Respiratory Commensal Bacteria Corynebacterium pseudodiphtheriticum Improves Resistance of Infant Mice to Respiratory Syncytial Virus and Streptococcus pneumoniae Superinfection

Kanmani, Paulraj; Clua, Patricia; Vizoso-Pinto, María Guadalupe; Rodríguez, Cecilia; Alvarez, Susana; Mel'nikov, V. G.; Takahashi, Hideki; Kitazawa, Haruki; Villena, Julio

doi:10.3389/fmicb.2017.01613

Cited by 103 publications

(128 citation statements)

References 40 publications

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“…In addition, viable Corynebacterium pseudodiphtheriticum significantly reduced S. pneumoniae cell counts in lungs and prevented its dissemination into the blood stream 101 . A similar protective effect against RSV‐pneumococcal superinfection, mediated by TLR‐3 activation, was observed in infant mice with the intranasal administration of viable, but also nonviable Lactobacillus rhamnosus or its purified peptidoglycan 101 . In addition, treatment of mice with anti‐IFN‐γ or anti‐IL‐10 monoclonal antibodies diminished their capacity to reduce lung bacterial cell counts and lung tissue injuries 102 .…”

Section: Airway Microbiomementioning

confidence: 98%

“…Conversely, changes in microbial community composition constitute a heightened element of risk towards viral respiratory infections and bacterial superinfections (Figure 4). 101,102 …”

Section: Airway Microbiomementioning

confidence: 99%

“…The airway microbiome comprises an abundance of bacterial species that, through the interplay among them and with local epithelial and immune cells, form a unique microecological system that provides a shield against respiratory infections [98][99][100]. Conversely, changes in microbial community composition constitute a heightened element of risk towards viral respiratory infections and bacterial superinfections (Figure 4) 101. Microbiome as a shield against respiratory infectionsCommensal bacteria may exert health benefits by directly blocking adhesion sites and indirectly countering bacterial or viral pathogens.In infant mice, nasal priming with viable Corynebacterium pseudodiphtheriticum, a commensal taxon, improved the resistance to primary RSV infection and to secondary pneumococcal pneumonia, by modulating the innate immune response through TLR-3 activation 101.…”

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confidence: 99%

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Viral strategies predisposing to respiratory bacterial superinfections

Rossi

Fanous

Colin

2020

Pediatric Pulmonology

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Acute respiratory infections are amongst the leading causes of childhood morbidity and mortality globally. Viruses are the predominant cause of such infections, but mixed etiologies with bacteria has for decades raised the question of the interplay between them in causality and determination of the outcome of such infections. In this review, we examine recent microbiological, biochemical, and immunological advances that contribute to elucidating the mechanisms by which infections by specific viruses enable bacterial infections in the airway, and exacerbate them. We analyze specific domains in which viruses play such facilitating role including enhancement of bacterial adhesion by unmasking cryptic receptors and upregulation of adhesion proteins, disruption of tight junction integrity favoring paracellular transmigration of bacteria and loss of epithelial barrier integrity, increased availability of nutrient, such as mucins and iron, alteration of innate and adaptive immune responses, and disabling defense against bacteria, and lastly, changes in airway microbiome that render the lung more vulnerable to pathogens. Separate exhaustive analysis of each domain focuses on individuals with cystic fibrosis (CF), in whom viruses may play a key role in paving the way for the primary injury that leads to permanence of bacterial pathogens, viruses may then serve as triggers for “CF exacerbations”; these constituting the signature and ultimately the outcome determinants of these patients.

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Section: Airway Microbiomementioning

confidence: 98%

“…Conversely, changes in microbial community composition constitute a heightened element of risk towards viral respiratory infections and bacterial superinfections (Figure 4). 101,102 …”

Section: Airway Microbiomementioning

confidence: 99%

mentioning

confidence: 99%

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Viral strategies predisposing to respiratory bacterial superinfections

Rossi

Fanous

Colin

2020

Pediatric Pulmonology

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“…35,36 Furthermore, nasal application of Coryne bacterium spp induced resistance against respiratory syncytial virus and secondary pneumococcal pneumonia in infant mice. 37 These findings emphasise the need for future research efforts to assess the combined effects of these commensal bacteria in modulation of the respiratory ecosystem, especially the containment of potential pathogens such as respiratory syncytial virus, Haemophilus spp, and Streptococcus spp, and of host immune responses underlying respiratory symptoms.…”

Section: (N=108) D (N=171) E (N=100) F (N=78)mentioning

confidence: 98%

Bacterial and viral respiratory tract microbiota and host characteristics in children with lower respiratory tract infections: a matched case-control study

