Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 190, Issue 2, Pages 286-294Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2019.10.006
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- NTH grant [1R41 -A1117990-02]
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Murine models of Mycobacterium tuberculosis (Mtb) infection demonstrate progression of M1-like (proinflammatory) and M2-like (anti-inflammatory) macrophage morphology following primary granuloma formation. The Mtb cell wall cording factor, trehalose 6,6'-dimycolate (TDM), is a physiologically relevant and useful molecule for modeling early macrophage-mediated events during establishment of the tuberculosis-induced granuloma pathogenesis. Here, it is shown that TDM is a major driver of the early M1-like macrophage response as seen during initiation of the granulomas of primary pathology. Proinflammatory cytokines tumor necrosis factor-alpha, IL-1 beta, IL-6, and IL-12p40 are produced in lung tissue after administration of TDM to mice. Furthermore, CD11b(+)CD45(+) macrophages with a high surface expression of the M1-like markers CD38 and CD86 were found present in regions of pathology in lungs of mice at 7 days post-TDM introduction. Conversely, only low phenotypic marker expression of M2-like markers CD206 and EGR-2 were present on macrophages. These findings suggest that TDM plays a role in establishment of the M1-like shift in the microenvironment during primary tuberculosis.
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