title: The adipocyte as an important target cell for Trypanosoma cruzi infection.
abstract: Adipose tissue plays an active role in normal metabolic homeostasis as well as in the development of human disease. Beyond its obvious role as a depot for triglycerides, adipose tissue controls energy expenditure through secretion of several factors. Little attention has been given to the role of adipocytes in the pathogenesis of Chagas disease and the associated metabolic alterations. Our previous studies have indicated that hyperglycemia significantly increases parasitemia and mortality in mice infected with Trypanosoma cruzi. We determined the consequences of adipocyte infection in vitro and in vivo. Cultured 3T3-L1 adipocytes can be infected with high efficiency. Electron micrographs of infected cells revealed a large number of intracellular parasites that cluster around lipid droplets. Furthermore, infected adipocytes exhibited changes in expression levels of a number of different adipocyte-specific or adipocyte-enriched proteins. The adipocyte is therefore an important target cell during acute Chagas disease. Infection of adipocytes by T. cruzi profoundly influences the pattern of adipokines. During chronic infection, adipocytes may represent an important long-term reservoir for parasites from which relapse of infection can occur. We have demonstrated that acute infection has a unique metabolic profile with a high degree of local inflammation in adipose tissue, hypoadiponectinemia, hypoglycemia, and hypoinsulinemia but with relatively normal glucose disposal during an oral glucose tolerance test.
authors.affiliation: Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
authors.forename: Terry P
authors.initials: TP
authors.lastname: Combs
authors.lastname: Nagajyothi
authors.forename: Shankar
authors.initials: S
authors.lastname: Mukherjee
authors.forename: Cecilia J G
authors.initials: CJ
authors.lastname: de Almeida
authors.forename: Linda A
authors.initials: LA
authors.lastname: Jelicks
authors.forename: William
authors.initials: W
authors.lastname: Schubert
authors.forename: Ying
authors.initials: Y
authors.lastname: Lin
authors.forename: David S
authors.initials: DS
authors.lastname: Jayabalan
authors.forename: Dazhi
authors.initials: D
authors.lastname: Zhao
authors.forename: Vicki L
authors.initials: VL
authors.lastname: Braunstein
authors.forename: Shira
authors.initials: S
authors.lastname: Landskroner-Eiger
authors.forename: Aisha
authors.initials: A
authors.lastname: Cordero
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Factor
authors.forename: Louis M
authors.initials: LM
authors.lastname: Weiss
authors.forename: Michael P
authors.initials: MP
authors.lastname: Lisanti
authors.forename: Herbert B
authors.initials: HB
authors.lastname: Tanowitz
authors.forename: Philipp E
authors.initials: PE
authors.lastname: Scherer
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000378:metabolism* / Q000469:parasitology; D000818:Animals; D001483:Base Sequence; D015153:Blotting, Western; D017931:DNA Primers; D007003:Hypoglycemia / Q000150:complications; D007150:Immunohistochemistry; D051379:Mice; D008855:Microscopy, Electron, Scanning; D014349:Trypanosoma cruzi / Q000472:pathogenicity*; D014352:Trypanosomiasis / Q000150:complications / Q000469:parasitology / Q000473:pathology*
chemical_list: D017931:DNA Primers