The biology of Trypanosoma cruzi-macrophage interaction

Tc, de Araújo-Jorge

doi:10.1590/s0074-02761989000400001

Cited by 53 publications

(25 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous studies carried out with P. falciparum and E. tenella suggest that N-acetyl glucosamine and galactose, respectively, play some role on the protozoan-host cell interaction process [9,10]. The observation that sialylated cells are more easily infected with tachyzoites of T. gondii is an additional evi- Incubation time of 2 h. P 6 0.01. dence that this negatively charged carbohydrate residue is involved on the interaction process, as previously reported for the P. falciparum-erythrocyte [10] and the T. cruzi-host cell (reviewed in [1]) interaction processes.…”

Section: Resultssupporting

confidence: 69%

“…For some protozoa, such as those of the genus Leishmania, it has been shown that there is a special tropism of the protozoa for macrophages and that parasite interiorization takes place through a typical phagocytic process. Other protozoa, as Trypanosoma cruzi, penetrate di¡erent types of cell using both a phagocytic process and another mechanism where the host cell also plays an important role on the interaction process (reviewed in [1]). Still other protozoa, as is the case of Toxoplasma gondii, have the capacity to invade a broad range of vertebrate cells using several mechanisms including one in which components of the cytoskeleton play a fundamental role [2^5].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Host cell surface sialic acid residues are involved on the process of penetration of Toxoplasma gondii into mammalian cells

Monteiro¹

1998

FEMS Microbiology Letters

View full text Add to dashboard Cite

Tachyzoites of Toxoplasma gondii are able to infect several cell types tested (wild-type chinese hamster ovary (CHO) cells and glycosylation mutants, Vero and LLCMK2 cells). However, the extent of infection varied. Mutant cells which present few or no surface-exposed sialic acid residues were infected to a lower extent. Similar results were obtained if sialic acid residues were removed by previous neuraminidase treatment. Addition of sialic acid residues to surface-exposed glycoconjugates using fetuin as a sialic acid donor and the trans-sialidase of Trypanosoma cruzi rendered the cells more easily infected by Toxoplasma gondii. These observations indicate that surface-exposed carbohydrate residues of the host cell are involved on the process of Toxoplasma gondii-host cell recognition. z

show abstract

Section: Resultssupporting

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Host cell surface sialic acid residues are involved on the process of penetration of Toxoplasma gondii into mammalian cells

Monteiro¹

1998

FEMS Microbiology Letters

View full text Add to dashboard Cite

show abstract

“…The parasite modulates the NO production by cytokine and LPS-activated macrophages (10,11). Processes involved in macrophage infection with T. cruzi are extensively studied (12). The membrane cysteine proteinase cruzipain of T. cruzi, which corresponds to the major antigen gp 57/51 (13)(14)(15)(16)(17), has been shown to be involved in macrophage infection during the first step of the parasite-macrophage recognition using anti-cruzipain antibodies (18,19) and synthetic irreversible inhibitors of the cysteine proteinases (20,21).…”

Section: Nitric Oxide (No)mentioning

confidence: 99%

Cystatins Up-regulate Nitric Oxide Release from Interferon-γ- activated Mouse Peritoneal Macrophages

