, a tolloid/BMP-1-like protein promotes sleep through an epidermal innate immune pathway and the expression of more than a dozen antimicrobial peptide (AMP) genes. In the adult, epidermal injury activates innate immunity and turns up AMP production to trigger sleep. We show for one AMP, NLP-29, that it acts through the neuropeptide receptor NPR-12 in neurons that depolarize the sleep-active RIS neuron to induce sleep. Sleep in turn increases the chance of surviving injury. Thus, we found a novel mechanism by which peripheral wounds signal to the nervous system to increase protective sleep. Such a long-range somnogen signaling function of AMPs might also boost sleep in other animals including humans.Highlights- Gain-of-function mutation in the tolloid/BMP-1-like NAS-38 protein increases sleep- NAS-38 activates innate immunity pathways to ramp up STAT-dependent antimicrobial peptide (AMP) expression- Wounding increases sleep through the innate immune response and AMPs- Antimicrobial peptides are long-range somnogens that act through neuronal neuropeptide receptors to depolarize a sleep-active neuron- Sleep increases the chance to survive injuryGraphical Abstract

scholarly journals Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36

2009 ◽  
Vol 206 (3) ◽  
pp. 637-653 ◽  
Author(s):  
Terry K. Means ◽  
Eleftherios Mylonakis ◽  
Emmanouil Tampakakis ◽  
Richard A. Colvin ◽  
Edward Seung ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Candida Albicans ◽  
Caenorhabditis Elegans ◽  
Antimicrobial Peptide ◽  
Host Defense ◽  
Fungal Pathogens ◽  
Cytokine Production ◽  
Scavenger Receptors ◽  
Evolutionarily Conserved ◽  
And Control

Receptors involved in innate immunity to fungal pathogens have not been fully elucidated. We show that the Caenorhabditis elegans receptors CED-1 and C03F11.3, and their mammalian orthologues, the scavenger receptors SCARF1 and CD36, mediate host defense against two prototypic fungal pathogens, Cryptococcus neoformans and Candida albicans. CED-1 and C03F11.1 mediated antimicrobial peptide production and were necessary for nematode survival after C. neoformans infection. SCARF1 and CD36 mediated cytokine production and were required for macrophage binding to C. neoformans, and control of the infection in mice. Binding of these pathogens to SCARF1 and CD36 was β-glucan dependent. Thus, CED-1/SCARF1 and C03F11.3/CD36 are β-glucan binding receptors and define an evolutionarily conserved pathway for the innate sensing of fungal pathogens.

Inactivation of human kininogen-derived antimicrobial peptides by secreted aspartic proteases produced by the pathogenic yeast Candida albicans

2015 ◽  
Vol 396 (12) ◽  
pp. 1369-1375 ◽  
Author(s):  
Oliwia Bochenska ◽  
Maria Rapala-Kozik ◽  
Natalia Wolak ◽  
Wojciech Kamysz ◽  
Daria Grzywacz ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Candida Albicans ◽  
Antimicrobial Peptides ◽  
Antimicrobial Peptide ◽  
Host Organism ◽  
Pathogenic Yeast ◽  
Aspartic Proteases ◽  
Antifungal Potential ◽  
Anticandidal Activity

Abstract Ten secreted aspartic proteases (Saps) of Candida albicans cleave numerous peptides and proteins in the host organism and deregulate its homeostasis. Human kininogens contain two internal antimicrobial peptide sequences, designated NAT26 and HKH20. In our current study, we characterized a Sap-catalyzed cleavage of kininogen-derived antimicrobial peptides that results in the loss of the anticandidal activity of these peptides. The NAT26 peptide was effectively inactivated by all Saps, except Sap10, whereas HKH20 was completely degraded only by Sap9. Proteolytic deactivation of the antifungal potential of human kininogens can help the pathogens to modulate or evade the innate immunity of the host.

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