Role of inducible nitric oxide synthase in leukocyte extravasation in vivo

被引:31
作者
Cockrell, A
Laroux, FS
Jourd'heuil, D
Kawachi, S
Gray, L
Van der Heyde, H
Grisham, MB
机构
[1] Louisiana State Univ, Med Ctr, Dept Mol & Cellular Physiol, Shreveport, LA 71130 USA
[2] Louisiana State Univ, Med Ctr, Dept Microbiol & Immunol, Shreveport, LA 71130 USA
关键词
D O I
10.1006/bbrc.1999.0484
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Several recent studies have suggested that nitric oxide (NO) derived from the inducible isoform of NO synthase (NOS) may act as an endogenous modulator of the inflammatory response by inhibiting adhesion of leukocytes to endothelial cells in vitro. Few studies have addressed specifically the role of iNOS in regulating leukocyte recruitment in vivo in a model of acute inflammation. Thus, the objective of this study was to assess the role of iNOS in modulating neutrophil (PMN) extravasation in an oyster glycogen-induced model of acute peritonitis in rats. Data obtained in the present study demonstrates that injection (IP) of oyster glycogen induces massive and selective PMN recruitment into the peritoneal cavity of rats at 6 hrs following OG administration. These extravasated cells were found to contain significant amounts of iNOS protein as assessed by Western blot analysis. Treatment of rats with the selective iNOS inhibitor L-iminoethyl-lysine (L-NIL) dramatically reduced NO levels in lavage fluid as measured by de. creases in nitrate and nitrite concentrations without significantly affecting iNOS protein levels. Although L-NIL inhibited NO production by >70%, it did not alter oyster glycogen-induced PMN recruitment when compared to vehicle-treated rats. We conclude that PMN-associated, iNOS-derived NO does not play an important role in modulating extravasation of these leukocytes in this model of acute inflammation. (C) 1999 Academic Press.
引用
收藏
页码:684 / 686
页数:3
相关论文
共 17 条
[11]  
LEFER DJ, 1999, IN PRESS AM J PHYS
[12]   ALTERED RESPONSES TO BACTERIAL-INFECTION AND ENDOTOXIC-SHOCK IN MICE LACKING INDUCIBLE NITRIC-OXIDE SYNTHASE [J].
MACMICKING, JD ;
NATHAN, C ;
HOM, G ;
CHARTRAIN, N ;
FLETCHER, DS ;
TRUMBAUER, M ;
STEVENS, K ;
XIE, QW ;
SOKOL, K ;
HUTCHINSON, N ;
CHEN, H ;
MUDGETT, JS .
CELL, 1995, 81 (04) :641-650
[13]   NITRIC-OXIDE SYNTHASE IN CIRCULATING VS EXTRAVASATED POLYMORPHONUCLEAR LEUKOCYTES [J].
MILES, AM ;
OWENS, MW ;
MILLIGAN, S ;
JOHNSON, GG ;
FIELDS, JZ ;
ING, TS ;
KOTTAPALLI, V ;
KESHAVARZIAN, A ;
GRISHAM, MB .
JOURNAL OF LEUKOCYTE BIOLOGY, 1995, 58 (05) :616-622
[14]  
Peng HB, 1998, J IMMUNOL, V161, P1970
[15]   Inhibition of endothelial vascular cell adhesion molecule-1 expression by nitric oxide involves the induction and nuclear translocation of IκBα [J].
Spiecker, M ;
Peng, HB ;
Liao, JK .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (49) :30969-30974
[16]   Nitric oxide attenuates adhesion molecule expression in human endothelial cells [J].
Takahashi, M ;
Ikeda, U ;
Masuyama, JI ;
Funayama, H ;
Kano, S ;
Shimada, K .
CYTOKINE, 1996, 8 (11) :817-821
[17]   MECHANICS OF STIMULATED NEUTROPHILS - CELL STIFFENING INDUCES RETENTION IN CAPILLARIES [J].
WORTHEN, GS ;
SCHWAB, B ;
ELSON, EL ;
DOWNEY, GP .
SCIENCE, 1989, 245 (4914) :183-186