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

DOWN-REGULATION OF IFN-g RECEPTOR ALPHA CHAIN EXPRESSION
AND CXCL-10 PRODUCTION BY CYSTOISOSPORA BELLI ANTIGENS
FERNANDA GONÇALVES GARCIA (1) ; MÁRCIA BENEDITA DE OLIVEIRA
SILVA (1) ; ANA CRISTINA LOPES TOSTA (1) ; DALMO CORREIA FILHO (1) ;
DAVID NASCIMENTO SILVA TEIXEIRA (1) .
(1) Universidade Federal do Triângulo Mineiro, UFTM, Uberaba, MG, Brasil.
Introduction: Extraintestinal cystoisosporosis has already been reported in
HIV/AIDS patients, generally involving preferential invasion of mesenteric and
tracheobronchial lymph nodes, liver and spleen by unizoic cysts of this parasite,
which may infect macrophages. It has been proposed that macrophages may
act as C. belli host cells in extraintestinal sites. However, the absence of an in
vivo experimental model has hampered the knowledge of parasite‟s biology.
Moreover, until present, there is no information about chemokine and cytokine
profile secreted by PBMCs in response to C. belli antigens.
Methods and Results: PBMCs were isolated from healthy volunteers and
stimulated with C. belli oocysts/sporozoites antigens. Cytokines in culture
supernatants were quantifyed by ELISA. The cell surface expression of IFN-g
receptor α-chain (CD119) was assessed by staining PBMCs with anti-CD119phycoerythrin
(PE) monoclonal antibody and analyzed with a FACSCalibur flow
cytometer using CellQuest software (BD Biosciences). This study was approved
by UFTM Research Ethical Committee. We demonstrate that C. belli antigens
markedly inhibited CXCL-10 production (403,7 pg/ml) by PBMCs when
compared to non stimulated cells (1030,0 pg/ml) (p=0,0093) without affecting IL-
12p40 and IFN-g secretion (p>0,05). Since, CXCL-10 is an IFN-g inducible
chemokine; we also analyzed the IFN-g receptor α-chain expression on CD14+
positive PBMCs. Results obtained showed that PBMCs stimulation with C. belli
antigens decreased CD119 expression.
Conclusion: Since IFN-g activates effector mechanisms against intracellular
pathogens, the impaired IFN-g response (reduction of CXCL-10 production and
CD119 expression) in cells stimulated by C. belli antigens may contributes to
survival of this pathogen inside host cells. Investigation of mechanisms involved
on IFN-g signaling inhibition by C. belli antigens may contribute for increase the
knowledge about C. belli evasion strategies. The results obtained on the
present work may improve the understanding of immunological events involved
on C. belli/hosts cells interactions.
Financial support: UFTM;CAPES/REUNI;FAPEMIG.