Host enzyme induction

Exposure to inducing agents is common but not uniform across the human population. The ultimate degree of enzyme induction depends both upon the extent of exposure and upon the receptivity of the host s cells to the inducing stimulus. Receptivity probably is strongly influenced by genetics. 

Host 3-Glucan Hydrolase Induction. A further response to microbial invasion of host tissues involves an increase in activity of certain host enzymes, especially the glycan hydrolases which are potentially able to depolymerise microbial polysaccharides. 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

Botrytis cinerea is responsible for gray mold disease in more than 200 host plants. This necrotrophic fungus displays the capacity to kill host cells through the production of toxins and reactive oxygen species and the induction of a plant-produced oxidative burst. Thanks to an arsenal of degrading enzymes, B. cinerea is then able to feed on various plant tissues (Choquer and others 2007). 

According to Albersheim and coworkers,10 the mechanism of induction of pathogeny is associated with an interaction, between the pathogen and the cell-wall saccharides of the host, which influences the production of enzymes degrading its cell walls. The production of enzyme is regulated both by the pathogen and the host. 

Yu SJ (1983) Induction of detoxifying enzymes by allelochemicals and host plants in the fall armyworm. Pestic Biochem Physiol 19 330-336 Yu SJ (1984) Interactions of allelochemicals with detoxification enzymes of insecticide-susceptible and resistant fall armyworms. Pestic Biochem Physiol 22 60-68 Yu SJ (1986) Consequences of induced foreign compound-metabolizing enzymes in insects. In Brattsten LB, Ahmad S (eds) Molecular aspects of insect-plant associations. Plenum, New York, pp 153-174... 

The use of a recombinant strains as biocatalysts has the advantage that once the fermentation conditions for the host microorganisms have been found, the conditions to be used for the recombinant strain are mostly close to these. Furthermore, the need for induction can be removed, undesired side reactions can be avoided and enzymes from pathogenic strains can safely be produced in recombinants of GRAS organisms. Therefore, biocatalysts that are amenable to genetic engineering are frequently preferred over those that are not. 

Yu S. J. (1983) Induction of detoxifying enzymes by allelochemicals and host plants in the fall armyworm. Pest. Biochem. Physiol. 19, 330-336. 

They act as antipathogenic agents and thus affect the process of pathogenesis. They may act on the host through the Induction of plant resistance mechanisms such as stimulation of lignification or enhancement of phytoalexin production. (Please refer to the chapter by Salt and Kuc in this volume for further discussion of this type of compound.) They may act on the pathogen to accentuate elicitor release or to prevent infection (host penetration), colonization (inhibition of phytotoxin synthesis, extracellular enzyme production and action, or phytoalexin degradation) or reproduction. 

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