Published online by Cambridge University Press: 15 September 2009
The concept that bacteria are rather simple organisms that interact with eukaryotic cells in a passive manner is now totally untenable, as more evidence emerges of active interaction and reaction between bacteria and host. It is also becoming clear that bacterial toxins do not merely operate as molecules of death for a cell. Toxin action may ultimately result in cell death, and indeed death of the host organism, but often the producer bacterium requires that the host cell is first organised in a particular manner. In these circumstances, the toxins sent out by the bacterium on its “behalf” have a mission to regulate the target cell in a very precise manner. Not much is known about the eukaryotic mechanisms that exist to control rather then kill bacteria, but such mechanisms must exist to regulate the homeostatic balance between a eukaryotic host and its commensal bacteria. Furthermore, a host weakened by diseases leading to immunodeficiency, such as HIV/AIDS, stress, or malnutrition, is more susceptible to infection – both by bacteria normally classified as pathogenic, but also by commensal bacteria, which in the circumstances are named as opportunistic pathogens.
Much more is known about the mechanisms that bacteria use to regulate cellular function. Many of these mechanisms have been described in detail in the chapters in this book. Several common themes are appearing. The most frequent targets for such toxins are intracellular proteins involved in the signal transduction pathways that integrate incoming signals at the cell surface.
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