Guest guest Posted July 1, 2006 Report Share Posted July 1, 2006 This is such a great investigation, it examined interaction of two chlamydial strains with tons of different mouse and human cell lines, illuminating why so many seemingly inconsistent results had been found in the past. Different strains interact with different cells quite differently. In some cases tryptophan limitation is occuring, in others there is another mechanism at play. http://iai.asm.org/cgi/reprint/74/1/225.pdf My hope is to assemble as thorough a cataloge as possible of host factors that cause hypometabolic states in bacteria. For Mtb in mice, its probably some aspect of immunity that does it; for Mtb in humans, its most likely hypoxia in acellular necrotic lung tissue that leads to the most severe hypometabolic phenotype, according to Mitchison. Thats all I have so far. For chlamydiae I suspect the macrophage is probably the most relevant cell and this paper shows the need to absolutely beware extrapolating from mouse macrophages, which were examined by AA Azenabor and also by the above paper. I dont know yet of anyone having examined causes of chlamydial death/hypometabolism in human macrophages (not monocytes). Quote Link to comment Share on other sites More sharing options...
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