CERELA   05438
CENTRO DE REFERENCIA PARA LACTOBACILOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Protein malnutrition significantly increases lung inflammatory damage induced by the viral pathogen-associated molecular pattern poly(I:C)
Autor/es:
CLUA, P; ZELAYA, H; SALVA, S; MARRANZINO, G; ALVAREZ, S; VILLENA, J
Lugar:
Mar del Plata, Buenos Aires (Argentina)
Reunión:
Congreso; LIX Reunión científica anual de la Sociedad Argentina de Investigación Clínica y LXII Reunión anual Sociedad Argentina de Inmunología; 2014
Institución organizadora:
Sociedad Argentina de Investigación Clínica (SAIC) y Sociedad Argentina de Inmunología (SAI).
Resumen:
Protein malnutrition significantly increases lung inflammatory damage induced by the viral pathogen-associated molecular pattern poly(I:C) Patricia Clua , Hortensia Zelaya, Susana Salva, Gabriela Marranzino, Susana Alvarez, and Julio Villena* Laboratory of Immunobiotechnology, Reference Centre for Lactobacilli (CERELA-CONICET), Tucuman, Argentina. * Corresponding author: Julio Villena. Address: Chacabuco 145. 4000 San Miguel de Tucumán, Tucumán, Argentina. Tel: 54-381-4311720; Fax: 54-381- 4005600. E-mail address: jcvillena@cerela.org.ar The respiratory inflammatory response triggered by the activation of Toll-like receptor (TLR)-3 in malnourished mice was evaluated. Weaned BALB/c mice were malnourished with a protein-free diet for 21 days (M mice). Aged-matched well-nourished mice consumed a balanced conventional diet for 21 days and were used as controls (W mice). To mimic the pro-inflammatory and physiopathological consequences of RNA viral infections in the lung, the administration of the artificial viral pathogen-associated molecular pattern poly(I:C) (pIC) was used. M and W mice were nasally challenged with 250 μg of pIC. Mice received three doses of pIC with 24 hours rest period between each administration. Lung tissue damage and respiratory and systemic immune responses were studied at several time points (12, 24 and 48 h) after the last administration of pIC. TLR3 activation induced a marked impairment of lung function that was accompanied by the production of pro-inflammatory mediators and inflammatory cell recruitment into the airways in both M and W mice. However, lung tissue injury was significantly higher in M than in W mice. Significantly increased levels of albumin concentrations as well as LDH activity were found in broncho-alveolar (BAL) samples of M mice (p