Man

Houten

Mérelle

et al. 2019

The Lancet Respiratory Medicine

160

169

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Background Lower respiratory tract infections (LRTIs) are a leading cause of childhood morbidity and mortality. Potentially pathogenic organisms are present in the respiratory tract in both symptomatic and asymptomatic children, but their presence does not necessarily indicate disease. We aimed to assess the concordance between upper and lower respiratory tract microbiota during LRTIs and the use of nasopharyngeal microbiota to discriminate LRTIs from health.Methods First, we did a prospective study of children aged between 4 weeks and 5 years who were admitted to the paediatric intensive care unit (PICU) at Wilhelmina Children's Hospital (Utrecht, Netherlands) for a WHO-defined LRTI requiring mechanical ventilation. We obtained paired nasopharyngeal swabs and deep endotracheal aspirates from these participants (the so-called PICU cohort) between Sept 10, 2013, and Sept 4, 2016. We also did a matched case-control study (1:2) with the same inclusion criteria in children with LRTIs at three Dutch teaching hospitals and in age-matched, sex-matched, and time-matched healthy children recruited from the community. Nasopharyngeal samples were obtained at admission for cases and during home visits for controls. Data for child characteristics were obtained by questionnaires and from pharmacy printouts and medical charts. We used quantitative PCR and 16S rRNA-based sequencing to establish viral and bacterial microbiota profiles, respectively. We did sparse random forest classifier analyses on the bacterial data, viral data, metadata, and the combination of all three datasets to distinguish cases from controls.Findings 29 patients were enrolled in the PICU cohort. Intra-individual concordance in terms of viral microbiota profiles (96% agreement [95% CI 93-99]) and bacterial microbiota profiles (58 taxa with a median Pearson's r 0·93 [IQR 0·62-0·99]; p<0·05 for all 58 taxa) was high between nasopharyngeal and endotracheal aspirate samples, supporting the use of nasopharyngeal samples as proxy for lung microbiota during LRTIs. 154 cases and 307 matched controls were prospectively recruited to our case-control cohort. Individually, bacterial microbiota (area under the curve 0·77), viral microbiota (0·70), and child characteristics (0·80) poorly distinguished health from disease. However, a classification model based on combined bacterial and viral microbiota plus child characteristics distinguished children with LRTIs from their matched controls with a high degree of accuracy (area under the curve 0·92).Interpretation Our data suggest that the nasopharyngeal microbiota can serve as a valid proxy for lower respiratory tract microbiota in childhood LRTIs, that clinical LRTIs in children result from the interplay between microbiota and host characteristics, rather than a single microorganism, and that microbiota-based diagnostics could improve future diagnostic and treatment protocols.

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“…Another study suggested that this was due to a priming effect, showing that nonviable L. rhamnosus or the bacterial cell wall component peptidoglycan can enhance inflammatory responses in a TLR3-dependent manner (240). In a similar manner, TLR3-dependent priming with the upper respiratory tract-resident species Corynebacterium pseudodiphtheriticum also improved the outcome of RSV and secondary S. pneumoniae infection (241). While these studies emphasized the effect of priming on pulmonary resistance to subsequent infection, it is plausible that these microbiota also influence host tolerance mechanisms.…”

Section: Lung Microbiome In Host Tolerancementioning

confidence: 98%

Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System

et al. 2018

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Much research on infectious diseases focuses on clearing the pathogen through the use of antimicrobial drugs, the immune response, or a combination of both. Rapid clearance of pathogens allows for a quick return to a healthy state and increased survival. Pathogen-targeted approaches to combating infection have inherent limitations, including their pathogen-specific nature, the potential for antimicrobial resistance, and poor vaccine efficacy, among others. Another way to survive an infection is to tolerate the alterations to homeostasis that occur during a disease state through a process called host tolerance or resilience, which is independent from pathogen burden. Alterations in homeostasis during infection are numerous and include tissue damage, increased inflammation, metabolic changes, temperature changes, and changes in respiration. Given its importance and sensitivity, the lung is a good system for understanding host tolerance to infectious disease. Pneumonia is the leading cause of death for children under five worldwide. One reason for this is because when the pulmonary system is altered dramatically it greatly impacts the overall health and survival of a patient. Targeting host pathways involved in maintenance of pulmonary host tolerance during infection could provide an alternative therapeutic avenue that may be broadly applicable across a variety of pathologies. In this review, we will summarize recent findings on tolerance to host lung infection. We will focus on the involvement of innate immune responses in tolerance and how an initial viral lung infection may alter tolerance mechanisms in leukocytic, epithelial, and endothelial compartments to a subsequent bacterial infection. By understanding tolerance mechanisms in the lung we can better address treatment options for deadly pulmonary infections.

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Respiratory Commensal Bacteria Corynebacterium pseudodiphtheriticum Improves Resistance of Infant Mice to Respiratory Syncytial Virus and Streptococcus pneumoniae Superinfection

Cited by 103 publications

References 40 publications

Viral strategies predisposing to respiratory bacterial superinfections

Viral strategies predisposing to respiratory bacterial superinfections

Bacterial and viral respiratory tract microbiota and host characteristics in children with lower respiratory tract infections: a matched case-control study

Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System

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