scholarly journals Immunobiotic Lactobacilli Improve Resistance of Respiratory Epithelial Cells to SARS-CoV-2 Infection

Pathogens ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1197
Author(s):  
Md. Aminul Islam ◽  
Leonardo Albarracin ◽  
Mikado Tomokiyo ◽  
Juan Carlos Valdez ◽  
Jacinto Sacur ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Poly I:C ◽  
Respiratory Pathogens ◽  
Respiratory Epithelial Cells ◽  
Beneficial Effects ◽  
In Vivo Experiments ◽  
Syncytial Virus ◽  
Respiratory Epithelial

Previously, we reported that immunomodulatory lactobacilli, nasally administered, beneficially regulated the lung antiviral innate immune response induced by Toll-like receptor 3 (TLR3) activation and improved protection against the respiratory pathogens, influenza virus and respiratory syncytial virus in mice. Here, we assessed the immunomodulatory effects of viable and non-viable Lactiplantibacillus plantarum strains in human respiratory epithelial cells (Calu-3 cells) and the capacity of these immunobiotic lactobacilli to reduce their susceptibility to the acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Immunobiotic L. plantarum MPL16 and CRL1506 differentially modulated IFN-β, IL-6, CXCL8, CCL5 and CXCL10 production and IFNAR2, DDX58, Mx1 and OAS1 expression in Calu-3 cells stimulated with the TLR3 agonist poly(I:C). Furthermore, the MPL16 and CRL1506 strains increased the resistance of Calu-3 cells to the challenge with SARS-CoV-2. L. plantarum MPL16 induced these beneficial effects more efficiently than the CRL1506 strain. Of note, neither non-viable MPL16 and CRL1506 strains nor the non-immunomodulatory strains L. plantarum CRL1905 and MPL18 could modify the resistance of Calu-3 cells to SARS-CoV-2 infection or the immune response to poly(I:C) challenge. To date, the potential beneficial effects of immunomodulatory probiotics on SARS-CoV-2 infection and COVID-19 outcome have been extrapolated from studies carried out in the context of other viral pathogens. To the best of our knowledge, this is the first demonstration of the ability of immunomodulatory lactobacilli to positively influence the replication of the new coronavirus. Further mechanistic studies and in vivo experiments in animal models of SARS-CoV-2 infection are necessary to identify specific strains of beneficial immunobiotic lactobacilli like L. plantarum MPL16 or CRL1506 for the prevention or treatment of the COVID-19.

scholarly journals Dolosigranulum pigrum Modulates Immunity against SARS-CoV-2 in Respiratory Epithelial Cells

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 634
Author(s):  
Md. Aminul Islam ◽  
Leonardo Albarracin ◽  
Vyacheslav Melnikov ◽  
Bruno G. N. Andrade ◽  
Rafael R. C. Cuadrat ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Specific Effect ◽  
Commensal Bacteria ◽  
Cellular Damage ◽  
Poly I:C ◽  
Respiratory Epithelial Cells ◽  
Promising Alternative ◽  
Immunological Mechanisms ◽  
Syncytial Virus ◽  
Respiratory Epithelial

In a previous work, we demonstrated that nasally administered Dolosigranulum pigrum 040417 beneficially modulated the respiratory innate immune response triggered by the activation of Toll-like receptor 3 (TLR3) and improved protection against Respiratory Syncytial Virus (RSV) in mice. In this work, we aimed to evaluate the immunomodulatory effects of D. pigrum 040417 in human respiratory epithelial cells and the potential ability of this immunobiotic bacterium to increase the protection against Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). The respiratory commensal bacterium D. pigrum 040417 differentially modulated the production of IFN-β, IL-6, CXCL8, CCL5 and CXCL10 in the culture supernatants of Calu-3 cells stimulated with poly(I:C) or challenged with SARS-CoV-2. The differential cytokine profile induced by the 040417 strain was associated with a significant reduction in viral replication and cellular damage after coronavirus infection. Of note, D. pigrum 030918 was not able to modify the resistance of Calu-3 cells to SARS-CoV-2 infection, indicating a strain-specific immunomodulatory effect for respiratory commensal bacteria. The findings of this work improve our understanding of the immunological mechanisms involved in the modulation of respiratory immunity induced by respiratory commensal bacteria, by demonstrating their specific effect on respiratory epithelial cells. In addition, the results suggest that particular strains such as D. pigrum 040417 could be used as a promising alternative for combating SARS-CoV-2 and reducing the severity of COVID-19.

