scholarly journals In vivo evidences that insulin regulates human polymorphonuclear neutrophil functions

2004 ◽  
Vol 76 (6) ◽  
pp. 1104-1110 ◽  
Author(s):  
S. Walrand ◽  
C. Guillet ◽  
Y. Boirie ◽  
M-P. Vasson
1998 ◽  
Vol 7 (6) ◽  
pp. 413-415 ◽  
Author(s):  
G. Camus ◽  
M. Nys ◽  
J-R. Poortmans ◽  
I. Venneman ◽  
T. Monfils ◽  
...  

1996 ◽  
Vol 88 ◽  
pp. 76
Author(s):  
Maria Leonor Meisel ◽  
Luis Martins ◽  
Helena Costa ◽  
Sara Correia ◽  
Maria João Peres ◽  
...  

1997 ◽  
Vol 186 (11) ◽  
pp. 1853-1863 ◽  
Author(s):  
Tao Tang ◽  
Alexander Rosenkranz ◽  
Karel J.M. Assmann ◽  
Michael J. Goodman ◽  
Jose-Carlos Gutierrez-Ramos ◽  
...  

Mac-1 (αmβ2), a leukocyte adhesion receptor, has been shown in vitro to functionally interact with Fcγ receptors to facilitate immune complex (IC)–stimulated polymorphonuclear neutrophil (PMN) functions. To investigate the relevance of Mac-1–FcγR interactions in IC-mediated injury in vivo, we induced a model of Fc-dependent anti–glomerular basement membrane (GBM) nephritis in wild-type and Mac-1–deficient mice by the intravenous injection of anti-GBM antibody. The initial glomerular PMN accumulation was equivalent in Mac-1 null and wild-type mice, but thereafter increased in wild-type and decreased in mutant mice. The absence of Mac-1 interactions with obvious ligands, intercellular adhesion molecule 1 (ICAM-1), and C3 complement, is not responsible for the decrease in neutrophil accumulation in Mac-1– deficient mice since glomerular PMN accumulation in mice deficient in these ligands was comparable to those in wild-type mice. In vitro studies showed that spreading of Mac-1–null PMNs to IC-coated dishes was equivalent to that of wild-type PMNs at 5–12 min but was markedly reduced thereafter, and was associated with an inability of mutant neutrophils to redistribute filamentous actin. This suggests that in vivo, Mac-1 is not required for the initiation of Fc-mediated PMN recruitment but that Mac-1–FcγR interactions are required for filamentous actin reorganization leading to sustained PMN adhesion, and this represents the first demonstration of the relevance of Mac-1–FcγR interactions in vivo. PMN-dependent proteinuria, maximal in wild-type mice at 8 h, was absent in Mac-1 mutant mice at all time points. Complement C3–deficient mice also had significantly decreased proteinuria compared to wild-type mice. Since Mac-1 on PMNs is the principal ligand for ic3b, an absence of Mac-1 interaction with C3 probably contributed to the abrogation of proteinuria in Mac-1–null mice.


2008 ◽  
Vol 149 (2) ◽  
pp. 243-249 ◽  
Author(s):  
Kohei Otake ◽  
Keiichi Uchida ◽  
Shigeyuki Yoshiyama ◽  
Mikihiro Inoue ◽  
Yoshiki Okita ◽  
...  

1985 ◽  
Vol 7 (4) ◽  
pp. 283-291 ◽  
Author(s):  
Joseph Nicotra ◽  
Anthony J. Orsini ◽  
Vincent A. DeBari

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