AIRWAY EPITHELIUM PARTICIPATION IN THE NEONATAL PREVENTION OF EXPERIMENTAL ASTHMA

GARCÍA, L ; LEIMGRUBER, CAROLINA1; URIBE ECHEVARRÍA; ELISA MARGARITA; ERREA, AGUSTINA; RUMBO, MARTÍN; MALDONADO, CRISTINA ALICIA

Mar del Plata

Congreso; LXII REUNIÓN ANUAL Sociedad Argentina de Inmunología-LIX REUNIÓN CIENTÍFICA ANUAL Sociedad Argentina de Investigación Clínica; 2014

Genetic and clinical data denotes airway epithelium (AE) rolein the onset of the allergic airway inflammation (AAI). Severalstudies proved that microbial stimulus can protect newborn mice(nbm) from the AAI as well as provide a long-term defense fromunrelated injuries in the AE. Our aim was to evaluate the impactof newborn microbial stimulus on epithelium host defense proteins(HDps), as Club cell secretory protein (CCSP), TLR4 andantimicrobial Surfactant D (SP-D) (IHQ/WB), cytokines (ELISA),and its correlation with AAI modulation. Balb/c NBM were exposedto intranasal (i.n.) PBS or LPS (200mg/ml-5μl), 3 times/ week ondays 3-13 after delivery (AD). At 4 and 6 weeks AD, they weresensitized by i.p. 100μl OVA/Alumm (1mg/1mg/ml), and thenassigned into 4 groups (n=10) and challenged for 10 consecutivedays with i.n. OVA (1mg/ml) (LPS/OVA and PBS/OVA groups) orvehicle (LPS and PBS groups). Bronchoalveolar lavage (BAL) andlung tissue were obtained ending the protocols. LPS mice, showedhigher immunoreactivity for CCSP, SP-D and TLR4 in bronchiolarClub cells (CC) vs PBS group; in BAL they exhibited higher levelsof TNFα and IFNγ; significantly TSLP, a Th2 promoter cytokineexpressed by AE, became negative (p