LTC4 MODULATES AN INFLAMMATORY RESPONSE AT THE GUT LEVEL VIA THE ACTIVATION OF CYSTEINYL LEUKOTRIENE RECEPTOR 1

SOLEDAD GORI; GABRIELA MORA; GABRIELA SALAMONE; MÓNICA VERMEULEN; JULIETA ALCAIN; SILVIA VANZULLI

Mar del Plata

Congreso; LXIV REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INMUNOLOGÍA (SAI); 2016

SAI

Leukotriene C4 (LTC4) is an important lipid mediator involvedin the genesis of chronic inflammatory responses. Its effects aremediated through the cysteinyl receptor 1 and 2 (CysLTR1/2). Inprevious works, it has been demonstrated that LTC4 is able tomodulate chemotaxis of dendritic cells (DC) and their activationstate, with the ability to interfere with their maturation. Here, westudied the capacity of LTC4 to break the gut tolerance. For this,BALB/c mice were orally inoculated with a single dose of PBS(Ct) or LTC4 (0.01 µM in 100µl of PBS) at the beginning of Ovalbumintolerance (100 mg/day in drinking water for 5 days). After12 days, histological examination of small intestine showed thatthe intestine was extensively modified by the exposure to LTC4,mainly evidenced through the shortening of villi, increased protrusionof goblet cells and edema in the lamina propria, together witha marked recruitment of leukocytes, mainly eosinophilic-granulocytes.Then, we decided to evaluate the populations recruited inmesenteric lymph node after treatment. In the first place, LTC4inhibited the CD11c+ CD103+ dendritic cells (DC), the main populationassociated to mucosal tolerance (mean% CD11c+CD103+ DC ±SEM: PBS 2.1 ± 0.25, LTC4 0.92 ± 0.1, p≤0.05, n = 4). Also, weobserved a greater expression of CysLTR1compared to CysLTR2(mean band ratio/b-actin; CysLTR1 vs CysLTR2: 1.2 ± 0.08; 0.4± 0.03; * p