scholarly journals Zygomycetes Hyphae Trigger an Early, Robust Proinflammatory Response in Human Polymorphonuclear Neutrophils through Toll-Like Receptor 2 Induction but Display Relative Resistance to Oxidative Damage

2007 ◽  
Vol 52 (2) ◽  
pp. 722-724 ◽  
Author(s):  
G. Chamilos ◽  
R. E. Lewis ◽  
G. Lamaris ◽  
T. J. Walsh ◽  
D. P. Kontoyiannis

ABSTRACT Human polymorphonuclear neutrophils (HPMNs) displayed attenuated hyphal damage associated with impaired O2 − release following exposure to Rhizopus oryzae versus that with Aspergillus fumigatus. Exposure of HPMNs to R. oryzae hyphae resulted in upregulation in Toll-like receptor 2 mRNA and a robust proinflammatory gene expression with rapid (1-h) induction of NF-κB pathway-related genes.

2013 ◽  
Vol 288 (35) ◽  
pp. 25362-25374 ◽  
Author(s):  
Melanie R. Shakespear ◽  
Daniel M. Hohenhaus ◽  
Greg M. Kelly ◽  
Nabilah A. Kamal ◽  
Praveer Gupta ◽  
...  

Author(s):  
Juu-Chin Lu ◽  
Chia-Yun Lu ◽  
Ying-Yu Wu

Peroxisome proliferator-activated receptor γ (PPARγ) is the master transcriptional regulator of adipocytes and the cellular target of thiazolidinedione (TZD) drugs. Suppression of proinflammatory actions, including proinflammatory gene expression and lipolysis in adipocytes, contributes to PPARγ-mediated anti-diabetic effects of TZDs. However, adverse side effects largely limited the clinical use of TZDs, despite their potent insulin-sensitizing effects. Therefore, it is important to understand how PPARγ is regulated. Thyroid hormone receptor-associated protein 3 (THRAP3) was previously reported to promote diabetic gene expression by acting as a transcriptional coregulator of PPARγ in adipocytes. Therefore, we tested if THRAP3 modulated anti-inflammatory functions of PPARγ in 3T3-L1 adipocytes. THRAP3 depletion increased basal and tumor necrosis factor α (TNFα)-induced lipolysis, proinflammatory gene expression, and phosphorylation of extracellular signal-regulated kinases (ERKs), suggesting elevated proinflammatory response after THRAP3 depletion in adipocytes. Moreover, TZD-mediated suppression of TNFα-induced lipolysis, proinflammatory gene expression, and ERK phosphorylation were attenuated or alleviated after THRAP3 depletion. Interestingly, the mRNA and protein levels of PPARγ were greatly reduced in THRAP3-depleted adipocytes. Actinomycin D treatment revealed that the stability of PPARγ mRNA was greatly reduced by THRAP3 depletion in adipocytes. Thus, in addition to modulating PPARγ function, THRAP3 may directly regulate the transcript of PPARγ in differentiated adipocytes.


2013 ◽  
Vol 34 (9) ◽  
pp. 2110-2124 ◽  
Author(s):  
Tony Valente ◽  
Marco Straccia ◽  
Nuria Gresa-Arribas ◽  
Guido Dentesano ◽  
Josep M. Tusell ◽  
...  

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