scholarly journals High-dose catecholamine treatment decreases polymorphonuclear leukocyte phagocytic capacity and reactive oxygen production.

1996 ◽  
Vol 3 (4) ◽  
pp. 423-428 ◽  
Author(s):  
C Wenisch ◽  
B Parschalk ◽  
A Weiss ◽  
K Zedwitz-Liebenstein ◽  
B Hahsler ◽  
...  
1996 ◽  
Vol 40 (9) ◽  
pp. 2039-2042 ◽  
Author(s):  
C Wenisch ◽  
B Parschalk ◽  
K Zedtwitz-Liebenstein ◽  
A Weihs ◽  
I el Menyawi ◽  
...  

Azithromycin was given as a single oral dose (20 mg/kg of body weight) to 12 volunteers in a crossover study with roxithromycin (8 to 12 mg/kg) and clarithromycin (8 to 12 mg/kg). Flow cytometry was used to study the phagocytic functions and the release of reactive oxygen products following phagocytosis by neutrophil granulocytes prior to administration of the three drugs, 16 h after azithromycin administration, and 3 h after clarithromycin and roxithromycin administration. Phagocytic capacity was assessed by measuring the uptake of fluorescein isothiocyanate-labeled bacteria. Reactive oxygen generation after phagocytosis of unlabeled bacteria was estimated by the amount of dihydrorhodamine 123 converted to rhodamine 123 intracellularly. Azithromycin resulted in decreased capacities of the cells to phagocytize Escherichia coli (median [range], 62% [27 to 91%] of the control values; P < 0.01) and generate reactive oxygen products (75% [34 to 26%] of the control values; P < 0.01). Clarithromycin resulted in reduced phagocytosis (82% [75 to 98%] of control values; P < 0.01) but did not alter reactive oxygen production (84% [63 to 113%] of the control values; P > 0.05). Roxithromycin treatment did not affect granulocyte phagocytosis (92% [62 to 118%] of the control values; P > 0.05) or reactive oxygen production (94% [66 to 128%] of the control value; P > 0.05). No relation between intra- and/or extracellular concentrations of azithromycin and/or roxithromycin and the polymorphonuclear phagocyte function and/or reactive oxygen production existed (P > 0.05 for all comparisons). These results demonstrate that the accumulation of macrolides in neutrophils can suppress the response of phagocytic cells to bacterial pathogens after a therapeutic dose.


Infection ◽  
1999 ◽  
Vol 27 (3) ◽  
pp. 183-186 ◽  
Author(s):  
C. Wenisch ◽  
B. Parschalk ◽  
S. Patruta ◽  
R. Brustbauer ◽  
W. Graninger

2010 ◽  
Vol 285 (30) ◽  
pp. 22864-22873 ◽  
Author(s):  
James J. Matsuda ◽  
Mohammed S. Filali ◽  
Jessica G. Moreland ◽  
Francis J. Miller ◽  
Fred S. Lamb

2002 ◽  
Vol 33 (9) ◽  
pp. 1268-1278 ◽  
Author(s):  
Albert P Senft ◽  
Timothy P Dalton ◽  
Daniel W Nebert ◽  
Mary Beth Genter ◽  
Alvaro Puga ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8
Author(s):  
Xiao-Tian Zhang ◽  
Chun-Jiang Yu ◽  
Jian-Wei Liu ◽  
Yan-Ping Zhang ◽  
Chao Zhang ◽  
...  

We analyzed the effects of a traditional Chinese medicine, Qizhi Jiangtang Jiaonang (QJJ), on insulin resistance (IR) in vitro. After an in vitro model of IR was established by treating human liver cancer cells (HepG2 cells) with palmitic acid, the cells were then treated with various concentrations of QJJ. Treatment with 400 µM palmitic acid for 24 h induced IR in HepG2 cells. The survival rate for HepG2 cells in the IR group was significantly lower than that of the untreated control group (P< 0.001); however, QJJ restored HepG2 cell survival (P< 0.001). As compared with HepG2 cells in the IR group, QJJ at all doses analyzed significantly increased glucose consumption (allP< 0.05). Moreover, treatment with all the QJJ doses significantly reduced the mean intracellular reactive oxygen species levels as compared with the IR group (allP< 0.05). Furthermore, high-dose QJJ reduced both TNF-αand IL-6 levels as compared to the IR group (allP< 0.05). QJJ ameliorated the altered PI3K, GLUT4, and RAGE expression observed with IR. In conclusion, QJJ can improve IR in HepG2 cells, which may be mediated through the IRS-1/PI3K/GLUT4 signaling pathway as well as regulation of NF-κB-mediated inflammation and oxidative stress.


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