Orally administered Lactobacillus rhamnosus modulates the respiratory immune response triggered by the viral pathogen-associated molecular pattern poly(I:C)

VILLENA JULIO; ERIKO CHIBA; YOHSUKE TOMOSADA; SUSANA SALVA; MARRANZINO GABRIELA; HARUKI KITAZAWA; ALVAREZ SUSANA

Kuala Lumpur

Congreso; 4th International Conference on Biotechnology for the Wellness Industry; 2012

Orally administered Lactobacillus rhamnosus CRL1505 (Lr05) is able to improve respiratory immunity and protect against pneumococcal challenge. In this study we evaluated whether Lr05 treatment is able to beneficially modulate respiratory immune response triggered by the viral pathogen-associated molecular pattern poly(I:C), considering that this synthetic double-stranded RNA analog induces similar pulmonary dysfunction to respiratory syncytial virus in BALB/c mice. Mice were orally treated with Lr05 (108 cells/mouse/day) during 5 consecutive days. After treatment, mice were intranasally administered three daily doses of poly(I:C) (250 μg/mouse). Mice with no Lr05 treatment were used as controls. Poly(I:C) administration resulted in an inflammatory cell influx into the lung with increases in both neutrophils and mononuclear cells in controls. We also observed increased levels of TNF-α, IFN-α, IFN-β, IFN-γ, IL-6, IL-8, IL-12 and MCP-1 in serum and broncho-alveolar lavage fluid (BAL) in challenged mice. Moreover, poly(I:C) administration increased albumin content and lactate dehydrogenase (LDH) activity in BAL and altered lung wet:dry weight ratio, indicating that long-term activation of TLR3 resulted in an increased permeability of the bronchoalveolar-capillarity barrier and lung injury. Administration of Lr05 before poly(I:C) challenge induced an improved production of IFN-γ, IFN-β and IL-6 together with a reduction of TNF-α and IL-8 in BAL. In addition, IL-10 was significantly higher in BAL of Lr05 treated mice when compared with controls (p<0.05). These changes in the respiratory cytokines induced an improved recruitment of immune cells into the lung during the first 12 hours after the challenge and lower levels of inflammatory cells at hour 24. Moreover, Lr05 treated mice showed lower lung injuries. Our results show that orally administered Lr05 is able to beneficially modulate inflammatory response triggered by TLR3/RIG-I activation in the respiratory tract