scholarly journals Slc11a1-mediated resistance toSalmonella entericaserovar Typhimurium andLeishmania donovaniinfections does not require functional inducible nitric oxide synthase or phagocyte oxidase activity

2004 ◽  
Vol 77 (3) ◽  
pp. 311-320 ◽  
Author(s):  
Jacqueline K. White ◽  
Pietro Mastroeni ◽  
Jean-François Popoff ◽  
Carlton A. W. Evans ◽  
Jenefer M. Blackwell
Immunity ◽  
1999 ◽  
Vol 10 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Michael U Shiloh ◽  
John D MacMicking ◽  
Susan Nicholson ◽  
Juliet E Brause ◽  
Strite Potter ◽  
...  

2000 ◽  
Vol 68 (7) ◽  
pp. 4361-4362 ◽  
Author(s):  
Rila Banerjee ◽  
Juan Anguita ◽  
Erol Fikrig

ABSTRACT Mice deficient in phox (gp91phox−/−) or NOS2 (NOS2−/−) were infected with the agent of human granulocytic ehrlichiosis (HGE) to evaluate the importance of these pathways in the eradication of HGE bacteria. NOS2−/− mice had delayed clearance of the HGE agent in comparison to control or gp91phox−/− mice, suggesting that reactive nitrogen intermediates play a role in the early control of HGE.


2000 ◽  
Vol 192 (2) ◽  
pp. 237-248 ◽  
Author(s):  
Pietro Mastroeni ◽  
Andrés Vazquez-Torres ◽  
Ferric C. Fang ◽  
Yisheng Xu ◽  
Shahid Khan ◽  
...  

The roles of the NADPH phagocyte oxidase (phox) and inducible nitric oxide synthase (iNOS) in host resistance to virulent Salmonella typhimurium were investigated in gp91phox−/−, iNOS−/−, and congenic wild-type mice. Although both gp91phox−/− and iNOS−/− mice demonstrated increased susceptibility to infection with S. typhimurium compared with wild-type mice, the kinetics of bacterial replication were dramatically different in the gp91phox−/− and iNOS−/− mouse strains. Greater bacterial numbers were present in the spleens and livers of gp91phox−/− mice compared with C57BL/6 controls as early as day 1 of infection, and all of the gp91phox−/− mice succumbed to infection within 5 d. In contrast, an increased bacterial burden was detected within reticuloendothelial organs of iNOS−/− mice only beyond the first week of infection. Influx of inflammatory CD11b+ cells, granuloma formation, and serum interferon γ levels were unimpaired in iNOS−/− mice, but the iNOS-deficient granulomas were unable to limit bacterial replication. The NADPH phagocye oxidase and iNOS are both required for host resistance to wild-type Salmonella, but appear to operate principally at different stages of infection.


2003 ◽  
Vol 71 (12) ◽  
pp. 7183-7187 ◽  
Author(s):  
K. H. Ramsey ◽  
I. M. Sigar ◽  
S. V. Rana ◽  
J. Gupta ◽  
S. M. Holland ◽  
...  

ABSTRACT Urinary nitrite and F2-isoprostanes, an index of oxidant stress, were elevated during chlamydial genital infection of mice. Enhancement of urinary nitrite and F2-isoprostanes was observed in phagocyte oxidase-deficient mice. Inhibition of inducible nitric oxide synthase reduced isoprostane excretion. We conclude that nitrogen radicals induce F2-isoprostane production and excretion during murine chlamydial genital infection.


2001 ◽  
Vol 69 (12) ◽  
pp. 7374-7379 ◽  
Author(s):  
K. H. Ramsey ◽  
I. M. Sigar ◽  
S. V. Rana ◽  
J. Gupta ◽  
S. M. Holland ◽  
...  

ABSTRACT It has been previously reported that although inducible nitric oxide synthase (iNOS) gene knockout (NOS2 −/−) mice resolve Chlamydia trachomatis genital infection, the production of reactive nitrogen species (RNS) via iNOS protects a significant proportion of mice from hydrosalpinx formation and infertility. We now report that higher in vivo RNS production correlates with mouse strain-related innate resistance to hydrosalpinx formation. We also show that mice with a deletion of a key component of phagocyte NADPH oxidase (p47 phox−/−) resolve infection, produce greater amounts of RNS in vivo, and sustain lower rates of hydrosalpinx formation than both wild-type (WT)NOS2 +/+ andNOS2 −/− controls. When we induced an in vivo chemical block in iNOS activity in p47 phox−/− mice usingN G-monomethyl-l-arginine (L-NMMA), a large proportion of these mice eventually succumbed to opportunistic infections, but not before they resolved their chlamydial infections. Interestingly, when compared to WT and untreated p47 phox−/− controls, L-NMMA-treated p47 phox−/− mice resolved their infections more rapidly. However, L-NMMA-treated p47 phox−/− mice lost resistance to chronic chlamydial disease, as evidenced by an increased rate of hydrosalpinx formation that was comparable to that forNOS2 −/− mice. We conclude that phagocyte oxidase-derived reactive oxygen species (ROS) regulate RNS during chlamydial urogenital infection in the mouse. We further conclude that while neither phagocyte oxidase-derived ROS nor iNOS-derived RNS are essential for resolution of infection, RNS protect from chronic chlamydial disease in this model.


2006 ◽  
Vol 175 (4S) ◽  
pp. 96-96
Author(s):  
Masayoshi Nomura ◽  
Hisae Nishii ◽  
Masato Tsutsui ◽  
Naohiro Fujimoto ◽  
Tetsuro Matsumoto

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