Chemokines in host–protozoan-parasite interactions

Brenier-Pinchart, Marie-Pierre; Pelloux, Hervé; Derouich-Guergour, Dorra; Ambroise-Thomas, P

doi:10.1016/s1471-4922(01)01902-x

Cited by 38 publications

(21 citation statements)

References 40 publications

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“…Several studies reported that Leishmania can trigger the expression of several chemokines in vitro and in vivo [20,31,32] and that these seem to play an important role in leukocyte recruitment and activation leading to healing and resistance to infection. We report here that SHP-1 deficiency provoked a higher induction of MIP1b, MIP-1a, MCP-1, IP-10 and MIP-2 mRNA expression in mice following Lm infection in comparison to that seen in wild-type mice.…”

Section: Discussionmentioning

confidence: 99%

“…Some of them (MCP-1/CCL2, MIP-1a/CCL3, IP-10/CXCL10, IL-8, KC/CXCL1, RANTES/CCL5, MIP-1b/CCL4, MIP-2/CXCL1 and TCA-3) have been shown to be induced by Leishmania infection in vitro and in vivo [20,31,32]. Lm infection induced mRNA expression of many chemokines (RANTES/CCL5, MIP-1a, MIP-1b/CCL4, MIP-2/CXCL1, IP-10 and MCP-1) in both types of mice (Fig.…”

Section: Regulation Of Lm-induced Chemokine Gene Expression By Shp-1mentioning

confidence: 99%

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Regulation of theLeishmania-induced innate inflammatory response by the protein tyrosine phosphatase SHP-1

et al. 2005

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Modulation of the phagocyte protein tyrosine phosphatase (PTP) SHP-1 by the parasite Leishmania favors its survival and propagation within its mammalian host. In vivo, the absence of SHP-1 leads to virtually absent footpad swelling, accompanied by enhanced inducible nitric oxide synthase expression. In this study, using an air pouch model, we show that viable motheaten SHP-1-deficient mice harbored a stronger inflammatory response against Leishmania infection than wild-type mice. This response was portrayed by higher pro-inflammatory cytokine (TNF-a, IL-1b and IL-6) expression and secretion and by greater chemokine and chemokine receptor expression. These inflammatory molecules were probably responsible for the stronger cellular recruitment, mainly of neutrophils, seen at the site of infection in viable motheaten mice within 6 h post inoculation. We also provide strong evidence that protein tyrosine phosphatases in general, and SHP-1 in particular, are important regulators of chemokine gene expression. Overall, this study suggests that the ability of Leishmania to induce SHP-1 activity in its host allows the taming of an otherwise strong innate inflammatory response that would be detrimental for its survival and progression.

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Section: Discussionmentioning

confidence: 99%

Section: Regulation Of Lm-induced Chemokine Gene Expression By Shp-1mentioning

confidence: 99%

Regulation of theLeishmania-induced innate inflammatory response by the protein tyrosine phosphatase SHP-1

et al. 2005

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“…The critical role of chemokines and their receptors in the development of immunity against a wide variety of pathogens has become a focus of interest in recent years [9,42]. Chemokines are often differentially induced in response to various stimuli or pathogens as a reflection of their varied ability to activate T cells and macrophages, influence T cell differentiation and recruit appropriate effector cells to the site of inflammation.…”

Section: Zoonotic Visceral Leishmaniasis (Zvl) Is Caused By Parasitesmentioning

confidence: 99%

Splenic immune responses during canine visceral leishmaniasis

Strauss-Ayali

Baneth

Jaffe³

2007

Vet. Res.