scholarly journals Differential Role of CbpA and PspA in Modulation of In Vitro CXC Chemokine Responses of Respiratory Epithelial Cells to Infection with Streptococcus pneumoniae

2006 ◽  
Vol 74 (12) ◽  
pp. 6739-6749 ◽  
Author(s):  
Rikki M. A. Graham ◽  
James C. Paton
Keyword(s):  
Streptococcus Pneumoniae ◽  
Epithelial Cells ◽  
Deletion Mutant ◽  
Protein A ◽  
A549 Cells ◽  
Respiratory Pathogens ◽  
Respiratory Epithelial Cells ◽  
Cxc Chemokine ◽  
Respiratory Epithelial

ABSTRACTRespiratory epithelial cells play an active part in the host response to respiratory pathogens, such asStreptococcus pneumoniae, by releasing chemokines responsible for neutrophil recruitment. In order to investigate the role of specific pneumococcal virulence factors in eliciting CXC chemokine responses, type II pneumocytes (A549) and nasopharyngeal cells (Detroit-562) were infected withS. pneumoniaeD39 or mutants lacking choline-binding protein A (CbpA), pneumococcal surface protein A (PspA), or specific domains thereof. In response to wild-type D39, both A549 and Detroit-562 cells showed a significant increase in CXC chemokine mRNA and interleukin-8 protein. This response was increased twofold when acbpAdeletion mutant (ΔCbpA) was used, suggesting that CbpA inhibits CXC chemokine induction. All three N-terminal domains of CbpA are required for this effect, as in-frame deletion of the respective region ofcbpAhad the same effect on the CXC chemokine response as deletion ofcbpAaltogether. Infection with apspAdeletion mutant (ΔPspA) led to a twofold decrease in the CXC chemokine response of A549 but not Detroit-562 cells, compared to infection with D39 at 2 h. Thus, PspA appears to have the ability to stimulate early CXC chemokine release from A549 cells. Deletion of the region ofpspAencoding the first N-terminal α-helical domain reduced the ability ofS. pneumoniaeto elicit a chemokine response to the same degree as deletion ofpspAaltogether. Thus, the N termini of CbpA and PspA exert differential effects on CXC chemokine induction in epithelial cells infected withS. pneumoniae.

scholarly journals Pneumococcal Interactions with Epithelial Cells Are Crucial for Optimal Biofilm Formation and ColonizationIn VitroandIn Vivo

2012 ◽  
Vol 80 (8) ◽  
pp. 2744-2760 ◽  
Author(s):  
Laura R. Marks ◽  
G. Iyer Parameswaran ◽  
Anders P. Hakansson
Keyword(s):  
Epithelial Cells ◽  
Biofilm Formation ◽  
Invasive Disease ◽  
Respiratory Epithelial Cells ◽  
Symptomatic Infection ◽  
Content Type ◽  
Abiotic Surfaces ◽  
Horizontal Spread ◽  
Respiratory Epithelial

ABSTRACTThe human nasopharynx is the main reservoir forStreptococcus pneumoniae(the pneumococcus) and the source for both horizontal spread and transition to infection. Some clinical evidence indicates that nasopharyngeal carriage is harder to eradicate with antibiotics than is pneumococcal invasive disease, which may suggest that colonizing pneumococci exist in biofilm communities that are more resistant to antibiotics. While pneumococcal biofilms have been observed during symptomatic infection, their role in colonization and the role of host factors in this process have been less studied. Here, we show for the first time that pneumococci form highly structured biofilm communities during colonization of the murine nasopharynx that display increased antibiotic resistance. Furthermore, pneumococcal biofilms grown on respiratory epithelial cells exhibited phenotypes similar to those observed during colonizationin vivo, whereas abiotic surfaces produced less ordered and more antibiotic-sensitive biofilms. The importance of bacterial-epithelial cell interactions during biofilm formation was shown using both clinical strains with variable colonization efficacies and pneumococcal mutants with impaired colonization characteristicsin vivo. In both cases, the ability of strains to form biofilms on epithelial cells directly correlated with their ability to colonize the nasopharynxin vivo, with colonization-deficient strains forming less structured and more antibiotic-sensitive biofilms on epithelial cells, an association that was lost when grown on abiotic surfaces. Thus, these studies emphasize the importance of host-bacterial interactions in pneumococcal biofilm formation and provide the first experimental data to explain the high resistance of pneumococcal colonization to eradication by antibiotics.

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