tetano
Editor, Senior Moderator
Int Immunopharmacol. 2014 Jan 3. pii: S1567-5769(13)00509-2. doi: 10.1016/j.intimp.2013.12.020. [Epub ahead of print]
Immunobiotic lactobacilli reduce viral-associated pulmonary damage through the modulation of inflammation-coagulation interactions.
Zelaya H1, Tsukida K2, Chiba E2, Marranzino G3, Alvarez S1, Kitazawa H2, Ag?ero G4, Villena J5.
Author information
Abstract
The exacerbated disease due to immune- and coagulative-mediated pulmonary injury during acute respiratory viruses infection results in severe morbidity and mortality. Identifying novel approaches to modulate virus-induced inflammation-coagulation interactions could be important alternatives for treating acute respiratory viruses infections. In this study we investigated the effect of the probiotic strain Lactobacillus rhamnosus CRL1505 on lung TLR3-mediated inflammation, and its ability to modulate inflammation-coagulation interaction during respiratory viral infection. Our findings reveal for the first time that a probiotic bacterium is able to influence lung immune-coagulative reaction triggered by TLR3 activation, by modulating the production of proinflammatory and anti-inflammatory cytokines as well as expression of tissue factor and thrombomodulin in the lung. We also demonstrated that the preventive treatment with the probiotic bacteria beneficially modulates the fine tune balance between clearing respiratory viruses (respiratory syncytial virus and influenza virus) and controlling immune-coagulative responses in the lung, allowing normal lung function to be maintained in the face of a viral attack. Our data also pinpoint a crucial role for IL-10 in the immune protection induced by L. rhamnosus CRL1505 during respiratory viral infections. These observations might be helpful to propose new preventive or therapeutic approaches to better control virus-inflammatory lung damage using probiotic functional foods.
Copyright ? 2013. Published by Elsevier B.V.
KEYWORDS:
APTT, BAL, DAB, DMEM, Dulbecco's modified Eagle's medium, ELISA, FBS, IFV, IL, IL-10, Inflammation?Coagulation, Influenza virus, LAB, LDH, Lactobacillus rhamnosus CRL1505, Lactobacillus rhamnosus CRL1506, Lr1505, Lr1506, MDCK, MIP, MOI, MPO, MRS, Madin?Darby canine kidney, Man?Rogosa?Sharpe, NAD, OD, PAI, PBS, PFU, PRRs, PT, Pen/Strep, Poly(I:C), RIG-I, RSV, Respiratory syncytial virus, TATc, TF, TFPI, TGF, TLR, TLR3, TM, TNF, Toll-like receptor, VCAM-1, activated partial thromboplastin time, bronchoalveolar lavage, diaminobenzidine, double-stranded RNA, dsRNA, enzyme-linked immunosorbent assay, fetal bovine serum, influenza virus, interleukin, lactate dehydrogenase, lactic acid bacteria, macrophage inflammatory protein, multiplicity of infection, myeloperoxidase, nicotinamide adenine dinucleotide, optical density, pattern-recognition receptors, penicillin?streptomycin, phosphate buffer saline, plaque-forming unit, plasminogen activator inhibitor, polyinosinic
olycytidylic acid, prothrombin time, respiratory syncytial virus, retinoic acid-inducible gene I, thrombin?antithrombin complexes, thrombomodulin, tissue factor, tissue factor pathway inhibitor, transforming growth factor, tumor necrosis factor, vWF, vascular cell adhesion molecule 1, von Willebrand factor
PMID:
24394565
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24394565
Immunobiotic lactobacilli reduce viral-associated pulmonary damage through the modulation of inflammation-coagulation interactions.
Zelaya H1, Tsukida K2, Chiba E2, Marranzino G3, Alvarez S1, Kitazawa H2, Ag?ero G4, Villena J5.
Author information
Abstract
The exacerbated disease due to immune- and coagulative-mediated pulmonary injury during acute respiratory viruses infection results in severe morbidity and mortality. Identifying novel approaches to modulate virus-induced inflammation-coagulation interactions could be important alternatives for treating acute respiratory viruses infections. In this study we investigated the effect of the probiotic strain Lactobacillus rhamnosus CRL1505 on lung TLR3-mediated inflammation, and its ability to modulate inflammation-coagulation interaction during respiratory viral infection. Our findings reveal for the first time that a probiotic bacterium is able to influence lung immune-coagulative reaction triggered by TLR3 activation, by modulating the production of proinflammatory and anti-inflammatory cytokines as well as expression of tissue factor and thrombomodulin in the lung. We also demonstrated that the preventive treatment with the probiotic bacteria beneficially modulates the fine tune balance between clearing respiratory viruses (respiratory syncytial virus and influenza virus) and controlling immune-coagulative responses in the lung, allowing normal lung function to be maintained in the face of a viral attack. Our data also pinpoint a crucial role for IL-10 in the immune protection induced by L. rhamnosus CRL1505 during respiratory viral infections. These observations might be helpful to propose new preventive or therapeutic approaches to better control virus-inflammatory lung damage using probiotic functional foods.
Copyright ? 2013. Published by Elsevier B.V.
KEYWORDS:
APTT, BAL, DAB, DMEM, Dulbecco's modified Eagle's medium, ELISA, FBS, IFV, IL, IL-10, Inflammation?Coagulation, Influenza virus, LAB, LDH, Lactobacillus rhamnosus CRL1505, Lactobacillus rhamnosus CRL1506, Lr1505, Lr1506, MDCK, MIP, MOI, MPO, MRS, Madin?Darby canine kidney, Man?Rogosa?Sharpe, NAD, OD, PAI, PBS, PFU, PRRs, PT, Pen/Strep, Poly(I:C), RIG-I, RSV, Respiratory syncytial virus, TATc, TF, TFPI, TGF, TLR, TLR3, TM, TNF, Toll-like receptor, VCAM-1, activated partial thromboplastin time, bronchoalveolar lavage, diaminobenzidine, double-stranded RNA, dsRNA, enzyme-linked immunosorbent assay, fetal bovine serum, influenza virus, interleukin, lactate dehydrogenase, lactic acid bacteria, macrophage inflammatory protein, multiplicity of infection, myeloperoxidase, nicotinamide adenine dinucleotide, optical density, pattern-recognition receptors, penicillin?streptomycin, phosphate buffer saline, plaque-forming unit, plasminogen activator inhibitor, polyinosinic
olycytidylic acid, prothrombin time, respiratory syncytial virus, retinoic acid-inducible gene I, thrombin?antithrombin complexes, thrombomodulin, tissue factor, tissue factor pathway inhibitor, transforming growth factor, tumor necrosis factor, vWF, vascular cell adhesion molecule 1, von Willebrand factorPMID:
24394565
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24394565