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-Dogs are the main reservoir host for zoonotic visceral leishmaniasis caused by Leishmania infantum. In this study we investigated the immune response in spleens of L. infantum-infected dogs by measuring the mRNA expression levels for a wide panel of cytokines, transcription factors and chemokines. mRNA levels and parasite load were followed during 7 months of experimental infection and 14 months post-treatment, and were compared to naturally-infected (NI) dogs. Similarly, serum anti-Leishmania IgG and IgG subclass levels were measured during experimental infection. An increase in IFN-γ, T-bet, IP-10 and RANTES was found in the experimentally and NI dogs, implicating a substantial type-1 immune response during canine visceral leishmaniasis. IL-4, a type-2 associated cytokine, increased as early as one month after experimental infection, while IL-5 was high at later stages. Interestingly, the expression levels of the Treg-associated cytokines, IL-10 and TGF-β, did not change during the infection. Total anti-Leishmania IgG and IgG subclasses increased during the experimental infection. However, no association with specific cytokine patterns was observed. Parasite load in the spleens increased as early as one month postinfection and remained high until treatment. The load was higher in the polysymptomatic NI dogs than in the experimentally-infected dogs. This study indicates that both type-1 and type-2 immune responses occur in the spleen during canine L. infantum infection, and suggests that the early elevation of IL-4 might have a role in the persistence of parasites in the presence of high IFN-γ expression.canine visceral leishmaniasis / IFN-γ / IL-4 / T-bet / IP-10

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“…In addition to their role in regulating the immune response during viral and bacterial infections, chemokines also appear to mediate the host immune response during protozoan infections (4). For example, recent studies have shown that P. falciparum infection during pregnancy is characterized by elevations in MIP-1␣, monocyte chemoattractant protein 1 (MCP-1), I-309, and interleukin-8 (IL-8) transcripts, which are associated with increased monocyte density in the placental intervillous space (1,42).…”

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confidence: 99%

Differential Regulation of β-Chemokines in Children with Plasmodium falciparum Malaria

et al. 2005

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Chemokines regulate the host immune response to a variety of infectious pathogens. Since the role of chemokines in regulating host immunity in children with Plasmodium falciparum malaria has not previously been reported, circulating levels of ␤-chemokines (MIP-1␣, MIP-1␤, and RANTES) and their respective transcriptional profiles in ex vivo peripheral blood mononuclear cells (PBMCs) were investigated. Peripheral blood MIP-1␣ and MIP-1␤ levels were significantly elevated in mild and severe malaria, while RANTES levels decreased with increasing disease severity. ␤-Chemokine gene expression profiles in blood mononuclear cells closely matched those of circulating ␤-chemokines, illustrating that PBMCs are a primary source for the observed pattern of ␤-chemokine production during acute malaria. Statistical modeling revealed that none of the chemokines was significantly associated with either parasitemia or anemia. Additional investigations in healthy children with a known history of malaria showed that children with prior severe malaria had significantly lower baseline RANTES production than children with a history of mild malaria, suggesting inherent differences in the ability to produce RANTES in these two groups. Baseline MIP-1␣ and MIP-1␤ did not significantly differ between children with prior severe malaria and those with mild malaria. Additional in vitro experiments in PBMCs from healthy, malaria-naïve donors revealed that P. falciparum-derived hemozoin (Hz; malarial pigment) and synthetic Hz (␤-hematin) promote a similar pattern of ␤-chemokine gene expression. Taken together, the results presented here demonstrate that children with severe malaria have a distinct profile of ␤-chemokines characterized by increased circulating levels of MIP-1␣ and MIP-1␤ and decreased RANTES. Altered patterns of circulating ␤-chemokines result, at least in part, from Hz-induced changes in ␤-chemokine gene expression in blood mononuclear cells.

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Chemokines in host–protozoan-parasite interactions

Cited by 38 publications

References 40 publications

Regulation of theLeishmania-induced innate inflammatory response by the protein tyrosine phosphatase SHP-1

Regulation of theLeishmania-induced innate inflammatory response by the protein tyrosine phosphatase SHP-1

Splenic immune responses during canine visceral leishmaniasis

Differential Regulation of β-Chemokines in Children with Plasmodium falciparum Malaria

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