Chemokine Gene Expression in Toll-Like Receptor-Competent and -Deficient Mice Infected with
            <i>Leishmania major</i>

Antoniazi, Simone Aparecida; Price, Helen P.; Kropf, Pascale; Freudenberg, Marina A.; Galanos, Chris; Smith, Deborah F.; Müller, Ingrid

doi:10.1128/iai.72.9.5168-5174.2004

Cited by 42 publications

(39 citation statements)

References 45 publications

(55 reference statements)

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“…Nevertheless, further studies showed that TLR4 was less important than TLR2 and cytokine expression was independent of this receptor 2 . KAVOOSI et al demonstrated in two studies that TLR4 is not activated by Leishmania 10,11 .…”

Section: Discussionmentioning

confidence: 99%

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Expression of TLR2 and TLR4 in lesions of patients with tegumentary american leishmaniasis

Tuon

Fernandes

Duarte

et al. 2012

Rev. Inst. Med. trop. S. Paulo

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SUMMARYObjectives: The aim of this study was to describe the pattern of expression of Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) in skin biopsies of patients with American tegumentary leishmaniasis (ATL) caused by Leishmania braziliensis. Methods: This prospective study evaluated 12 patients with ATL caused by Leishmania braziliensis confirmed by polymerase chain reaction. Immunohistochemistry was performed to determine the expression of TLR2 and TLR4. The number of NK cells, dendritic cells and macrophages in the tissue were calculated. The cytokine expression was determined using the anti-TNF-α, anti-IFN-γ, anti-IL-1 and anti-IL-6. Double immunostaining reactions were used to determine the cell expressing TLR2 and TLR4. Results: The numbers of cells expressing TLR2 and TLR4 were 145.48 ± 82.46 cell/mm 2 and 3.26 ± 4.11 cell/mm 2 respectively (p < 0.05). There was no correlation of TLR2 and TLR4 with the amount of cytokines and the number of NK cells, dendritic cells or macrophages. The double immunostaining revealed that TLR2 was expressed by macrophages. Conclusion: In human cutaneous leishmaniasis caused by Leishmania braziliensis, TLR2 is the most common TLR expressed during active disease, mainly by macrophages although without correlation with the amount of cytokines and number of cells.

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Section: Discussionmentioning

confidence: 99%

“…Nevertheless, discrepancy in TLR signaling has been observed when in vitro and in vivo studies have been published 2,[10][11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Expression of TLR2 and TLR4 in lesions of patients with tegumentary american leishmaniasis

Tuon

Fernandes

Duarte

et al. 2012

Rev. Inst. Med. trop. S. Paulo

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“…Studies using mouse L. major model have shown that the draining lymph nodes from diseaseresistant C3H and C57BL/6 mice contain significantly higher amounts of MCP-1, IP-10, and lymphotactin mRNA than those from susceptible BALB/c mice [38,40]. L. major-infected C57BL/6 mice also display increased levels of CXCL10 in their lesions [42]. On the other hand, C57BL/6 mice lacking the MCP-1 receptor CCR2 show decreased migration of Th1-inducing dendritic cells from the site of infection to the lymph nodes, mount a Th2 response, and develop non-healing lesions [38].…”

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confidence: 99%

CXCR3^–/– mice mount an efficient Th1 response but fail to control Leishmania major infection

