Interplay of bacterial toxins with host defence: molecular mechanisms of immunomodulatory signalling.
Mucosal surfaces are protected by a first line of defence termed the innate immune system, which controls the resident microflora to effectively prevent microbial diseases. Inflammatory processes are activated as a consequence of a complex interplay between microbes and host target cells. Many bacterial pathogens have developed mechanisms to avoid host recognition. Some are even able to exploit the immune response through sophisticated interactions with the host signalling cascades in order to increase their replication and propagation. While in the past major emphasis on bacterial protein toxins was directed towards their cytotoxic role, it is increasingly evident that toxins can also modulate various cellular functions at non-cytolytic concentrations. Here, we review important aspects on the molecular mechanisms of immunomodulatory interference by bacterial toxins, with emphasis on the signalling induced in the intestinal epithelium.
Backert
Steffen
S
Institute of Medical Microbiology, Otto von Guericke University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany. Steffen.Backert@medizin.uni-magdeburg.de
König
Wolfgang
W
D000818:Animals; D001419:Bacteria / Q000276:immunology / Q000472:pathogenicity*; D001424:Bacterial Infections / Q000276:immunology / Q000382:microbiology*; D001427:Bacterial Toxins / Q000276:immunology* / Q000633:toxicity; D006801:Humans; D007113:Immunity, Innate; D007155:Immunologic Factors; D007413:Intestinal Mucosa / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D020935:MAP Kinase Signaling System; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000502:physiology
D001427:Bacterial Toxins; D007155:Immunologic Factors; D051193:Toll-Like Receptors