Myeloid Differentiation Factor 88

Publication Title: 
American Journal of Physiology. Heart and Circulatory Physiology

In this study, we evaluated whether blocking myeloid differentiation factor-88 (MyD88) could decrease cardiac myocyte apoptosis following pressure overload. Adenovirus expressing dominant negative MyD88 (Ad5-dnMyD88) or Ad5-green fluorescent protein (GFP) (Ad5-GFP) was transfected into rat hearts (n = 8/group) immediately followed by aortic banding for 3 wk. One group of rats (n = 8) was subjected to aortic banding for 3 wk without transfection. Sham surgical operation (n = 8) served as control.

Author(s): 
Ha, Tuanzhu
Hua, Fang
Li, Yuehua
Ma, Jing
Gao, Xiang
Kelley, Jim
Zhao, Aiqiu
Haddad, Georges E.
Williams, David L.
Browder, I. William
Kao, Race L.
Li, Chuanfu
Publication Title: 
The Journal of Clinical Endocrinology and Metabolism

CONTEXT: Type 1 diabetes (T1DM) is associated with increased cardiovascular mortality. It is a pro-inflammatory state as evidenced by increased circulating biomarkers and monocyte activity. The toll-like receptors (TLRs) are pattern recognition receptors, expressed abundantly on monocytes. TLR2 and TLR4 are important in atherosclerosis. However, there is a paucity of data examining TLR2 and TLR4 expression in T1DM and examining its contribution to the proinflammatory state.

Author(s): 
Devaraj, Sridevi
Dasu, Mohan R.
Rockwood, Jason
Winter, William
Griffen, Steven C.
Jialal, Ishwarlal
Publication Title: 
The Journal of Biological Chemistry

Macrophage-specific Abca1 knock-out (Abca1(-)(M)(/-)(M)) mice were generated to determine the role of macrophage ABCA1 expression in plasma lipoprotein concentrations and the innate immune response of macrophages. Plasma lipid and lipoprotein concentrations in chow-fed Abca1(-)(M)(/-)(M) and wild-type (WT) mice were indistinguishable.

Author(s): 
Zhu, Xuewei
Lee, Ji-Young
Timmins, Jenelle M.
Brown, J. Mark
Boudyguina, Elena
Mulya, Anny
Gebre, Abraham K.
Willingham, Mark C.
Hiltbold, Elizabeth M.
Mishra, Nilamadhab
Maeda, Nobuyo
Parks, John S.
Publication Title: 
Inflammatory Bowel Diseases

BACKGROUND: Bacteria play a role in inflammatory bowel disease and other forms of intestinal inflammation. Although much attention has focused on the search for a pathogen or inciting inflammatory bacteria, another possibility is a lack of beneficial bacteria that normally confer anti-inflammatory properties in the gut. The purpose of this study was to determine whether normal commensal bacteria could inhibit inflammatory pathways important in intestinal inflammation.

Author(s): 
Petrof, Elaine O.
Claud, Erika C.
Sun, Jun
Abramova, Tatiana
Guo, Yuee
Waypa, Tonya S.
He, Shu-Mei
Nakagawa, Yasushi
Chang, Eugene B.
Publication Title: 
International Immunopharmacology

Yamoa (ground bark of Funtumia elastica tree) is marketed and sold as a dietary supplement with anecdotal therapeutic effects in the treatment of asthma and hay fever. We determined that Yamoa and Yamoa-derived polysaccharides affected innate immunity, in part, by priming gammadelta T cells. Gene expression patterns in purified bovine gammadelta T cells and monocytes induced by Yamoa were similar to those induced by ultrapure lipopolysaccharide (uLPS).

Author(s): 
Graff, Jill C.
Kimmel, Emily M.
Freedman, Brett
Schepetkin, Igor A.
Holderness, Jeff
Quinn, Mark T.
Jutila, Mark A.
Hedges, Jodi F.
Publication Title: 
Hepatology (Baltimore, Md.)

