Lactobacillus rhamnosus CRL1505 peptidoglycan modulates the inflammation-coagulation response triggered by poly(I:C)

ZELAYA, HORTENSIA; TADA, ASUKA; CLUA, PATRICIA; MARRANZINO, GABRIELA; SALVA, SUSANA; ALVAREZ, SUSANA; KITASAWA, HARUKI; AGÜERO, GRACIELA; VILLENA, JULIO

Buenos Aires

Congreso; IV LASID Meeting-LXIII Argentinean Society for Immunology Meeting-II French-Argentinean Immunology Meeting; 2015

Sociedad Argentina de Inmunología

Background: Lactobacillus rhamnosus CRL1505 beneficially modulates inflammation-coagulation response during respiratoty viral infections. This study evaluated the capacity of peptidoglycan obtaines from the CRL1505 strain (Pg1505) to modulate the immuno-goagulative response triggered by the viral pathogen associated molecular pattern poly(I:C).Methods: adult BALB/c mice were nasally treated with Pg1505 for 2 days. Treated and untreated control mice were them nasally challenged with poly(I:C). Mice received three of doses of poly(I:C) with 24 hours rest period between each administration. The immune-coagulative response was studied after the last administration of poly(I:C).Results: ply(I:C) challenge significantly increased blood and respiratory proinflammatory mediators, decreased prothombin activity (PT) and increased von Willebrand Factor (vWF) levels in plasma. Furthermore, tissue factor (TF) expression was elevated in lungs. These changes induced a significant damage in lung tissue. Pg1505-treated mice showed significantly reduced level of PT and lung TNF-alpha, vWF and TF while the levels of IL-10 and thrombomodulin were higher than control mice. Those changes induced by Pg1505 correlated with a significant reduction of lung tissue damage. In vivo and complementary in vitri studies with RAW cells indicated that macrophages would be a key population for the protective effect of Pg1505, since reduced production of inflammatory mediators as well as TF were found in Pg1505-treated macrophages after poly(I:C) challenge.Conclusions: peptidoglycan from L. rhamnosus CRL1505 is able to beneficially modulate the immuno-coagulative response in the respiratory tract after TLR3 activation through its capacity to regulate respiratory macrophages production of inflammatory and procoagulant mediators.