IFN-γ-Dependent Nitric Oxide Production Is Not Linked to Resistance in Experimental African Trypanosomiasis

Hertz, Cheryl J.; Mansfield, John M.

doi:10.1006/cimm.1998.1429

Cited by 71 publications

(57 citation statements)

References 45 publications

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“…15,31 In the case of complement activation, complement component B is situated in close proximity to C3 (Tir1) but is not on the microarray. Our results also substantiate the findings of others, indicating that interferons 13,32 and arginase 12 are factors associated with susceptibility or resistance. However, the study by Duleu et al suggested that macrophages of the susceptible strain express higher levels of arginase I and II, whereas we found that arginase I was more highly expressed in the tolerant C57BL/6 strain.…”

Section: Discussionsupporting

confidence: 92%

“…8,9 Until recently, most investigators have focused their research on the innate and adaptive immune response to T. congolense infection, investigating components such as trypanosome-specific and nonspecific antibody production, subsets of T cells, complement pathway, cytokine and nitric oxide production, and specific proteins such as heat-shock protein 70.1 and arginase. [10][11][12][13][14][15][16][17][18] Although these studies have led to important findings, the measurement of a small number of components in any one study has limited the ability to integrate individual results. Microarray-based gene expression assays provide the ability to study the expression of large numbers of genes simultaneously.…”

Section: Introductionmentioning

confidence: 99%

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Gene expression profiling in a mouse model for African trypanosomiasis

Kierstein¹,

Noyes²,

Naessens³

et al. 2006

Genes Immun

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This study aimed to provide the foundation for an integrative approach to the identification of the mechanisms underlying the response to infection with Trypanosoma congolense, and to identify pathways that have previously been overlooked. We undertook a large-scale gene expression analysis study comparing susceptible A/J and more tolerant C57BL/6 mice. In an initial time course experiment, we monitored the development of parasitaemia and anaemia in every individual. Based on the kinetics of disease progression, we extracted total RNA from liver at days 0, 4, 7, 10 and 17 post infection and performed a microarray analysis. We identified 64 genes that were differentially expressed in the two strains in non-infected animals, of which nine genes remained largely unaffected by the disease. Gene expression profiling at stages of low, peak, clearance and recurrence of parasitaemia suggest that susceptibility is associated with high expression of genes coding for chemokines (e.g. Ccl24, Ccl27 and Cxcl13), complement components (C1q and C3) and interferon receptor alpha (Ifnar1). Additionally, susceptible A/J mice expressed higher levels of some potassium channel genes. In contrast, messenger RNA levels of a few immune response, metabolism and protease genes (e.g. Prss7 and Mmp13) were higher in the tolerant C57BL/6 strain as compared to A/J.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Gene expression profiling in a mouse model for African trypanosomiasis

Kierstein¹,

Noyes²,

Naessens³

et al. 2006

Genes Immun

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“…A similar mechanism may operate for migration of T. brucei brucei across the BBB. In support of this hypothesis, it has been reported that IFN-γ -/-mice express low levels of NO and TNF-α (18,33). In addition, IFN-γ can induce chemokines (in astrocytes, macrophages, and microglial cells), which are involved in leukocyte recruitment into the brain (24,34).…”

Section: Discussionmentioning

confidence: 83%

Cerebral vessel laminins and IFN-γ define Trypanosoma brucei brucei penetration of the blood-brain barrier

Masocha

Robertson²,

Rottenberg³

et al. 2004

J. Clin. Invest.

120

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“…24 No.9 No role for NO in T. brucei control could be established through knockout mice studies; iNOS À/À mice behaved similarly to fully immune-competent control mice [44][45][46]. However, treatment studies using a specific NOS inhibitor (L-NAME), in addition to one knockout-mice study, highlighted the role of NO in T. brucei-induced immunosuppression and anaemia [46][47][48].…”

Section: Reviewmentioning

confidence: 99%

“…In this regard, IFN-g has been described as a susceptibility factor in a BALB/c T. congolense model characterized by early host death, and a link has been established between early death and unrestrained IFN-g production that results in an unbalanced IFN-g-IL-10 response [26]. T. congolense infections in IFN-g À/À C57Bl/6 and BALB/c mice that were treated with anti-IFN-g antibodies highlighted these different aspects of IFN-g involvement as a result of different genetic backgrounds [25,28,45].…”

Section: Reviewmentioning

confidence: 99%