Lipoarabinomannans (LAM) is believed as a potential virulence factor of Mycobacterium tuberculosis. LAM exhibits marked differences in biological activities depending on the types, arabinofuranosyl-terminated LAM (AraLAM) derived from a rapidly growing Mycobacterium sp. and heavily mannosylated LAM (ManLAM) derived from the Erdman strain. Collaboration between macrophages and T cells, especially macrophage activation by gamma interferon (IFN-r) and chemoattraction of T cells at the very inflammatory foci would be essential in defence against M. tubercu/osis. Chemokines Mig and IP-10 are inducible by IFN-r from macrophages and have been shown to act in vitro as T cell chemoattractants. However, little is known of LAMs capacity to induce chemokines Mig and IP-10 in macrophages. In this experiment, Mig and IP10 mRNA was expressed in the delayed-type hypersensitivity (DTH) against BCG in BCG-immune mice. In some experiments, both Mig and IP-10 mRNA was evidently induced with different time courses in THP-1 cells stimulated with whole live M. tubercu/osis H37Rv (Erdman). To investigate whether Mig and IP-10 genes are differentially induced depending on the type of LAM, PCR amplification was used to detect mRNA of Mig and IP-10 from the THP-1 human monocytic cells stimulated with LAM. AraLAM, but not ManLAM, induced weakly Mig and IP-10 mRNA in the THP-1 cells. The induction of Mig and IP-10 was dependent upon the dose of AraLAM and exhibited different time courses. The mRNA for Mig and IP-10 was induced within 2 hr and 4 hr from the initiation of treatrnent and has disappeared by 8 hr and 24 hr under the experimental conditions used in this study, respectively. IFN-y at 100 U/ml, but not at 10 U/ml, was itself a good stimulus of both Mig and IP- 10 expression, and synergized with either AraLAM or ManLAM for induction of both Mig and IP-10. The expression patterns of MCP-3 were somewhat similar to those of Mig and IP10 in all of the experiments. These data indicate that IFN-r may contribute to effective macrophage function if macrophages are not fully affected by ManLAM, and chemokines Mig and IP-10 may a role in recruitment of T cells at inflammatory foci of tuberculosis.
Animals ; Chemokines* ; Chemotactic Factors ; Cooperative Behavior ; Humans ; Hypersensitivity ; Interferons ; Macrophage Activation ; Macrophages ; Mice ; Mycobacterium ; Mycobacterium bovis ; Mycobacterium tuberculosis ; Polymerase Chain Reaction ; RNA, Messenger* ; T-Lymphocytes ; Tuberculosis ; Virulence

No abstract available.
Meibomian Glands* ; Thermodynamics*

No abstract available.
HLA-D Antigens* ; Humans*

No abstract available.
Korea*

No abstract available.
Aneurysm* ; Carotid Artery, Internal* ; Epistaxis*

No abstract available.
Rectus Abdominis* ; Thigh*

No abstract available.
Rectus Abdominis* ; Thigh*

No abstract available.

"Mig is a gamma interferon-inducible T cell chemoattractant that is a member of the chemokine family of cytokines. In order to gain a better understanding of the molecular mechanisms that regulate expression of the Mig gene, we have characterized the Mig gene and compared its structure and regulatory sequences with that of its ciosest IP10 gene. The genomic organization of the Mig gene reveals three introns that interrupt the transcribed sequence into four functional domains with a single ""CAT""- and ""TATA""-like structure. Primer extension analysis was used to identify the transcriptional initiation site that is located 50 bp upstream to the methionine codon that begins the long open reading frame. Comparison of the intron-exon structure of this gene to the gene for IP10 establishes that both genes are interrupted in precisely the same positions within homologous codons. The similarity of the intron-exon structure of the Mig and IP10 genes further support the hypothesis that Mig and IP10 genes have evolved from a common ancestral gene by gene duplication. The 5'-flanking region of Mig gene shows no overall sequence similarity with that from its closest IP10 gene whose production is also affected by gamma interferon. However, there are regions including a sequence with similarity to the NFxB binding site, AP-1 binding site, and ISRE. The r-RF-1 binding site is well conserved from -204 to -194 from the transcription start site in the Mig gene. Given the importance of IFN-r for effective immunity in tuberculosis and induction of Mig and IP10 genes in macrophages by IFN-r, we demonstrated induction of the genes Mig and IP10 with different message levels in the THP-1 human monocytic cell lines stimulated with whole M. tuberculosis. Despite the very similarity in genomic organization and the overlap in biological activities between MIG and IP10, our data described herein further support the suggestion that these chemokines rnay role nonredundantly in vivo. Moreover, our studies done on the Mig gene should provide the structural framework for future studies and begin to dissect cis-acting DNA sequences that are critical for gene regulation mediated by cell surface receptors."
Base Sequence ; Binding Sites ; Cell Line ; Chemokine CXCL9* ; Chemokines ; Codon ; Cytokines ; Gene Duplication ; Genome ; Humans* ; Interferons ; Introns ; Macrophages ; Methionine ; Open Reading Frames ; Transcription Factor AP-1 ; Transcription Initiation Site ; Tuberculosis

No abstract available.
Arthroplasty ; Femoral Fractures ; Hip