Chronic inflammation plays a critical role in promoting obesity-related disorders, such as fatty liver disease. The inflammatory cells that mediate these effects remain unknown. This study investigated the accumulation of immature myeloid cells in the liver and their role in liver inflammation. We found that the accumulation of immature myeloid cells, i.e., CD11b(+)Ly6C(hi)Ly6G(-) cells, in the liver of B6 mice fed a high-fat diet contribute to liver inflammation.

Author(s): 
Deng, Zhong-Bin
Liu, Yuelong
Liu, Cunren
Xiang, Xiaoyu
Wang, Jianhua
Cheng, Ziqiang
Shah, Spandan V.
Zhang, Shuangyin
Zhang, Liming
Zhuang, Xiaoying
Michalek, Sue
Grizzle, William E.
Zhang, Huang-Ge
Publication Title: 
Diabetes Care

OBJECTIVE: Individuals with type 2 diabetes have a myriad of metabolic aberrations including increased inflammation, increasing their cardiovascular risk. Toll-like receptors (TLRs) and their ligands play a key role in insulin resistance and atherosclerosis. However, there is a paucity of data examining the expression and activity of TLRs in type 2 diabetes. Thus, in the present study, we examined TLR2 and TLR4 mRNA and protein expression, their ligands, and signaling in monocytes of recently diagnosed type 2 diabetic patients.

Author(s): 
Dasu, Mohan R.
Devaraj, Sridevi
Park, Samuel
Jialal, Ishwarlal
Publication Title: 
The American Journal of Pathology

In this study we observed that mice pretreated with tumor exosomes had a significant acceleration of tumor metastasis in the lung. Tumor metastasis correlated significantly with an increase in recruitment of more Myeloid-derived suppressor cells (MDSCs) in the lung of C57BL/6j (B6) mice pretreated with tumor exosomes. These effects were blunted when MyD88 knockout (KO) mice were pretreated with tumor exosomes.

Author(s): 
Liu, Yuelong
Xiang, Xiaoyu
Zhuang, Xiaoying
Zhang, Shuangyin
Liu, Cunren
Cheng, Ziqiang
Michalek, Sue
Grizzle, William
Zhang, Huang-Ge
Publication Title: 
Journal of Lipid Research

We previously showed that macrophages from macrophage-specific ATP-binding cassette transporter A1 (ABCA1) knockout (Abca1(-M/-M)) mice had an enhanced proinflammatory response to the Toll-like receptor (TLR) 4 agonist, lipopolysaccharide (LPS), compared with wild-type (WT) mice. In the present study, we demonstrate a direct association between free cholesterol (FC), lipid raft content, and hyper-responsiveness of macrophages to LPS in WT mice. Abca1(-M/-M) macrophages were also hyper-responsive to specific agonists to TLR2, TLR7, and TLR9, but not TLR3, compared with WT macrophages.

Author(s): 
Zhu, Xuewei
Owen, John S.
Wilson, Martha D.
Li, Haitao
Griffiths, Gary L.
Thomas, Michael J.
Hiltbold, Elizabeth M.
Fessler, Michael B.
Parks, John S.
Publication Title: 
Laboratory Investigation; a Journal of Technical Methods and Pathology

Toll-like receptor-2 (TLR2) is a pivotal pathogen recognition receptor that has a key role in inflammation, diabetes, and injury. Hyperglycemia, inflammation, and oxidative stress induce TLR2-myeloid differentiation factor-88 (MyD88) expression and signaling, and are major pathophysiological mechanisms in the impaired diabetic wound-healing process. The aim of the study was to examine the contribution of TLR2-MyD88 expression and signaling to the prolonged inflammation observed in diabetic wounds.

Author(s): 
Dasu, Mohan R.
Thangappan, Ravi K.
Bourgette, Alika
DiPietro, Luisa A.
Isseroff, Rivkah
Jialal, Ishwarlal

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