Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1993-6-4
pubmed:abstractText
The granulomatous immune response in tuberculosis is characterized by delayed hypersensitivity and is mediated by various cytokines released by the stimulated mononuclear phagocytes, including tumor necrosis factor-alpha (TNF alpha) and IL-1 beta. We have demonstrated that Mycobacterium tuberculosis cell wall component lipoarabinomannan (LAM), mycobacterial heat shock protein-65 kD, and M. tuberculosis culture filtrate, devoid of LPS as assessed by the Amebocyte Lysate assay, stimulate the production of TNF alpha and IL-1 beta proteins and mRNA from mononuclear phagocytes (THP-1 cells). The effect of LAM on the release of these cytokines was specific, as only LAM stimulation was inhibited by anti-LAM monoclonal antibody. Interestingly, we found that LAM and Gram-negative bacterial cell wall-associated endotoxin LPS may share a similar mechanism in their stimulatory action as demonstrated by inhibition of TNF alpha and IL-1 beta release by monoclonal antibodies to CD14. Anti-CD14 monoclonal antibody MY4 inhibited both TNF alpha and IL-1 beta release with LAM and LPS but no effect was observed with other mycobacterial proteins. An isotype antibody control did not inhibit release of cytokines under the same experimental conditions. M. tuberculosis and its components upregulated IL-1 beta and TNF alpha mRNAs in THP-1 cells. Nuclear run-on assay for IL-1 beta demonstrated that LAM increased the transcription rate. The induction of IL-1 beta was regulated at the transcriptional level, in which these stimuli acted through cis-acting element(s) on the 5' flanking region of the IL-1 beta genomic DNA. M. tuberculosis cell wall component LAM acts similarly to LPS in activating mononuclear phagocyte cytokine TNF alpha and IL-1 beta release through CD14 and synthesis at the transcriptional level; both cytokines are key participants in the host immune response to tuberculosis.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1373520, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1541542, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1548069, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1556131, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1588290, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1624801, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1690136, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1698311, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-1850379, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2110362, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2111816, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2113553, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2138940, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2161430, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2205576, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2387094, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2402637, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2451266, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2469122, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2471708, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2492162, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2503277, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2647299, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2786503, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-2989698, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3015413, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3053456, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3119471, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3128482, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3147796, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3258884, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3264123, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3312018, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3484390, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3485575, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-3488815, http://linkedlifedata.com/resource/pubmed/commentcorrection/7683696-6960240
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2076-83
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:7683696-Antibodies, Monoclonal, pubmed-meshheading:7683696-Antigens, CD, pubmed-meshheading:7683696-Antigens, CD14, pubmed-meshheading:7683696-Antigens, Differentiation, Myelomonocytic, pubmed-meshheading:7683696-Cell Nucleus, pubmed-meshheading:7683696-Chloramphenicol O-Acetyltransferase, pubmed-meshheading:7683696-Escherichia coli, pubmed-meshheading:7683696-Humans, pubmed-meshheading:7683696-Interleukin-1, pubmed-meshheading:7683696-Kinetics, pubmed-meshheading:7683696-Leukemia, pubmed-meshheading:7683696-Lipopolysaccharides, pubmed-meshheading:7683696-Mycobacterium tuberculosis, pubmed-meshheading:7683696-RNA, Messenger, pubmed-meshheading:7683696-RNA, Neoplasm, pubmed-meshheading:7683696-Transfection, pubmed-meshheading:7683696-Tumor Cells, Cultured, pubmed-meshheading:7683696-Tumor Necrosis Factor-alpha
pubmed:year
1993
pubmed:articleTitle
Mechanisms of stimulation of interleukin-1 beta and tumor necrosis factor-alpha by Mycobacterium tuberculosis components.
pubmed:affiliation
Department of Medicine, Bellevue Hospital Center, New York University Medical Center, New York 10016.
More...