Susceptibility to Leishmania major Infection in Interleukin-4-Deficient Mice

Science ◽  
1996 ◽  
Vol 271 (5251) ◽  
pp. 987-990 ◽  
Author(s):  
N. Noben-Trauth ◽  
P. Kropf ◽  
I. M ller
Keyword(s):  
Leishmania Major ◽  
Interleukin 4 ◽  
Major Infection ◽  
Deficient Mice

scholarly journals Migration-Inhibitory Factor Gene-Deficient Mice Are Susceptible to Cutaneous Leishmania major Infection

2001 ◽  
Vol 69 (2) ◽  
pp. 906-911 ◽  
Author(s):  
Abhay R. Satoskar ◽  
Marcelo Bozza ◽  
Miriam Rodriguez Sosa ◽  
Guoshing Lin ◽  
John R. David
Keyword(s):  
Migration Inhibitory Factor ◽  
Protective Immunity ◽  
Leishmania Major ◽  
Inhibitory Factor ◽  
Interleukin 4 ◽  
Wild Type ◽  
Leishmanicidal Activity ◽  
Ifn Γ ◽  
Deficient Mice

ABSTRACT To determine the role of endogenous migration-inhibitory factor (MIF) in the development of protective immunity against cutaneous leishmaniasis, we analyzed the course of cutaneous Leishmania major infection in MIF gene-deficient mice (MIF−/−) and wild-type (MIF+/+) mice. Following cutaneous L. major infection, MIF−/− mice were susceptible to disease and developed significantly larger lesions and greater parasite burdens than MIF+/+ mice. Interestingly, antigen-stimulated lymph node cells from MIF−/− mice produced more interleukin-4 (IL-4) and gamma interferon (IFN-γ) than those from MIF+/+ mice, although the differences were statistically not significant. IFN-γ-activated resting peritoneal macrophages from MIF−/− mice showed impaired macrophage leishmanicidal activity and produced significantly lower levels of nitric oxide and superoxide in vitro. The macrophages from MIF−/− mice, however, produced much more IL-6 than macrophages from wild-type mice. These findings demonstrate that endogenous MIF plays an important role in the development of protective immunity against L. majorin vivo. Furthermore, they indicate that the susceptibility of MIF−/− mice to L. major infection is due to impaired macrophage leishmanicidal activity rather than dysregulation of Th1 and Th2 responses.

Leishmania major infection in interleukin-4 and interferon-gamma depleted mice

1999 ◽  
Vol 21 (8) ◽  
pp. 423-431 ◽  
Author(s):  
Rene Chatelain ◽  
Smita Mauze ◽  
Kari Varkila ◽  
Robert L. Coffman
Keyword(s):  
Interferon Gamma ◽  
Leishmania Major ◽  
Interleukin 4 ◽  
Major Infection

scholarly journals Arginase I Induction during Leishmania major Infection Mediates the Development of Disease

2005 ◽  
Vol 73 (9) ◽  
pp. 6085-6090 ◽  
Author(s):  
Virginia Iniesta ◽  
Jesualdo Carcelén ◽  
Isabel Molano ◽  
Pablo M. V. Peixoto ◽  
Eloy Redondo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mouse Model ◽  
Differential Expression ◽  
Leishmania Major ◽  
Interleukin 4 ◽  
Major Infection ◽  
Time Of Infection ◽  
Oxide Synthase ◽  
Arginase I

ABSTRACT In a previous work, we demonstrated that the induction of arginase I favored the replication of Leishmania inside macrophages. Now we have analyzed the differential expression of this enzyme in the mouse model of L. major infection. Ours results show that arginase I is induced in both susceptible and resistant mice during the development of the disease. However, in BALB/c-infected tissues, the induction of this protein parallels the time of infection, while in C57BL/6 mice, the enzyme is upregulated only during footpad swelling. The induction of the host arginase in both strains is mediated by the balance between interleukin-4 (IL-4) and IL-12 and opposite to nitric oxide synthase II expression. Moreover, inhibition of arginase reduces the number of parasites and delays disease outcome in BALB/c mice, while treatment with l-ornithine increases the susceptibility of C57BL/6 mice. Therefore, arginase I induction could be considered a marker of disease in leishmaniasis.

scholarly journals High Levels of Susceptibility and T Helper 2 Response in MyD88-Deficient Mice Infected with Leishmania major Are Interleukin-4 Dependent

2003 ◽  
Vol 71 (12) ◽  
pp. 7215-7218 ◽  
Author(s):  
Andrea Debus ◽  
Joachim Gläsner ◽  
Martin Röllinghoff ◽  
André Gessner
Keyword(s):  
Knockout Mice ◽  
Leishmania Major ◽  
Parasite Burden ◽  
Interleukin 4 ◽  
Myeloid Differentiation ◽  
Interleukin 12 ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Deficient Mice

ABSTRACT Myeloid differentiation protein 88 (MyD88) is a general adaptor for the signaling cascade through receptors of the Toll/IL-1R family. When infected with Leishmania major parasites, MyD88-deficient mice displayed a dramatically enhanced parasite burden in their tissues similar to that found in susceptible BALB/c mice. In contrast, MyD88 knockout mice did not develop ulcerating lesions despite a lack of interleukin-12 (IL-12) production and a predominant T helper 2 cell response. Blockade of IL-4 produced early (day 1) after infection restored a protective T helper 1 response in MyD88 knockout mice.

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