Experimental model of infection

Experimental Model of Infection with T. gondii and Modulation of Immune Response... 

Simpson RM, Leno M, Hubbard BS, Kindt TJ (1996) Cutaneous manifestations of human T cell leukemia virus type I infection in an experimental model. J Infect Dis 173 722-726. 

In soft tissue infection caused by group A Streptococcus, streptococcal toxic shock syndrome may occur. Although penicillin and cefazolin are efficacious, experimental models of group A streptococcal infection show clindamycin to be more effective than penicillin. ... 

MOI, TOI Modeling of infection and protein expression kinetics with experimental validation. Determination of critical rate constants. 22... 

Elevated DNA oxidation has been observed in several experimental models of cancer, including Helicobacter pylori infection-induced stomach cancer," rodent renal cancer," ... 

The experimental evidence in mouse and rabbit models of infection indicates that the 35-kDa protein encoded by VACV, rabbitpox vims and MYXV inhibit the chemokine-mediated infiltration of immune cells into primary sites of infection but have little influence on the progression of disease [17,20,21]. The expression of the 35-kDa protein from VACV Western Reserve (WR), a strain that does not encode the vCKBP, causes a slight attenuation of the vims associated with reduced inflammatory pathology in the lungs [22]. 

At least two environmental factors may contribute to the development of HP as a promoting factor viral infections and inhalation injury. Experimental models of HP have shown that animals challenged with respiratory syncytial virus or Sendai virus exhibit a more severe inflammatory response to subsequent Saccharopolyspora rectivirgula exposure, which may persist long after the viral infection has declined (11,12). Also, studies in humans have revealed that common respiratory vimses, primarily Influenza A, are often present in the lower airways of patients with HP (13). The reasons why viral infections may potentiate HP are unknown, but it may be related to vims-induced mucociliary dysfunction, increased expression of costimulatory molecules by alveolar macrophages, and increased secretion of chemokines, enhancing the recruitment of lymphocytes to the lungs (13,14). 

The administration of recombinant cytokines or cytokine receptors in experimental animal models of infection has proven to be a powerful tool to study the biological effects of specific cytokine mediators. However, cytokine- based immunotherapy is often complicated by significant toxicity, especially when cytokines or cytokine antagonists are given systemically. This is particularly true... 

The impact of anti-IgE antibodies on parasite burdens has been examined in animal models of infections with 5. mansoni, the lung fluke Paragonimus wetermani, and Strongyloides ratti. Despite undetectable levels of IgE posttreatment, treatment with anti-IgE resulted in reduced parasite burdens in mice infected with P. westermani (95) and decreased worm burden and a decrease in the number of eggs produced per worm in mice infected with S. mansoni (96). Experimental infections with S. ratti were not affected by anti-IgE treatment (97). Potential... 

Although bacterial clearance studies and models of infection are useful for showing how particle inhalation can alter host resistance to infection, analysis of cell type and function after in vivo or in vitro particle exposure can produce more detailed information about the molecular and cellular processes affected by the toxicant. Overall interpretation of these experiments is difficult because some studies show suppression of phagocytosis and downregulation of immune cytokines, whereas others indieate an increase in these functions, suggesting a state of activation. These eontradictory results can often be explained by differences in experimental protoeols and culture techniques, the endpoints under study, species from which the eells are derived, and the type of particle used. It is well to keep the old toxicology adage in mind, however, that the dose makes the poison, and that subtoxic concentrations of substances can often be beneficial or at least stimulatory. 

Although infection with C. parvum is considered predominantly secretory, histopathologic studies have revealed varying degrees of villous atrophy and infiltration of inflammatory cells beneath the epithelial mucosa [85, 86], Prostaglandins, which are known to induce cAMP-mediated apical chloride secretion and inhibit electroneutral sodium chloride and water absorption in enterocytes, have been demonstrated to be elevated in a porcine model of cryptosporidiosis [87], Inflammatory cytokines such as IL-1, IL-8 and TNF-a are induced in intestinal epithelial cell lines infected with Cryptosporidium and in animal models of cryptosporidiosis and have been postulated to play a role in pathogenesis [88, 89], Expression of TNF-a and IL-1 mRNA in the majority of jejunal biopsies of adult volunteers after experimental infection were also observed, although this did not correlate with the enteric symptoms [90]. 

The lack of absorption and, consequently, the lack of systemic therapeutic activity was also demonstrated in a model of experimental tuberculosis in the guinea pig [75], Here again, oral rifampicin but not oral rifaximin did protect the animals from the development of the infection (table 3) [76],... 

In Vivo Properties. The efficacy of dalbaheptides has been assessed in various models of experimental infections. In general there was good correlation between the ED50S in the septicemia model in mice and the MICs on test strains. 

In this chapter, the experimental procedures required to establish a mouse model of cutaneous and soft tissue infection are detailed. This model has provided invaluable insights into the pathogenicity of the agent for the hitman host. 

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