et al. 2005

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Chemokines play a critical role in recruitment of leukocytes to the site of infection, which is essential for host defense. We analyzed the role of CXC chemokine receptor 3 (CXCR3) in the control of cutaneous leishmaniasis using CXCR3 -/-C57BL/6 mice. We found that Leishmania major-infected CXCR3 -/-mice mount an efficient Th1 response as evident by markedly increased serum levels of Th1-associated IgG2a and significant production of IFN-c and IL-12 by the draining lymph node cells, restrict systemic spread of infection, but fail to control parasite replication at the site of infection and develop chronic non-healing lesions. Furthermore, the inability of CXCR3 -/-mice to control cutaneous L. major growth was associated with fewer CD4 + and CD8 + T cells and significantly lower levels of IFN-c in their lesions as compared to CXCR3 +/+ mice. These results demonstrate that CXCR3 plays a critical role in the host defense against cutaneous leishmaniasis caused by L. major. Furthermore, they also suggest that the susceptibility of CXCR3 -/-mice to L. major is due to impaired CD4 + and CD8 + T cell trafficking and decreased production of IFN-c at the site of infection rather than to their inability to mount a parasite-specific Th1 response. IntroductionLeishmania species are obligate intracellular parasites that are of extensive public health importance in the tropical and subtropical regions of the world [1]. In humans, cutaneous leishmaniasis caused by Leishmania major commonly manifests as a self-healing skin lesion followed by the development of long-term immunity. Several studies have shown that an IL-12-driven Th1 response and IFN-c production are critical for the control of L. major infection in genetically resistant mice, such as CBA/J, C57BL/6, and C3H [2][3][4][5]. On the other hand, the development of non-healing lesions in susceptible BALB/c mice is associated with the preferential induction of a Th2-like response associated with production of 6].The chemokine superfamily comprises a large number of small soluble proteins that are involved in the development and homeostasis of the hematopoietic system, angiogenesis, tissue repair, and regulation of the host immune response [7,8]. Recent studies have shown that chemokines play a critical role in the development of innate as well as acquired immunity against a variety [18]. Three CXC chemokines, CXCL9 (Mig), CXCL10 (IFN-inducible protein 10, IP-10) and CXCL11 (IFN-inducible T cell alpha chemoattractant, I-TAC), signal via CXCR3 [19,20], activate Ras/extracellular signal-regulated kinase (ERK), Src, and the phosphatidylinositol 3-kinase/Akt pathway, and mediate their biological functions such as cell migration and proliferation [21]. Many clinical studies have implicated a role for CXCR3 in the pathogenesis of several inflammatory diseases such as multiple sclerosis, psoriasis, and rheumatoid arthritis by facilitating the recruitment of pathogenic T cells to the site of inflammation [22][23][24][25]. Moreover, experimental studies using a cardiac transplanta...

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“…Case of ISPs interfering in trypsin-like action of sand fly midguts has been reported [25]. Moreover, a few parasites of Leishmania family also have mechanisms that intensify their resistance to proteolytic attack without inhibiting the overall proteolytic activity in the midgut [28].…”

Section: Alternative Pathogenicity Of Parasitesmentioning

confidence: 99%

“…In this diagnostic method, promastigotes of L. donovani are grown to log phase and lysed and the soluble protein is used as sample [18]. With Western blotting, one can find even minor antigenic differences among various organisms and thus detect cross-reactive antigens [28]. Though, the process is time consuming, technically cumbersome, and expensive [8] tonsils, and skin; and even as widely disseminated disease [4,8].…”

Section: Western Blotmentioning

confidence: 99%

Altercating Leishmaniasis: Cultivating Improved Vaccines

Dhingra¹,

Satapathy²

2014

AJIDM

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The exponentially rising cases of Leishmaniasis over the past decades, has attracted scientists and clinicians to mitigate the contagious infection by modern treatments and new generation vaccinations. Leishmania, the causative pathogen of this infection predominantly expresses its diseased condition in form of cutaneous leishmaniasis. Although systemic leishmaniasis, is a more deadly form, but cases of its manifestation are limited; thereby staging the focus onto more intricate study of cutaneous leishmaniasis. Designing a vaccine against Leishmania has witnessed more than two generations of vaccine, but each attempt has failed more than it's cases of success. The proposed drawbacks root to the difficulty in ensuring an efficient transition of research from simple laboratory experiments carried out in-vitro/in-vivo in small animals to that of the humans. There have been extensive case studies of this disease and thus every immunological aspect has been our focus. This paper is an attempt to decipher the ideas and methodologies adopted till date and further target the genetic spans and molecular moieties, for crafting an alternative vaccine based on efforts to mock the pathogenic pathways.

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Chemokine Gene Expression in Toll-Like Receptor-Competent and -Deficient Mice Infected with Leishmania major

Cited by 42 publications

References 45 publications

Expression of TLR2 and TLR4 in lesions of patients with tegumentary american leishmaniasis

Expression of TLR2 and TLR4 in lesions of patients with tegumentary american leishmaniasis

CXCR3^–/– mice mount an efficient Th1 response but fail to control Leishmania major infection

Altercating Leishmaniasis: Cultivating Improved Vaccines

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Chemokine Gene Expression in Toll-Like Receptor-Competent and -Deficient Mice Infected with Leishmania major

Cited by 42 publications

References 45 publications

Expression of TLR2 and TLR4 in lesions of patients with tegumentary american leishmaniasis

Expression of TLR2 and TLR4 in lesions of patients with tegumentary american leishmaniasis

CXCR3–/– mice mount an efficient Th1 response but fail to control Leishmania major infection

Altercating Leishmaniasis: Cultivating Improved Vaccines

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Product

Resources

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CXCR3^–/– mice mount an efficient Th1 response but fail to control Leishmania major infection