INVESTIGADORES
VILLAR Silvina Raquel
congresos y reuniones científicas
Título:
LEVELS OF PRO-INFLAMMATORY CYTOKINES IN THE ADRENAL GLANDS DURIGN EXPERIMENTAL TRYPANOSOMA CRUZI INFECTION
Autor/es:
SILVINA R VILLAR1, AILIN LEPLETIER2, EDUARDO ROGGERO1, FLORENCIA GONZÁLEZ1, WILSON SAVINO2, ANA R PÉREZ1, OSCAR BOTTASSO1.
Lugar:
Los cocos- Córdoba
Reunión:
Congreso; LXI Reunión anual de la Sociedad Argenina de Inmunología.; 2013
Institución organizadora:
Sociedad Argenina de Inmunología
Resumen:
The pro-inflammatory cytokines produced mainly by immune cells are able to
establish a communication between the immune and endocrine systems via the
hypothalamic-pituitary-adrenal (HPA). Evidence indicates that adrenal GCs secretion can be modulated in situ, in an ACTH-independent fashion, by cytokines such
as TNF-α, IL-6 and IL-1β.
Previous studies have shown increased levels of GCs in mice infected with Trypanosoma cruzi (Tc). We hence aimed
to assess the levels of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and
the type of inflammatory infiltrates at the adrenal gland. C57BL/6 mice were
infected with Tc or inoculated with saline (Co). Assessments were made at day
17 post-infection (n=6/group). Data, expressed as mean ± SEM, belong to a representative
from three independent experimental rounds. Histological analysis revealed adrenal
hyperplasia (H&E), accompanied by increased plasma levels of GC (ELISA, m g /
dL) = Co: 0.34 ± 0.04, Tc: 1 ± 0.18 (p<0.05) without changes in plasma ACTH levels
(RIA, mg / dL) = Co: 93.7 ± 21, Tc: 69.5 ± 20.1. Real time PCR for pro-inflammatory
cytokines at the adrenal tissue showed increased levels of TNF-α and IL-1β,
without changes in IL-6 [ΔCt, TNF- α = Co: 5.1 ± 0.8, Tc: 57 ± 4.5, IL-1β = Co:
26.8 ± 6.2, Tc: 55.9 ± 7.4, IL-6 = Co: 19.0 ± 8.2, Tc: 17.3 ± 3.7, p<0.05
all cases]. Immunohistochemistry with anti-CD68 and anti-CD1b monoclonal
antibodies allowed to identify macrophages and dendritic cells, in the adrenal
cortex somehow augmented in the Tc group. The increased adrenal production of
pro-inflammatory cytokines may be partly explained by the presence of
infiltrating macrophages and dendritic cells.