A human astrocytoma cell line is highly susceptible to infection with Trypanosoma cruzi.

Astrocytes play a vital role in neuronal protection, homeostasis, vascular interchange and the local immune response. Some viruses and parasites can cross the blood-brain barrier and infect glia. Trypanosoma cruzi, the aetiological agent of Chagas disease, can seriously compromise the central nervous system, mainly in immune-suppressed individuals, but also during the acute phase of the infection. In this report, the infective capacity of T. cruzi in a human astrocyte tumour-derived cell line was studied. Astrocytes exposed to trypomastigotes (1:10 ratio) produced intracellular amastigotes and new trypomastigotes emerged by day 4 post-infection (p.i.). At day 6 p.i., 93% of the cells were infected. Using flow cytometry, changes were observed in both the expression of major histocompatibility complex class I and II molecules and the chemokine secretion pattern of astrocytes exposed to the parasite. Blocking the low-density lipoprotein receptor on astrocytes did not reduce parasite intracellular infection. Thus, T. cruzi can infect astrocytes and modulate the immune response during central nervous system infection.

A human astrocytoma cell line is highly susceptible to infection with Trypanosoma cruzi

Astrocytes play a vital role in neuronal protection, homeostasis, vascular interchange and the local immune response. Some viruses and parasites can cross the blood-brain barrier and infect glia. Trypanosoma cruzi, the aetiological agent of Chagas disease, can seriously compromise the central nervous system, mainly in immune-suppressed individuals, but also during the acute phase of the infection. In this report, the infective capacity of T. cruzi in a human astrocyte tumour-derived cell line was studied. Astrocytes exposed to trypomastigotes (1:10 ratio) produced intracellular amastigotes and new trypomastigotes emerged by day 4 post-infection (p.i.). At day 6 p.i., 93% of the cells were infected. Using flow cytometry, changes were observed in both the expression of major histocompatibility complex class I and II molecules and the chemokine secretion pattern of astrocytes exposed to the parasite. Blocking the low-density lipoprotein receptor on astrocytes did not reduce parasite intracellular infection. Thus, T. cruzi can infect astrocytes and modulate the immune response during central nervous system infection.

Microfilariae of Wuchereria bancrofti in cyst fluid of tumors of the brain: a report of three cases.

Microfilariae of various nematodes, including Loa loa, Dirofilariae, and Onchocerca volvulus, have been identified in the central nervous system (CNS). The CNS, however, is a rare site for the isolation of microfilariae of Wuchereria bancrofti. To the best of our knowledge, the presence of microfilariae of W. bancrofti in tumor cyst fluids or cerebrospinal fluid has not been reported to date. We report three cases in which microfilariae were identified in the cyst fluid of tumors of the brain. Cyst fluid aspirated from space-occupying lesions in the thalamus and C6-D1 spinal segments in a 46-yr-old man and a 35-yr-old man, respectively, showed numerous microfilariae of W. bancrofti, along with fragments of tumor suggestive of glioma. In the third case, in a 12-yr-old boy, the fluid from the space-occupying lesion in the third ventricle showed microfilariae in a necrotic dirty background with a few squames and cholesteral crystals. Histopathologic examination of the tumor showed an anaplastic astrocytoma and a low-grade astrocytoma in the first two cases, respectively, and a craniopharyngioma in the third case. No microfilariae were identified on the histology sections.

Colchicine decreases the infection by Toxoplasma gondii in cultured glial cells.

Addition of colchicine (2.5 x 10(-8)-1.25 x 10(-6) M) to cultures of glial cells infected with Toxoplasma gondii decreased the number of parasites up to 80% (P < 0.05) in comparison with controls. Our results indicate that colchicine could interfere with the infectious, or replicative mechanisms, or both, of Toxoplasma and place it as a candidate in the search for additional antitoxoplasmic therapy for those cases where the parasitic load is massive. Further studies in vivo must be made to confirm this finding and provide support for therapeutic trials.

Tumor necrosis factor alpha, interleukin 1 alpha, and interleukin 6 mRNA expressed by human astrocytoma cells after infection by three different strains of Toxoplasma gondii.

The role of cytokines in the pathogenesis of toxoplasmosis remains unknown to a large extent, especially in the case of reactivation that occurs in immunocompromised patients. To assess the importance of tumor necrosis factor alpha (TNF alpha), interleukin 1 alpha (IL1 alpha), and interleukin 6 (IL6), we studied the expression of these three cytokines by human astrocytoma cells after infection by three different strains of Toxoplasma gondii. The virulent RH strain, the intermediate 76K strain, and the cystogenic Prugniaud strain did not induce significantly different levels of expression of the cytokine messenger RNAs when the cytokines were studied at 1, 3, 6, and 24 h after parasitic infection. These results could indicate that infection by T. gondii strains of different virulence do not involve strong differences in TNF alpha, IL1 alpha, or IL6 expression by human astrocytoma cells.