Mingfang Lu
National Institutes of Health
12 Papers
102 Citations
Mingfang Lu is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Acyloxyacyl hydrolase & Lipopolysaccharide. The author has an hindex of 11, co-authored 12 publications. Previous affiliations of Mingfang Lu include Fudan University & University of Texas Southwestern Medical Center.
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Papers
Toll-like receptor agonists promote prolonged triglyceride storage in macrophages.
Ying-ling Huang,Joel A. Morales-Rosado,Jessica Ray,Timothy G. Myers,Terry Kho,Mingfang Lu,Robert S. Munford +6 more
TL;DR: TLR agonist-induced TAG storage is a multifaceted process that persists long after most early pro-inflammatory responses have subsided and may contribute to the formation of “lipid-laden” macrophages in infected tissues.
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Altered inactivation of commensal LPS due to acyloxyacyl hydrolase deficiency in colonic dendritic cells impairs mucosal Th17 immunity.
TL;DR: This article found that LPS-containing Gramnegative microbiota augmented the differentiation of Ag-specific Th17 cells, and identified a colonic DC subset (CD103+CD11b+ALDH−) displaying a unique capacity to both express AOAH and polarize Th 17 cells.
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Persistently active microbial molecules prolong innate immune tolerance in vivo.
TL;DR: It is shown that prolonged macrophage reprogramming is maintained in vivo by the persistence of stimulatory LPS molecules within the cells' in vivo environment, where naïve cells can acquire LPS via cell-cell contact or from the extracellular fluid.
The transport and inactivation kinetics of bacterial lipopolysaccharide influence its immunological potency in vivo.
Mingfang Lu,Robert S. Munford +1 more
TL;DR: Its immunological potency, as measured by its ability to stimulate polyclonal Ab production, was greatly influenced by the kinetics of both lymphatic drainage and enzymatic inactivation.
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Chapter 2 Kill the Bacteria…and Also Their Messengers?
TL;DR: A previously neglected aspect of recovery from infectious diseases: how animals dispose of the dead microbes in their tissues is considered and the rate at which stimulatory microbial molecules undergo inactivation may influence the duration and severity of diseases caused by other infectious agents.