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2016 ; 38
(2
): 221-37
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Mouse models of human TB pathology: roles in the analysis of necrosis and the
development of host-directed therapies
#MMPMID26542392
Kramnik I
; Beamer G
Semin Immunopathol
2016[Mar]; 38
(2
): 221-37
PMID26542392
show ga
A key aspect of TB pathogenesis that maintains Mycobacterium tuberculosis in the
human population is the ability to cause necrosis in pulmonary lesions. As
co-evolution shaped M . tuberculosis (M.tb) and human responses, the complete TB
disease profile and lesion manifestation are not fully reproduced by any animal
model. However, animal models are absolutely critical to understand how infection
with virulent M.tb generates outcomes necessary for the pathogen transmission and
evolutionary success. In humans, a wide spectrum of TB outcomes has been
recognized based on clinical and epidemiological data. In mice, there is clear
genetic basis for susceptibility. Although the spectra of human and mouse TB do
not completely overlap, comparison of human TB with mouse lesions across
genetically diverse strains firmly establishes points of convergence. By
embracing the genetic heterogeneity of the mouse population, we gain tremendous
advantage in the quest for suitable in vivo models. Below, we review genetically
defined mouse models that recapitulate a key element of M.tb
pathogenesis-induction of necrotic TB lesions in the lungs-and discuss how these
models may reflect TB stratification and pathogenesis in humans. The approach
ensures that roles that mouse models play in basic and translational TB research
will continue to increase allowing researchers to address fundamental questions
of TB pathogenesis and bacterial physiology in vivo using this well-defined,
reproducible, and cost-efficient system. Combination of the new generation mouse
models with advanced imaging technologies will also allow rapid and inexpensive
assessment of experimental vaccines and therapies prior to testing in larger
animals and clinical trials.
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