Mycobacterial TDM: A Coat to Modulate Post Primary Pathogenesis?

Actor, Jeffrey K.

doi:10.4172/2161-1068.1000e106

Cited by 3 publications

(1 citation statement)

References 24 publications

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“…Cord factor (trehalose 6,6′-dimycolate, TDM) is the most abundant glycolipid produced on the surface of mycobacterial organisms. TDM plays multiple roles in the pathogenesis of MTB [ 34 , 35 ], including the formation of caseation in the lung after infection [ 36 ]. TDM formulated into an emulsion, or placed on beads, and injected intravenously into mice induces a lung pathology that mimics many aspects of early MTB infection, including granulomatous response and the production of proinflammatory cytokines.…”

Section: Introductionmentioning

confidence: 99%

Lactoferrin: A Modulator for Immunity against Tuberculosis Related Granulomatous Pathology

Actor

2015

Mediators of Inflammation

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There is great need for a therapeutic that would limit tuberculosis related pathology and thus curtail spread of disease between individuals by establishing a “firebreak” to slow transmission. A promising avenue to increase current therapeutic efficacy may be through incorporation of adjunct components that slow or stop development of aggressive destructive pulmonary pathology. Lactoferrin, an iron-binding glycoprotein found in mucosal secretions and granules of neutrophils, is just such a potential adjunct therapeutic agent. The focus of this review is to explore the utility of lactoferrin to serve as a therapeutic tool to investigate “disruption” of the mycobacterial granuloma. Proposed concepts for mechanisms underlying lactoferrin efficacy to control immunopathology are supported by data generated based on in vivo models using nonpathogenic trehalose 6,6′-dimycolate (TDM, cord factor).

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Section: Introductionmentioning

confidence: 99%