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<https://discovery.ucl.ac.uk/id/eprint/17419> <http://purl.org/dc/terms/title> "Studies of the intercellular signalling actions of Mycobacterium tuberculosis chaperonins"^^<http://www.w3.org/2001/XMLSchema#string> .
<https://discovery.ucl.ac.uk/id/eprint/17419> <http://purl.org/ontology/bibo/abstract> "Mycobacterial chaperonin 60 (Cpn60) is an intracellular molecule essential for\r\ncellular function due to its protein folding actions. However, it has recently been\r\nestablished that Cpn60 can be released by certain bacteria and act as an extracellular\r\nsignalling protein. Mycobacterium tuberculosis has two genes coding for Cpn60\r\nproteins: cpn60.1 and cpn60.2 (also known as hsp65). It was recently shown that\r\nCpn60.1 and Cpn60.2 are pro-inflammatory activators of myeloid cells and that the\r\neffects of Cpn60.1, but not Cpn60.2, depend on CD14. This PhD project shows that\r\nM. tuberculosis Cpn60.1 and Cpn60.2 proteins strongly bind to human peripheral\r\nblood monocytes but their binding sites are different. Both M. tuberculosis Cpn60\r\nproteins depend on MyD88 for the maximal activation of intracellular signalling\r\npathways but have different TLR requirements: Cpn60.1 signals exclusively through\r\nTLR4 while Cpn60.2 needs the presence of TLR2 and TLR4 for maximal induction\r\nof pro-inflammatory cytokines. A study has recently established that an M.\r\ntuberculosis mutant with an inactivated cpn60.1 gene is unable to induce granulomas\r\nin animal models suggesting that Cpn60.1 has inflammation-modulatory effects on\r\nmyeloid cells. This PhD project identified that recombinant M. tuberculosis Cpn60.1\r\nhas bipolar effects on human circulating monocytes. At high concentrations Cpn60.1\r\ninduces the synthesis of TNF-α and promotes the phosphorylation of NF-κB p65,\r\np44/42MAPK and p38 MAPK while at picomolar concentrations, Cpn60.1 inhibits the\r\nlipopolysaccharide-induced formation of TNF-α and the phosphorylation of NF-κB\r\np65 without affecting the activation of MAP kinases. Gene expression analysis show\r\nthat low concentrations of Cpn60.1 completely suppress cell activation while higher\r\nconcentrations of Cpn60.1 down-regulate the expression of major pro-inflammatory\r\ncytokine and chemokine genes in human monocytes. It is therefore concluded that M.\r\ntuberculosis Cpn60.1 is an unusual protein with the ability to induce bipolar effects\r\nwhich may help explain the pathology of granuloma formation in tuberculosis."^^<http://www.w3.org/2001/XMLSchema#string> .
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