Verdot

Lalmanach

Vercruysse

et al. 1996

Journal of Biological Chemistry

102

View full text Add to dashboard Cite

Up-regulation of nitric oxide (NO) production by activated murine macrophages was observed during infection by Trypanosoma cruzi, the etiological agent of Chagas' disease. Cell infection by T. cruzi depends at least in part on cruzipain, a membrane-associated papain-related proteinase which is sensitive to inhibition by synthetic inhibitors of cysteine proteinases. Using the natural cysteine proteinase inhibitor chicken cystatin, a representative member of cystatin family 2, to investigate the effect of cruzipain on macrophage infection and NO release, we found that the inhibitor alone up-regulated NO release from interferon-␥-activated macrophages. A 12-fold increase in NO production was observed in the presence of 1 M chicken cystatin. This overproduction was concentration-dependent and could be detected at concentrations as low as 10 nM and remained in the presence of polymyxin B. Representative members of the other cystatin families, i.e. stefin B (family 1), T-kininogen, and its inhibitory domains (family 3), were also able to enhance NO production from interferon-␥-activated macrophages. Neither E64, an irreversible inhibitor of cysteine proteinases, nor inhibitors of aspartyl and serine proteinases (aprotinin, pepstatin, and soybean trypsin inhibitor) enhanced NO production. Upon complexation with saturating amounts of reduced-alkylated papain, cystatins still remained active in increasing NO production, suggesting that the cystatin inhibitory site was not involved in the mechanism.The results demonstrate that members of all 3 cystatin families share another common property unrelated to their function of cysteine proteinase inhibitors, i.e. upregulation of NO production, which biological significance remains to be elucidated. Nitric oxide (NO)1 is a multipotent physiologic molecule detected in the immune, neuronal, and vascular systems and in many other tissues (1). NO is synthesized by a wide variety of cell types from L-arginine by NO synthases (NOS), three distinct isoforms of which have now been identified (2, 3). Two isoforms are constitutive and Ca 2ϩ -calmodulin dependent: the first is membrane-bound, and was initially discovered in endothelial cells; the second is soluble and was first identified in neurons. The third isoform is an inducible Ca 2ϩ -independent NOS first discovered in murine macrophages and induced by appropriate stimulation with cytokines (4 -7).Among other cells, macrophages allow the intracellular multiplication of Trypanosoma cruzi, the etiological agent of Chagas' disease, a major public health problem in South and Central America (8). A close relationship has been demonstrated between NO production in activated murine macrophages and T. cruzi infection (9). The parasite modulates the NO production by cytokine and LPS-activated macrophages (10, 11). Processes involved in macrophage infection with T. cruzi are extensively studied (12). The membrane cysteine proteinase cruzipain of T. cruzi, which corresponds to the major antigen gp 57/51 (13-17), has been shown to be involved i...

show abstract

“…Without additional information, mere recruitment of inflammatory cells cannot be assumed to point to a role of the chemokines mentioned above in the pathogenesis of myocarditis. It should also borne in mind that T cells and macrophages are active in host defense against T. cruzi infection in mice (Kierszenbaum et al 1974;de Araujo-Jorge 1989;Russo and Starobinas 1991;Tarleton 1991Tarleton , 1995Kuhn 1994).…”

Section: Involvement Of Chemokines and Chemokine Receptors In The Devmentioning

confidence: 99%

Mechanisms of pathogenesis in Chagas disease

Kierszenbaum

2007

Acta Parasitologica

View full text Add to dashboard Cite

Chagas disease, caused by the obligate unicellular parasite Trypanosoma cruzi, presents itself in a diverse collection of clinical manifestations, ranging from severe, fatal heart and digestive tract pathologies to unapparent or minor alterations that do not compromise survival. Over the years, a number of mechanisms have been proposed to explain the pathogenesis of chagasic tissue lesions, all of which have faced some criticism or been received with skepticism. This article excludes the autoimmunity hypothesis for Chagas disease because it has been extensively reviewed elsewhere, and summarizes the various alternative hypotheses that have been advanced over the years. For each of these hypotheses, an outline of its main tenets and key findings that support them is presented. This is followed by the results and comments that have challenged them and the caveats that stand on their way to wider acceptance. It is hoped that this writing will draw attention to our shortcomings in understanding the pathogenesis of Chagas disease, which, unfortunately, continues to figure among the most serious health problems of the American continent.

show abstract

The biology of Trypanosoma cruzi-macrophage interaction

Cited by 53 publications

References 0 publications

Host cell surface sialic acid residues are involved on the process of penetration of Toxoplasma gondii into mammalian cells

Host cell surface sialic acid residues are involved on the process of penetration of Toxoplasma gondii into mammalian cells

Cystatins Up-regulate Nitric Oxide Release from Interferon-γ- activated Mouse Peritoneal Macrophages

Mechanisms of pathogenesis in Chagas disease

Contact Info

Product

Resources

About