EOH Events

EOH Departmental Calendar

Event
Thu 4/2/2020 11:00AM - 12:00PM
EOH Journal Club
Human & mouse single-nucleus transcriptomics reveal TREM2-dependent & TREM2-independent - ONLINE EOH Journal Club
Human & mouse single-nucleus transcriptomics reveal TREM2-dependent & TREM2-independent - ONLINE
Thu 4/2/2020 11:00AM - 12:00PM


Join Zoom Meeting - https://pitt.zoom.us/j/356770679 Meeting ID: 356 770 679

Presenter: Yi Lu

Paper: Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer’s disease

Authors: Yingyue Zhou, Wilbur M. Song, Prabhakar S. Andhey, et Al.

Abstract:
Glia have been implicated in Alzheimer’s disease (AD) pathogenesis. Variants of the microglia receptor triggering receptor expressed on myeloid cells 2 (TREM2) increase AD risk, and activation of disease-associated microglia (DAM) is dependent on TREM2 in mouse models of AD. We surveyed gene-expression changes associated with AD pathology and TREM2 in 5XFAD mice and in human AD by single-nucleus RNA sequencing. We confirmed the presence of Trem2-dependent DAM and identified a previously undiscovered Serpina3n+C4b+ reactive oligodendrocyte population in mice. Interestingly, remarkably differential phenotypes were evident in human AD. Microglia signature was reminiscent of IRF8-driven reactive microglia in peripheral- nerve injury. Oligodendrocyte signatures suggested impaired axonal myelination and metabolic adaptation to neuronal degeneration. Astrocyte profiles indicated weakened metabolic coordination with neurons. Notably, the reactive phenotype of microglia was less evident in TREM2-R47H and TREM2-R62H carriers than in non-carriers,

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Thu 4/9/2020 11:00AM - 12:00PM
EOH Journal Club
Organophosphorus pesticide chlorpyrifos intake promotes obesity and insulin resistance - ONLINE EOH Journal Club
Organophosphorus pesticide chlorpyrifos intake promotes obesity and insulin resistance - ONLINE
Thu 4/9/2020 11:00AM - 12:00PM


Join Zoom Meeting https://pitt.zoom.us/j/152532472  Meeting ID: 152 532 472

Presenter: Jenna Kuhn

Paper: Organophosphorus pesticide chlorpyrifos intake promotes obesity and insulin resistance through impacting gut and gut microbiota

Authors: Yiran Liang, Jing Zhan, Donghui Liu, Mai Luo, Jiajun Han, Xueke Liu, Chang Liu, Zheng Cheng, Zhiqiang Zhou, and Peng Wang

Abstract:
Background
Disruption of the gut microbiota homeostasis may induce low-grade inflammation leading to obesity-associated diseases. A major protective mechanism is to use the multi-layered mucus structures to keep a safe distance between gut epithelial cells and microbiota. To investigate whether pesticides would induce insulin resistance/obesity through interfering with mucus-bacterial interactions, we conducted a study to determine how long-term exposure to chlorpyrifos affected C57Bl/6 and CD-1 (ICR) mice fed high- or normal-fat diets. To further investigate the effects of chlorpyrifos-altered microbiota, antibiotic treatment and microbiota transplantation experiments were conducted.

Results
The results showed that chlorpyrifos caused broken integrity of the gut barrier, leading to increased lipopolysaccharide entry into the body and finally low-grade inflammation, while genetic background and diet pattern have limited influence on the chlorpyrifos-induced results. Moreover, the mice given chlorpyrifos-altered microbiota had gained more fat and lower insulin sensitivity.

Conclusions
Our results suggest that widespread use of pesticides may contribute to the worldwide epidemic of inflammation-related diseases.

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Thu 4/16/2020 11:00AM - 12:00PM
EOH Journal Club
M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung - ONLINE EOH Journal Club
M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung - ONLINE
Thu 4/16/2020 11:00AM - 12:00PM


Join Zoom Meeting https://pitt.zoom.us/j/848181150 Meeting ID: 848 181 150

Presenter: Grace Ge

Paper: M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung epithelial cells

Authors:  Jiajun Cui, Wenhua Xu, Jian Chen, Hui Li, Lu Dai, Jacqueline A. Frank,Shaojun Peng, Siying Wang, Gang Chen

Abstract: The alterations in microenvironment upon chronic arsenic exposure may
contribute to arsenic-induced lung carcinogenesis. Immune cells, such as
macrophages, play an important role in mediating the microenvironment in the lungs.
Macrophages carry out their functions after activation. There are two activation status
for macrophages: classical (M1) or alternative (M2); the latter is associated with
tumorigenesis. Our previous work showed that long-term arsenic exposure induces
transformation of lung epithelial cells. However, the crosstalk between epithelial cells
and macrophages upon arsenic exposure has not been investigated. In this study,
using a co-culture system in which human lung epithelial cells are cultured with
macrophages, we determined that long-term arsenic exposure polarizes macrophages
towards M2 status through ROS generation. Co-culture with epithelial cells further
enhanced the polarization of macrophages as well as transformation of epithelial cells,
while blocking macrophage M2 polarization decreased the transformation. In addition,
macrophage M2 polarization decreased autophagy activity, which may account for
increased cell transformation of epithelial cells with co-culture of macrophages.


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Recent Events

EOH Journal Club

EOH Journal Club - Spring 2017 - Antonella Marrocco

Thursday 2/16 11:00AM - 12:00PM
EOH Journal Club Seminar - Spring 2017

Date: Thursday February 16, 2017

Time: 11am - 12pm

Presenter: Antonella Marrocco

Paper: Mitochondrial respiratory-chain adaptations in macrophages contribute to antibacterial host defense

Authors: Johan Garaude, Rebeca Acín-Pérez, Sarai Martínez-Cano, Michel Enamorado, Matteo Ugolini, Estanislao Nistal-Villán, Sandra Hervás-Stubbs, Pablo Pelegrín, Leif E Sander, José A Enríquez & David Sancho  

Abstract: Macrophages tightly scale their core metabolism after being activated, but the precise regulation of the mitochondrial electron-transport chain (ETC) and its functional implications are currently unknown. Here we found that recognition of live bacteria by macrophages transiently decreased assembly of the ETC complex I (CI) and CI-containing super-complexes and switched the relative contributions of CI and CII to mitochondrial respiration. This was mediated by phagosomal NADPH oxidase and the reactive oxygen species (ROS)-dependent tyrosine kinase Fgr. It required Toll-like receptor signaling and the NLRP3 inflammasome, which were both connected to bacterial viability–specific immune responses. Inhibition of CII during infection with Escherichia coli normalized serum concentrations of interleukin 1β (IL-1β) and IL-10 to those in mice treated with dead bacteria and impaired control of bacteria. We have thus identified ETC adaptations as an early immunological-metabolic checkpoint that adjusts innate immune responses to bacterial infection.

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Last Updated On Friday, January 20, 2017 by Orbell, Adam W
Created On Friday, January 20, 2017

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