| Native X-DING-CD4 protein secreted by HIV-1 resistant CD4+ T cells blocks activity of IL-8 promoter in human endothelial cells infected with enteric bacteria. | |
| | |
MedLine Citation:
|
PMID: 22031506 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
|
Onsets of bacterial infections devastate the compromised immune system in AIDS patients. Damaged gut mucosa permits dissemination of bacterial toxins into deeper layers and hyper-activation of the immune system. We previously reported that the unfractionated supernatants of HIV-resistant CD4(+) T cells impeded the NF-κB/DNA binding in macrophages induced by either HIV-1 or LPS. The active component of this soluble material was identified as X-DING-CD4 (extracellular DING from CD4 T cells). We hypothesized that the anti-inflammatory effect of the X-DING-CD4 protein might extend to non-immune cells, for example endothelial cells, undergoing persistent endotoxin stimulation in the course of advanced HIV disease. To test this proposition, we evaluated the efficiency of NF-κB and Ap-1 binding to the IL-8 promoter in LPS-activated endothelial cells and control human macrophages exposed to native X-DING-CD4 protein. We found a deficiency of NF-κB- but not AP-1-DNA binding in the systems where cells were treated with native soluble X-DING-CD4 protein. The X-DING-CD4-mediated inhibition of the IL-8 promoter also resulted in a reduction of the soluble IL-8 protein in endothelial cells and human macrophages infected with a subset of enteric bacteria frequently causing diarrhea in progressive HIV disease. Bacterial endotoxin did not induce the endogenous X-DING-CD4 mRNA activity in human macrophages and transformed CD4(+)T cells, indicating that the reduction of LPS-mediated IL-8 promoter activation was not related to de novo X-DING-CD4 protein synthesis, but depended on function of the exogenous X-DING-CD4 protein. This study provides evidence that the X-DING-CD4 protein might be developed as a novel biotherapeutic to control LPS-mediated inflammation in advanced HIV disease. |
| | |
Authors:
|
Anna Ivanova; Rasheda Y Shilpi; Rakhee Sachdeva; Guanhua Li; Malgorzata Simm |
Related Documents
:
|
19998456 - Cd24 is upregulated in inflammatory bowel disease and stimulates cell motility and colo... 15771296 - Erbb-1 expression in experimental model of inflammatory bowel disease in rats. 20594136 - Mycobacteria in crohn's disease: how innate immune deficiency may result in chronic inf... 18200516 - Vitamin d derivatives induce apoptosis and downregulate icam-1 levels in peripheral blo... 2706756 - Cardiac dysfunction caused by factors released from endotoxin-activated macrophages. 9862326 - Lack of th2 cytokine increase during spontaneous remission of experimental allergic enc... |
Publication Detail:
|
Type: JOURNAL ARTICLE Date: 2011-10-26 |
Journal Detail:
|
Title: Innate immunity Volume: - ISSN: 1753-4267 ISO Abbreviation: - Publication Date: 2011 Oct |
Date Detail:
|
Created Date: 2011-10-27 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101469670 Medline TA: Innate Immun Country: - |
Other Details:
|
Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
|
Protein Chemistry Laboratory, St. Luke's/Roosevelt Hospital, Columbia University, New York, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: The punishment of gene doping - The relation between WADA prohibited lists, German Medicinal Product...
Next Document: Protein and RNA engineering to customize microbial molecular reporting.