Cargando…

Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2

Individuals with chronic obstructive pulmonary disease (COPD) are more susceptible to exacerbation crisis triggered by secondary lung infections due to the dysfunction of antiviral signaling, principally via suppression of IFN-γ. Although the probiotic is known for controlling pulmonary inflammation...

Descripción completa

Detalles Bibliográficos
Autores principales: Olímpio, Fabiana, Andreata-Santos, Robert, Rosa, Paloma Cristina, Santos, Wellington, Oliveira, Carlos, Aimbire, Flavio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9643982/
https://www.ncbi.nlm.nih.gov/pubmed/36346611
http://dx.doi.org/10.1007/s12602-022-09998-2
_version_ 1784826645198143488
author Olímpio, Fabiana
Andreata-Santos, Robert
Rosa, Paloma Cristina
Santos, Wellington
Oliveira, Carlos
Aimbire, Flavio
author_facet Olímpio, Fabiana
Andreata-Santos, Robert
Rosa, Paloma Cristina
Santos, Wellington
Oliveira, Carlos
Aimbire, Flavio
author_sort Olímpio, Fabiana
collection PubMed
description Individuals with chronic obstructive pulmonary disease (COPD) are more susceptible to exacerbation crisis triggered by secondary lung infections due to the dysfunction of antiviral signaling, principally via suppression of IFN-γ. Although the probiotic is known for controlling pulmonary inflammation in COPD, the influence of the Lactobacillus rhamnosus (Lr) on antiviral signaling in bronchial epithelium exposed to cigarette smoke extract (CSE) and viruses, remains unknown. Thus, the present study investigated the Lr effect on the antiviral signaling and the secretion of inflammatory mediators from bronchial epithelial cells (16HBE cells) exposed to CSE and SARS-CoV-2. The 16HBE cells were cultured, treated with Lr, stimulated with CSE, and infected with SARS-CoV-2. The cellular viability was evaluated using the MTT assay and cytotoxicity measured by lactate dehydrogenase (LDH) activity. The viral load, TLR2, TLR3, TLR4, TLR7, TLR8, MAVS, MyD88, and TRIF were quantified using specific PCR. The pro-inflammatory mediators were measured by a multiplex biometric immunoassay, and angiotensin converting enzyme 2 (ACE2) activity, NF-κB, RIG-I, MAD5, and IRF3 were measured using specific ELISA kits. Lr decreased viral load, ACE2, pro-inflammatory mediators, TLR2, TLR4, NF-κB, TLR3, TLR7, and TLR8 as well as TRIF and MyD88 expression in CSE and SARS-CoV-2 -exposed 16HBE cells. Otherwise, RIG-I, MAD5, IRF3, IFN-γ, and the MAVS expression were restored in 16HBE cells exposed to CSE and SARS-CoV-2 and treated with Lr. Lr induces antiviral signaling associated to IFN-γ secreting viral sensors and attenuates cytokine storm associated to NF-κB in bronchial epithelial cells, supporting its emerging role in prevention of COPD exacerbation.
format Online
Article
Text
id pubmed-9643982
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Springer US
record_format MEDLINE/PubMed
spelling pubmed-96439822022-11-14 Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2 Olímpio, Fabiana Andreata-Santos, Robert Rosa, Paloma Cristina Santos, Wellington Oliveira, Carlos Aimbire, Flavio Probiotics Antimicrob Proteins Article Individuals with chronic obstructive pulmonary disease (COPD) are more susceptible to exacerbation crisis triggered by secondary lung infections due to the dysfunction of antiviral signaling, principally via suppression of IFN-γ. Although the probiotic is known for controlling pulmonary inflammation in COPD, the influence of the Lactobacillus rhamnosus (Lr) on antiviral signaling in bronchial epithelium exposed to cigarette smoke extract (CSE) and viruses, remains unknown. Thus, the present study investigated the Lr effect on the antiviral signaling and the secretion of inflammatory mediators from bronchial epithelial cells (16HBE cells) exposed to CSE and SARS-CoV-2. The 16HBE cells were cultured, treated with Lr, stimulated with CSE, and infected with SARS-CoV-2. The cellular viability was evaluated using the MTT assay and cytotoxicity measured by lactate dehydrogenase (LDH) activity. The viral load, TLR2, TLR3, TLR4, TLR7, TLR8, MAVS, MyD88, and TRIF were quantified using specific PCR. The pro-inflammatory mediators were measured by a multiplex biometric immunoassay, and angiotensin converting enzyme 2 (ACE2) activity, NF-κB, RIG-I, MAD5, and IRF3 were measured using specific ELISA kits. Lr decreased viral load, ACE2, pro-inflammatory mediators, TLR2, TLR4, NF-κB, TLR3, TLR7, and TLR8 as well as TRIF and MyD88 expression in CSE and SARS-CoV-2 -exposed 16HBE cells. Otherwise, RIG-I, MAD5, IRF3, IFN-γ, and the MAVS expression were restored in 16HBE cells exposed to CSE and SARS-CoV-2 and treated with Lr. Lr induces antiviral signaling associated to IFN-γ secreting viral sensors and attenuates cytokine storm associated to NF-κB in bronchial epithelial cells, supporting its emerging role in prevention of COPD exacerbation. Springer US 2022-11-08 /pmc/articles/PMC9643982/ /pubmed/36346611 http://dx.doi.org/10.1007/s12602-022-09998-2 Text en © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Article
Olímpio, Fabiana
Andreata-Santos, Robert
Rosa, Paloma Cristina
Santos, Wellington
Oliveira, Carlos
Aimbire, Flavio
Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2
title Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2
title_full Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2
title_fullStr Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2
title_full_unstemmed Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2
title_short Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2
title_sort lactobacillus rhamnosus restores antiviral signaling and attenuates cytokines secretion from human bronchial epithelial cells exposed to cigarette smoke and infected with sars-cov-2
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9643982/
https://www.ncbi.nlm.nih.gov/pubmed/36346611
http://dx.doi.org/10.1007/s12602-022-09998-2
work_keys_str_mv AT olimpiofabiana lactobacillusrhamnosusrestoresantiviralsignalingandattenuatescytokinessecretionfromhumanbronchialepithelialcellsexposedtocigarettesmokeandinfectedwithsarscov2
AT andreatasantosrobert lactobacillusrhamnosusrestoresantiviralsignalingandattenuatescytokinessecretionfromhumanbronchialepithelialcellsexposedtocigarettesmokeandinfectedwithsarscov2
AT rosapalomacristina lactobacillusrhamnosusrestoresantiviralsignalingandattenuatescytokinessecretionfromhumanbronchialepithelialcellsexposedtocigarettesmokeandinfectedwithsarscov2
AT santoswellington lactobacillusrhamnosusrestoresantiviralsignalingandattenuatescytokinessecretionfromhumanbronchialepithelialcellsexposedtocigarettesmokeandinfectedwithsarscov2
AT oliveiracarlos lactobacillusrhamnosusrestoresantiviralsignalingandattenuatescytokinessecretionfromhumanbronchialepithelialcellsexposedtocigarettesmokeandinfectedwithsarscov2
AT aimbireflavio lactobacillusrhamnosusrestoresantiviralsignalingandattenuatescytokinessecretionfromhumanbronchialepithelialcellsexposedtocigarettesmokeandinfectedwithsarscov2