Mechanistic Study on the Role of Soluble Microbial Products in Sulfate Radical-Mediated Degradation of Pharmaceuticals

2018 ◽  
Vol 53 (1) ◽  
pp. 342-353 ◽  
Author(s):  
Lingwei Gao ◽  
Daisuke Minakata ◽  
Zongsu Wei ◽  
Richard Spinney ◽  
Dionysios D. Dionysiou ◽  
...  
Keyword(s):  
Sulfate Radical ◽  
Mechanistic Study ◽  
Soluble Microbial Products ◽  
Microbial Products

Role of Toll-like receptor 1, 2 and 4 on thromboxane B2 production by different microbial products

2018 ◽  
Vol 56 (08) ◽  
pp. e254-e255
Author(s):  
J Zhang ◽  
A Wieser ◽  
H Li ◽  
I Liß ◽  
AL Gerbes ◽  
...  
Keyword(s):  
Thromboxane B2 ◽  
Toll Like Receptor ◽  
Microbial Products

scholarly journals Liver Injury and the Macrophage Issue: Molecular and Mechanistic Facts and Their Clinical Relevance

2021 ◽  
Vol 22 (14) ◽  
pp. 7249
Author(s):  
Siyer Roohani ◽  
Frank Tacke
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Current Knowledge ◽  
Hepatocellular Cancer ◽  
Complete Recovery ◽  
Hepatic Macrophages ◽  
Liver Injuries ◽  
Microbial Products ◽  
Injured Liver

The liver is an essential immunological organ due to its gatekeeper position to bypassing antigens from the intestinal blood flow and microbial products from the intestinal commensals. The tissue-resident liver macrophages, termed Kupffer cells, represent key phagocytes that closely interact with local parenchymal, interstitial and other immunological cells in the liver to maintain homeostasis and tolerance against harmless antigens. Upon liver injury, the pool of hepatic macrophages expands dramatically by infiltrating bone marrow-/monocyte-derived macrophages. The interplay of the injured microenvironment and altered macrophage pool skews the subsequent course of liver injuries. It may range from complete recovery to chronic inflammation, fibrosis, cirrhosis and eventually hepatocellular cancer. This review summarizes current knowledge on the classification and role of hepatic macrophages in the healthy and injured liver.

scholarly journals Thymic stromal lymphopoietin is released by human epithelial cells in response to microbes, trauma, or inflammation and potently activates mast cells

2007 ◽  
Vol 204 (2) ◽  
pp. 253-258 ◽  
Author(s):  
Zoulfia Allakhverdi ◽  
Michael R. Comeau ◽  
Heidi K. Jessup ◽  
Bo-Rin Park Yoon ◽  
Avery Brewer ◽  
...  
Keyword(s):  
Mast Cells ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Immunoglobulin E ◽  
Interleukin 1 ◽  
Allergic Inflammation ◽  
Thymic Stromal Lymphopoietin ◽  
Microbial Products ◽  
Necrosis Factor

Compelling evidence suggests that the epithelial cell–derived cytokine thymic stromal lymphopoietin (TSLP) may initiate asthma or atopic dermatitis through a dendritic cell–mediated T helper (Th)2 response. Here, we describe how TSLP might initiate and aggravate allergic inflammation in the absence of T lymphocytes and immunoglobulin E antibodies via the innate immune system. We show that TSLP, synergistically with interleukin 1 and tumor necrosis factor, stimulates the production of high levels of Th2 cytokines by human mast cells (MCs). We next report that TSLP is released by primary epithelial cells in response to certain microbial products, physical injury, or inflammatory cytokines. Direct epithelial cell–mediated, TSLP-dependent activation of MCs may play a central role in “intrinsic” forms of atopic diseases and explain the aggravating role of infection and scratching in these diseases.

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