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However, in a skin necrosis infection model, immunization with the AT62 vaccine resulted in smaller lesions and reduced mouse weight loss compared to controls.
Importantly, the colon of C57BL/6 mice with colitis induced by TNBS or oxazolone had increased SRB colonization, and the administration of D. indonesiensis to mice with TNBS-induced colitis clearly exacerbated the alterations in colonic architecture observed in the established disease, and also increased mouse weight loss.
A mouse weight loss of over 25% was used as the experimental end-point.
Rag1 −/− and Nfil3 −/− ; Rag1 −/− mice were orally challenged with 5 × 10 CFU of C. rodentium and mouse weight loss was monitored.
Mouse weight loss was not significant in any of the test groups, showing that all of the treatments were well-tolerated.
Specifically, mouse weight loss correlated with the magnitude of the host response, and infectious viral particle production at a given time point correlated with the velocity of the host response at the next time-point.
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In obese, insulin-resistant mice, weight loss increased PPAR-γ expression [17], and both starvation and endurance training activated PPAR-δ in healthy animals [18, 19].
When CD8 cells are depleted, weight loss decreases [5], [6]; when virus-specific CD8 cells are adoptively transferred into RSV infected mice, weight loss increases [19].
In vivo, these agents did not induce excessive water accumulation and had no systemic effects on the mice (weight loss, hypoglycaemia) that may have caused growth inhibition.
Among the immunized mice, weight loss was the lightest in the group challenged with a lethal dose of 2009 H1N1, with maximal weight loss being 7.2% and weight recovering starting from day 6 following challenge.
For metastasis experiments, external evidence of lung metastases in 50% of control mice (weight loss and/or laboured breathing) indicated, from experience, that the experimental end point had been reached.
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