Host Defense Peptide LL-37, in Synergy with Inflammatory Mediator IL-1beta, Augments Immune Responses by Multiple Pathways.

Host Defense Peptide LL-37, in Synergy with Inflammatory Mediator IL-1beta, Augments Immune Responses by Multiple Pathways. Research Abstract Details 

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Host Defense Peptide LL-37, in Synergy with Inflammatory Mediator IL-1beta, Augments Immune Responses by Multiple Pathways. Abstract Text:

Jie Yu,Neeloffer Mookherjee,Kathleen Wee,Dawn M E Bowdish,Jelena Pistolic,Yuexin Li,Linda Rehaume,Robert E W Hancock,Jie Yu,Neeloffer Mookherjee,Kathleen Wee,Dawn M E Bowdish,Jelena Pistolic,Yuexin Li,Linda Rehaume,Robert E W Hancock,Jie Yu,Neeloffer Mookherjee,Kathleen Wee,Dawn M E Bowdish,Jelena Pistolic,Yuexin Li,Linda Rehaume,Robert E W Hancock,

The human cathelicidin LL-37 is a cationic host defense peptide and serves as an important component of innate immunity. It has been demonstrated to be a multifunctional modulator of innate immune responses, although the mechanism(s) underlying this have not been well characterized. In this study, it was demonstrated that LL-37 synergistically enhanced the IL-1beta-induced production of cytokines (IL-6, IL-10) and chemokines such as macrophage chemoattractant proteins (MCP-1, MCP-3) in human PBMC, indicating a role in enhancing certain innate immune responses. Similarly, LL-37 synergistically enhanced chemokine production in the presence of GM-CSF, but IFN-gamma, IL-4, or IL-12 addition led to antagonism, indicating that the role of LL-37 in reinforcing specific immune responses is selective and restricted to particular endogenous immune mediators. The inhibition of G protein-coupled receptors and PI3K substantially suppressed the ability of IL-1beta and LL-37 to synergistically enhance the production of chemokine MCP-3. Consistent with this, the combination of IL-1beta and LL-37 enhanced the activation/phosphorylation of kinase Akt and the transcription factor CREB. The role of transcription factor NF-kappaB was revealed through the demonstration of enhanced phosphorylation of IkappaBalpha and the consequent nuclear translocation of NF-kappaB subunits p50 and p65, as well as the antagonistic effects of an inhibitor of IkappaBalpha phosphorylation. These results together indicate that the human host defense peptide LL-37 can work in synergy with the endogenous inflammatory mediator IL-1beta to enhance the induction of specific inflammatory effectors by a complex mechanism involving multiple pathways, thus reinforcing certain innate immune responses.

Host Defense Peptide LL-37, in Synergy with Inflammatory Mediator IL-1beta, Augments Immune Responses by Multiple Pathways. Publishing Authors By Initials

J Yu,N Mookherjee,K Wee,DM Bowdish,J Pistolic,Y Li,L Rehaume,RE Hancock,J Yu,N Mookherjee,K Wee,DM Bowdish,J Pistolic,Y Li,L Rehaume,RE Hancock,J Yu,N Mookherjee,K Wee,DM Bowdish,J Pistolic,Y Li,L Rehaume,RE Hancock,

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Host Defense Peptide LL-37, in Synergy with Inflammatory Mediator IL-1beta, Augments Immune Responses by Multiple Pathways. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 179

Page Numbers: 7684-91

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Dec

YEAR: 2007

Host Defense Peptide LL-37, in Synergy with Inflammatory Mediator IL-1beta, Augments Immune Responses by Multiple Pathways. Information

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LANGUAGE: eng

NlmUniqueID: 2985117

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AFFILIATION: Department of Microbiology and Immunology, Centre for Microbial Diseases and Immunity Research, University of British Columbia, Vancouver, British Columbia, Canada.

Country: United States

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MEDLINETA: J Immunol

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