Kazem Behbehani

Bio: Kazem Behbehani is an academic researcher from University of London. The author has an hindex of 1, co-authored 1 publications receiving 37 citations.

Developmental cycles of Trypanosoma (Schizotrypanum) cruzi (Chagas, 1909) in mouse peritoneal macrophages in vitro.

Abstract: Mouse peritoneal macrophage cells suspended in a TC 199 calf serum medium and cultured in Leighton tubes, were infected with Trypanosoma (Schizotrypanum) cruzi culture forms in order to study the development of this parasite in vitro. Three cycles of development were thought to occur: 1. Epimastigotes or trypomastigotes were taken up by macrophages and transformed into amastigotes. These multiplied by binary fission and ruptured the infected cell after 4‐5 days. Released amastigotes were taken up by uninfected macrophages and the cycle was repeated. 2. A small proportion of intracellular amastigotes developed into ‘ovoid forms’ which transformed progressively into promastigotes, epimastigotes and trypomastigotes. 3. Some amastigotes became ‘round forms’ from which sphaeromastigotes developed. These transformed directly into trypomastigotes without the formation of epimastigotes.

Immunity to Trypanosoma cruzi.

Abstract: Publisher Summary Trypanosoma cruzi (T. cruzi), the causative agent of Chagas disease, is a digenetic trypanosomatid, which circulates in the bloodstream of the vertebrate host as trypomastigotes and has an obligatory intracellular phase in which the parasite multiplies as amastigotes, which differentiate into trypomastigotes. From an immunological point of view, therefore, the parasite presents stages that are directly exposed to the effector elements of the immune response, such as antibodies and macrophages, as well as stages that are sequestrated within host cells. T. cruzi infection is characterized by an acute phase with large numbers of parasites and by a sub-patent chronic phase in which circulating and tissue stages are difficult to detect. The mechanisms involved in the resistance to the parasite and in the control of parasitism during the chronic phase are not known. Chagas disease is life-long and spontaneous cures do not occur. There is increasing evidence that auto-immune processes participate in the pathogenesis of the cardiac and digestive forms of the disease. These many obscure aspects and challenging problems explain the increasing use of T. cruzi as a model for the study of humoral and cellular immunity in both basic and applied immunology.

Killing in vitro of Trypanosoma cruzi by macrophages from mice immunized with T. cruzi or BCG, and absence of cross-immunity on challege in vivo.

Abstract: Peritoneal macrophages from T. cruzi-immune mice were resistant to infection in vitro with culture forms of the parasite. Macrophage resistance appeared in infected mice about 21 days postinfection when parasitemia was still rising. Resistance in vitro was nonspecific since macrophages from BCG-immune mice were resistant to T. cruzi, and since macrophages from T. cruzi-immune mice were resistant to infection in vitro with Listeria were not resistant to challenge with T. cruzi even when the parasites were opsonized.

Mammalian cell invasion and intracellular trafficking by Trypanosoma cruzi infective forms

Abstract: Trypanosoma cruzi, the etiological agent of Chagas’ disease, occurs as different strains or isolates that may be grouped in two major phylogenetic lineages: T. cruzi I, associated with the sylvatic cycle and T. cruzi II, linked to the human disease. In the mammalian host the parasite has to invade cells and many studies implicated the flagellated trypomastigotes in this process. Several parasite surface components and some of host cell receptors with which they interact have been identified. Our work focused on how amastigotes, usually found growing in the cytoplasm, can invade mammalian cells with infectivities comparable to that of trypomastigotes. We found differences in cellular responses induced by amastigotes and trypomastigotes regarding cytoskeletal components and actin-rich projections. Extracellularly generated amastigotes of T. cruzi I strains may display greater infectivity than metacyclic trypomastigotes towards cultured cell lines as well as target cells that have modified expression of different classes of cellular components. Cultured host cells harboring the bacterium Coxiella burnetii allowed us to gain new insights into the trafficking properties of the different infective forms of T. cruzi, disclosing unexpected requirements for the parasite to transit between the parasitophorous vacuole to its final destination in the host cell cytoplasm.