Abstract
There are several examples that illustrate the principle that the host immune/inflammatory response is necessary for the manifestation of disease caused by infection (Table 1). For example, it is well recognized that some infections trigger autoimmune disease. While the microbe is the trigger, the host response is the bullet that leads to the actual disease. Others have shown that infection with Clostridium difficile causes enteritis but administration of antibodies that impair the homing of immune/inflammatory cells to the gut prevents the manifestation of diarrhoea1. Even the prototype for a microbial virulence factor, cholera toxin, cannot exert its pathogenic effect without an intact host response. Infection of mice deficient in stem cell factor or its receptor does not induce fluid accumulation in the intestinal lumen after administration of the cholera toxin2. Thus, the host response must often be considered an essential element of microbial pathogenicity.
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Ernst, P.B. (2000). The inflammatory activity in Helicobacter pylori infection is predominantly host-related. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3927-4_22
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DOI: https://doi.org/10.1007/978-94-011-3927-4_22
Publisher Name: Springer, Dordrecht
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