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Modulation of Neutrophil Apoptosis by Antimicrobial Peptides
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- Isao Nagaoka
- Department of Host Defense and Biochemical Research, Juntendo University, Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan
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- Kaori Suzuki
- Department of Host Defense and Biochemical Research, Juntendo University, Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan
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- François Niyonsaba
- Atopy (Allergy) Research Center, Juntendo University, Graduate School of Medicine, Tokyo 113-8421, Japan
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- Hiroshi Tamura
- Seikagaku Biobusiness Corporation, Tokyo 104-0033, Japan
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- Michimasa Hirata
- Institute of Ohtaka Enzyme Co., Hokkaido 047-0156, Japan
Description
<jats:p>Peptide antibiotics possess the potent antimicrobial activities against invading microorganisms and contribute to the innate host defense. Human antimicrobial peptides, α-defensins (human neutrophil peptides, HNPs), human β-defensins (hBDs), and cathelicidin (LL-37) not only exhibit potent bactericidal activities against Gram-negative and Gram-positive bacteria, but also function as immunomodulatory molecules by inducing cytokine and chemokine production, and inflammatory and immune cell activation. Neutrophil is a critical effector cell in host defense against microbial infection, and its lifespan is regulated by various pathogen- and host-derived substances. Here, we provided the evidence that HNP-1, hBD-3, and LL-37 cannot only destroy bacteria but also potently modulate (suppress) neutrophil apoptosis, accompanied with the phosphorylation of ERK-1/-2, the downregulation of tBid (an proapoptotic protein) and upregulation of Bcl-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mtext>x</mml:mtext><mml:mtext>L</mml:mtext></mml:msub></mml:math>(an antiapoptotic protein), and the inhibition of mitochondrial membrane potential change and caspase 3 activity, possibly via the actions on the distinct receptors, the P2Y<jats:sub>6</jats:sub>nucleotide receptor, the chemokine receptor CCR6, and the low-affinity formyl-peptide receptor FPRL1/the nucleotide receptor P2X<jats:sub>7</jats:sub>, respectively. Suppression of neutrophil apoptosis results in the prolongation of their lifespan and may be advantageous for the host defense against bacterial invasion.</jats:p>
Journal
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- ISRN Microbiology
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ISRN Microbiology 2012 1-12, 2012-03-27
Wiley
