Artículo

Non-Viable Lactobacillus Casei Beneficially Modulates Poly I:C Immune Response in Co-Cultures of Human Cells

Vintiñi, Elisa Ofelia ; Medina, Marcela Susana Icon

Otros responsables

Fecha

12/2017

Editorial

Shiraz Inst Cancer Res

Revista

Iranian Journal Of Immunology

Título del libro

Nombre del evento

Fecha del evento

Institución organizadora

ISSN

1735-1383

eISSN

1735-367X

ISBN

Idioma

Inglés

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Clasificación temática

Resumen

Background: Polyinosinic:polycytidylic acid (Poly-IC) has been used as a viralstimulus to mimic in vivo and in vitro infection induced by some viruses. Objective: To determine whether non-viable Lactobacillus casei CRL431 (LcM) can modulate the immune response induced by Poly I:C in co-culture models of peripheral blood mononuclear cells (PBMC) and A549 cells. Methods: T and NK cell activation was evaluated by flow cytometry and levels of TNF-α, IFN-γ, IL-10, IL-29, and IL-17 by ELISA. Cells in direct contact with A549 (PBMC-A549) and cells with no contact with it (PBMC//A549) were used for this purpose. PBMCs alone and both co-culture systems were stimulated for 24 h with the following stimuli: LPS (10 µg/ml), LcM (106 UFC/ml), Poly I:C (2 µg/ml), Poly I:C+LcM, and LcM (3 h)+Poly I:C. Moreover, unstimulated cells were used as a control. Results: Poly I:C and LcM (3 h)+Poly I:C in PBMC-A549 showed a significant increase in the percentage of CD8+ expression (p<0.05). All stimuli induced significant activation from T CD4+, CD8+ cells compared with unstimulated PBMCs in both co-culture cells system. However, activation percentages were higher in direct co-culture. Poly I:C induced a higher level of proinflammatoryTNF-α and IFN-γ cytokines as well as IL-17 and IL-29 with lower IL-10levels in both co-culture systems while LcM induced a beneficial pattern of cytokines that would regulate Poly I:C effect. Conclusion: This in vitro model allowed us to highlight the potential of LcM as a modulator of anti-viral immune response and suggest its potential use in formulations against RNA respiratory viruses.

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