Overall, these insights coupled with the availability of characterized non-binding mutants of SitA provide a platform for future investigations of the physiological role of SitA during colonization and/or invasion in animal models of disease caused by S. pseudintermedius.
Experimental use of this system would open up new horizons in genome biology, including the establishment of cellular and animal models of diseases caused by translocations and copy-number variations.
It is known that chinchillas are sensitive to P. aeruginosa infection and are therefore frequently used as an animal model of diseases caused by P. aeruginosa, including otitis media, otitis interna, pneumonia, septicaemia enteritis, and sudden death [ 9- 12].
We and others have previously demonstrated that aerosol infection of BALB/c mice with B. thailandensis is an excellent surrogate model for the acute pneumonic form of disease caused by B. pseudomallei and is capable of reproducing the major lung pathology of murine melioidosis [20], [21].
Several chapters in section 4 describe in vitro and animal model systems for the study of diseases caused by superantigens, including autoimmune disease, neuropathology, toxic shock, and others.
Thus, we have developed a new useful model system for addressing the pathological mechanism of diseases caused by the downregulation of Bmpr1a-mediated signaling.
Mottled-dappled (Mo-dp) is a mouse model of Menkes disease caused by a large, previously uncharacterized deletion in the 5′ region of Atp7a, the mouse ortholog of ATP7A.
Genome-scale metabolic models of disease-causing organisms have been constructed and evaluated to identify potential drug targets [ 3- 5].
The team introduced BHB to mouse models of inflammatory diseases caused by NLP3.
The inability to construct animal models of human diseases caused by mutated mitochondrial DNA (mtDNA) has been a major obstacle to investigating pathogenetic mechanisms associated with specific mtDNA mutations.
Age‐dependent paralysis in a transgenic worm model of Huntington's disease caused by expression of aggregation‐prone Q35 was reduced by elc‐1 knockdown (Fig. 5B).
