Nasal priming with immunobiotic Lactobacillus rhamnosus modulates inflammation-coagulation interactions and reduces influenza virus-associated pulmonary damage

ZELAYA H; TADA, A; VIZOSO-PINTO, MG; SALVA, S; ALVAREZ, S; KITAZAWA, H; AGÜERO, G; VILLENA, J

Mar del Plata, Buenos Aires (Argentina)

Congreso; LIX Reunión científica anual de la Sociedad Argentina de Investigación Clínica y LXII Reunión anual Sociedad Argentina de Inmunología; 2014

Sociedad Argentina de Investigación Clínica y Sociedad Argentina de Inmunología

Nasal priming with immunobiotic Lactobacillus rhamnosus modulates inflammation-coagulation interactions and reduces influenza virus-associated pulmonary damage Hortensia Zelaya1,4, Asuka Tada2, María Guadalupe Vizoso-Pinto3,4, Susana Salva1, Susana Alvarez1,4, Haruki Kitazawa2, Graciela Agüero4 and Julio Villena1,2 * 1CERELA-CONICET, Argentina, 2Food Immunology Group, Japan, 3INSIBIO-CONICET, Argentina, 4UNT, Argentina * Corresponding author. Mailing address for Julio Villena: Laboratory of Immunobiotechnology, Reference Centre for Lactobacilli (CERELA-CONICET). Tucuman, Argentina. Phone: +54-381-4310465. Fax: +54-381-4005600. E-mail address: jcvillena@cerela.org.ar Five to fifteen percent of global population is affected by seasonal influenza yearly. Thus, influenza represents a major public health problem. Symptoms are variable ranging from mild respiratory distress to massive organ failure resulting in death. Seasonal influenza is usually self-limiting but in susceptible patients it may progress to acute lung injury, which is characterized by augmented pulmonary microvascular permeability leading to pulmonary edema, hypoxemia and respiratory failure. Available drugs are of limited efficacy in this setting, therefore, the development of novel therapeutic or preventive alternatives are a milestone in influenza research. We examined the effect of nasal administration of live and heat-killed (HK) Lactobacillus rhamnosus 1505 (Lr1505) on influenza infection and found that both treatments were able to protect mice challenged with influenza virus (IFV). Furthermore, we unraveled several mechanisms by which this immunobiotic strain protected infected mice by reducing pulmonary injury and lung viral loads: a) inflammatory cytokines were down-regulated diminishing inflammation (p