NDLI: Antibacterial cathelicidin peptide CAP11 inhibits the lipopolysaccharide (LPS)-induced suppression of neutrophil apoptosis by blocking the binding of LPS to target cells

Content Provider	Springer Nature Link
Author	Nagaoka, I. Yomogida, S. Tamura, H. Hirata, M.
Copyright Year	2004
Abstract	Objective: The action of antibacterial cathelicidin CAP11 (cationic antibacterial polypeptide of 11 kDa) on the lipopolysaccharide (LPS)-induced suppression of neutrophil apoptosis was evaluated in vitro.Methods: Human neutrophils (106 cells/ml) were incubated alone or with mononuclear cells (6 × 105 cells/ml) in the presence of LPS (10 ng/ml) and CAP11 (0.1 ~ 10 μg/ml), and neutrophil apoptosis was determined.Results: LPS suppressed neutrophil apoptosis, accompanied with the activation of NF-κB, phosphorylation of extracellular signal-related protein kinase (ERK), expression of Bcl-XL (an anti-apoptotic protein) and inhibition of caspase 3 activity. Interestingly, CAP11 (>1 μg/ml) reversed the actions of LPS to trigger these changes, and induced neutrophil apoptosis (p < 0.0001). Moreover, neutralizing antibodies against Mac-1 (CD11b/CD18) and Toll-like receptor (TLR) 4 completely blocked the LPS-induced suppression of neutrophil apoptosis (p < 0.0001), suggesting a major role of Mac-1 and TLR4 in the LPS-mediated neutrophil activation. In addition, LPS activated monocytes to produce proinflammatory cytokines (IL-1β, TNF-α and IL-8) and inhibited neutrophil apoptosis. Importantly, CAP11 (>1 μg/ml) reduced the cytokine production, thereby inducing neutrophil apoptosis (p < 0.0001). Finally, CAP11 (>1 μg/ml) strongly suppressed the LPS-binding to neutrophils and monocytes (p < 0.01).Conclusions: CAP11 is able to block the LPS-induced survival of neutrophils via the suppression of anti-apoptotic signaling in neutrophils and cytokine production from monocytes by inhibiting the binding of LPS to target cells.
Starting Page	609
Ending Page	622
Page Count	14
File Format	PDF
ISSN	10233830
Journal	Inflammation Research
Volume Number	53
Issue Number	11
e-ISSN	1420908X
Language	English
Publisher	Birkhäuser-Verlag
Publisher Date	2004-01-01
Publisher Place	Basel
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neutrophil Apoptosis Antibacterial peptide Cathelicidin Lipopolysaccharide Immunology Pharmacology/Toxicology Allergology Dermatology Neurology Rheumatology
Content Type	Text
Resource Type	Article
Subject	Pharmacology Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

A FQHPSFI peptide selectively binds to LPS-activated alveolar macrophages and inhibits LPS-induced MIP-2 production

Geniposide inhibits interleukin-6 and interleukin-8 production in lipopolysaccharide-induced human umbilical vein endothelial cells by blocking p38 and ERK1/2 signaling pathways

Ivermectin inhibits LPS-induced production of inflammatory cytokines and improves LPS-induced survival in mice

N-methyl pyrrolidone (NMP) inhibits lipopolysaccharide-induced inflammation by suppressing NF-κB signaling

CPPD crystal-induced suppression of neutrophil apoptosis is regulated by the ERK1/2 and PI3-kinase/Akt pathways

Quercetin inhibits LPS-induced delay in spontaneous apoptosis and activation of neutrophils

Augmentation of the bactericidal activities of human cathelicidin CAP18/LL-37-derived antimicrobial peptides by amino acid substitutions

β-1,4-Galactosyltransferase-involved in lipopolysaccharide-induced adhesion of schwann cells

A peptide derived from neutrophil inhibitory factor (NIF) blocks neutrophil adherence to endothelial cells

Antibacterial cathelicidin peptide CAP11 inhibits the lipopolysaccharide (LPS)-induced suppression of neutrophil apoptosis by blocking the binding of LPS to target cells

Similar Documents

A FQHPSFI peptide selectively binds to LPS-activated alveolar macrophages and inhibits LPS-induced MIP-2 production

Geniposide inhibits interleukin-6 and interleukin-8 production in lipopolysaccharide-induced human umbilical vein endothelial cells by blocking p38 and ERK1/2 signaling pathways

Ivermectin inhibits LPS-induced production of inflammatory cytokines and improves LPS-induced survival in mice

N-methyl pyrrolidone (NMP) inhibits lipopolysaccharide-induced inflammation by suppressing NF-κB signaling

CPPD crystal-induced suppression of neutrophil apoptosis is regulated by the ERK1/2 and PI3-kinase/Akt pathways

Quercetin inhibits LPS-induced delay in spontaneous apoptosis and activation of neutrophils

Augmentation of the bactericidal activities of human cathelicidin CAP18/LL-37-derived antimicrobial peptides by amino acid substitutions

β-1,4-Galactosyltransferase-involved in lipopolysaccharide-induced adhesion of schwann cells

A peptide derived from neutrophil inhibitory factor (NIF) blocks neutrophil adherence to endothelial cells

Antibacterial cathelicidin peptide CAP11 inhibits the lipopolysaccharide (LPS)-induced suppression of neutrophil apoptosis by blocking the binding of LPS to target cells