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immunology of infectious and parasitic diseases - XXXVII Congress ...

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LYMPHOID ORGANS BEHAVIOR AND DINAMIC OF LYMPHOCYTE<br />

POPULATIONS IN EXPERIMENTAL TRYPANOSOMA CRUZI ORAL<br />

INFECTION<br />

JULIANA BARRETO DE ALBUQUERQUE (PG)1; DÉSIO AURÉLIO FARIAS<br />

DE OLIVEIRA1; DANIELLE SILVA DOS SANTOS1; LUIZ RICARDO<br />

BERBERT1; CARLA EPONINA DE CARVALHO PINTO2; JOSÉ JURBERG1;<br />

VANDA CUNHA1; WILSON SAVINO1; JULIANA DE MEIS1<br />

1Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Brazil;<br />

2Immunobiology Institute, Federal Fluminense University, Brazil<br />

Introduction: Trypanosoma cruzi (T. cruzi), the causative agent <strong>of</strong> Chagas´<br />

disease, infects about 10 million <strong>of</strong> people worldwide (WHO, 2010). The oral<br />

transmission by ingestion <strong>of</strong> contaminated food is causing outbreaks in several<br />

Brazilian states <strong>and</strong> other Latin America countries, <strong>and</strong> is potentially<br />

unrestricted to endemic regions (Int J Parasitol 39:615-623, 2009). Although we<br />

have previously described regional immune response in lymphoid organs in<br />

intraperitoneal (IP) murine infection (PLoS Negl Trop Dis 3(7):e417, 2009),<br />

there is a lack <strong>of</strong> data in oral infection/intragastric (IG). Here we analyze<br />

peripheral lymphoid organs behavior <strong>and</strong> dinamic <strong>of</strong> lymphocyte subpopulations<br />

in mice infected by IG or IP route. Methods <strong>and</strong> Results: BALB/c mice were<br />

infected with 5x104 T. cruzi trypomastigotes IP or IG <strong>and</strong> parasitemia was<br />

followed. After 9 (IP:n=8, IG:n=8), 12 (IP:n=3, IG:n=5), 15 (IP:n=1, IG:n=2), 17<br />

(IP:n=1, IG:n=3) <strong>and</strong> 27 days (IG:n=3), subcutaneous (SCLN) <strong>and</strong> mesenteric<br />

lymph nodes (MLN), spleen (Sp) <strong>and</strong> Peyer patches (PP) were harvested for<br />

cell counting <strong>and</strong> flow cytometry. Hearts were harvested at 15 dpi (IP:n=3,<br />

IG:n=2) <strong>and</strong> sections stained with Hematoxilin <strong>and</strong> Eosin. IG infected mice<br />

presented lower parasitemia <strong>and</strong> mortality than IP infected mice. In IP infection,<br />

95% <strong>of</strong> mice died before 18 dpi, while in IG group, 90% were still alive 27 dpi.<br />

SCLN (controls=19,5x106±2,9 cells; IP=57,6x106±9,1 cells; IG =31,8x106±3,2<br />

cells) <strong>and</strong> Sp (controls=239,1x106±49,7 cells; IP=776,3x106±180,9 cells;<br />

IG=307,5x106±80,3 cells) showed increased number <strong>of</strong> cells in both groups 9<br />

dpi <strong>and</strong> similar pr<strong>of</strong>ile in later days; however, hypertrophy <strong>of</strong> these tissues as<br />

well as T <strong>and</strong> CD19+ cells expansion was less evident IG mice than IP. In<br />

mucosal-associated lymphoid tissues, such as PP, after 9 dpi the atrophy was<br />

more evident in IP mice than IG (controls=1,5x106±0,4 cells; IP=0,5 x 106±0,2<br />

cells; IG=0,8x106±0,1 cells), due to decrease in CD19+ <strong>and</strong> CD4+ cells. MLN<br />

atrophy was only observed in after 15 dpi (controls= 40,1x106±4,5 cells; IP<br />

=11x 106 cells; IG=19,3x106±9,3 cells), due to depletion <strong>of</strong> CD19+ cells. Heart<br />

histological analysis showed similar alterations in 15 dpi (parasite nests,<br />

inflammatory infiltrate <strong>and</strong> tissue damage) in both groups, even with the lower

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