scholarly journals Tissue distribution of basigin and monocarboxylate transporter 1 in the adult male mouse: A study using the wild-type and basigin gene knockout mice

2006 ◽  
Vol 288A (5) ◽  
pp. 527-535 ◽  
Author(s):  
Masaaki Nakai ◽  
Li Chen ◽  
Romana A. Nowak
Keyword(s):  
Tissue Distribution ◽  
Adult Male ◽  
Knockout Mice ◽  
Male Mouse ◽  
Gene Knockout ◽  
Monocarboxylate Transporter ◽  
Wild Type ◽  
Monocarboxylate Transporter 1 ◽  
Adult Male Mouse ◽  
Gene Knockout Mice

scholarly journals Critical Role of Cytotoxic T Lymphocytes in Immune Clearance of Rickettsial Infection

2001 ◽  
Vol 69 (3) ◽  
pp. 1841-1846 ◽  
Author(s):  
David H. Walker ◽  
Juan P. Olano ◽  
Hui-Min Feng
Keyword(s):  
T Lymphocytes ◽  
Knockout Mice ◽  
Gene Knockout ◽  
Wild Type ◽  
Spleen Cells ◽  
Rickettsial Infection ◽  
Cd8 T Lymphocytes ◽  
Gene Knockout Mice ◽  
Ifn Γ ◽  
Ctl Activity

ABSTRACT Cytotoxic T-lymphocyte (CTL) activity developed against the major infected target cells of rickettsial infections, endothelial cells and macrophages. Spleen cells from mice immune to Rickettsia conorii exerted specific major histocompatibility complex (MHC) class I-matched CTL activity against R. conorii-infected SVEC-10 endothelial cells, with peak activity on day 10. Similarly, spleen cells from Rickettsia australis-immune mice exerted specific CTL activity against an R. australis-infected macrophage-like cell line. Gamma interferon (IFN-γ) gene knockout mice were more than 100-fold more susceptible to R. australis infection than wild-type C57BL/6 mice. MHC class I gene knockout mice were the most susceptible, more than 50,000-fold more susceptible to a lethal outcome of R. australis infection than wild-type C57BL/6 mice. These results indicate that CTL activity was more critical to recovery from rickettsial infection than were the effects of IFN-γ. The observation that perforin gene knockout mice were more than 100-fold more susceptible than wild-type C57BL/6 mice indicates that perforin-mediated activity accounts for a large component, but not all, of the CTL-mediated antirickettsial effect. CTL activity was expressed by immune CD8 T lymphocytes. Adoptive transfer of immune CD8 T lymphocytes from IFN-γ gene knockout mice intoR. australis-infected IFN-γ gene knockout mice dramatically reduced the infectious rickettsial content in the organs, confirming that CD8 T lymphocytes provide immunity against rickettsiae besides that provided by the secretion of IFN-γ. CTLs appear to be crucial to recovery from rickettsial infection.

scholarly journals Phagocyte-Derived Reactive Oxygen Species Do Not Influence the Progression of Murine Blood-Stage Malaria Infections

2005 ◽  
Vol 73 (8) ◽  
pp. 4941-4947 ◽  
Author(s):  
S. M. Potter ◽  
A. J. Mitchell ◽  
W. B. Cowden ◽  
L. A. Sanni ◽  
M. Dinauer ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Knockout Mice ◽  
Plasmodium Berghei ◽  
Gene Knockout ◽  
Reactive Oxygen ◽  
Plasmodium Yoelii ◽  
Oxygen Species ◽  
Wild Type ◽  
Gene Knockout Mice

ABSTRACT Phagocyte-derived reactive oxygen species have been implicated in the clearance of malaria infections. We investigated the progression of five different strains of murine malaria in gp91phox−/− mice, which lack a functional NADPH oxidase and thus the ability to produce phagocyte-derived reactive oxygen species. We found that the absence of functional NADPH oxidase in the gene knockout mice had no effect on the parasitemia or total parasite burden in mice infected with either resolving (Plasmodium yoelii and Plasmodium chabaudi K562) or fatal (Plasmodium berghei ANKA, Plasmodium berghei K173 and Plasmodium vinckei vinckei) strains of malaria. This lack of effect was apparent in both primary and secondary infections with P. yoelii and P. chabaudi. There was also no difference in the presentation of clinical or pathological signs between the gp91phox−/− or wild-type strains of mice infected with malaria. Progression of P. berghei ANKA and P. berghei K173 infections was unchanged in glutathione peroxidase-1 gene knockout mice compared to their wild-type counterparts. The rates of parasitemia progression in gp91phox−/− mice and wild-type mice were not significantly different when they were treated with l-N G -methylarginine, an inhibitor of nitric oxide synthase. These results suggest that phagocyte-derived reactive oxygen species are not crucial for the clearance of malaria parasites, at least in murine models.

scholarly journals Role of IL-6 and TNF in thermoregulation and survival during sepsis in mice

1998 ◽  
Vol 275 (1) ◽  
pp. R269-R277 ◽  
Author(s):  
Lisa R. Leon ◽  
Andrew A. White ◽  
Matthew J. Kluger
Keyword(s):  
Knockout Mice ◽  
Gene Knockout ◽  
Cecal Ligation ◽  
Wild Type ◽  
Profound Hypothermia ◽  
Male And Female ◽  
Female Mice ◽  
Tnf Α ◽  
Gene Knockout Mice

Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have been implicated as key mediators in inflammation, morbidity, and mortality associated with sepsis. We examined the role of IL-6 and TNF-α signaling on hypothermia, fever, cachexia, anorexia, and survival during sepsis induced by cecal ligation and puncture (CLP) in male and female gene knockout mice. Male wild-type mice developed an initial hypothermia and subsequent fever during sepsis. Male IL-6 knockout mice did not develop fever; rather, they maintained a profound hypothermia during sepsis. Male TNF p55/p75 receptor (TNFR) knockout mice had attenuated hypothermia, but developed a virtually identical fever as wild-type mice. Cachexia did not differ between male wild-type and IL-6 or TNFR knockout mice, whereas anorexia was prolonged in IL-6 knockout mice. Due to the rapid lethality of sepsis in female mice, survival was the only variable we were able to statistically compare among female genotypes. Female wild-type mice had significantly decreased survival compared with male wild-type mice. Survival was significantly enhanced in male and female TNFR knockout mice compared with their wild-type controls. Lack of IL-6 did not affect male or female lethality. These data support the hypothesis that IL-6 is a key mediator of fever and food intake, whereas TNF is responsible for the initial hypothermia and lethality of sepsis in both sexes of mice. The enhanced lethality of CLP-treated female mice supports a role for sex steroids during sepsis.

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