Nasal priming with immunobiotic Lactobacillus rhamnosus modulates inflammation–coagulation interactions and reduces influenza virus-associated pulmonary damage

Zelaya, Hortensia; Tada, Asuka; Vizoso-Pinto, María Guadalupe; Salva, Susana; Kanmani, Paulraj; Agüero, Graciela; Alvarez, Susana; Kitazawa, Haruki; Villena, Julio

doi:10.1007/s00011-015-0837-6

Cited by 63 publications

(69 citation statements)

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“…Later, proinflammatory cytokines and infiltrated cells started to decrease in immunobiotic-treated animals in contrast to control mice, in which those parameters continued increasing. The trend toward lower inflammatory factors and cells registered later during IFV infection in L. rhamnosus CRL1505-treated mice correlated with a reduced severity of pulmonary damage when compared to control mice (41, 42). …”

Section: Beneficial Effects Of Immunobiotics On Ifv Infectionmentioning

confidence: 80%

“…Thus, the proper balance of cytokines is a key factor in determining the outcome of IFV infection. In this regard, we observed that orally (41) or nasally (42) administered immunobiotic L. rhamnosus CRL1505 differentially regulated the levels and kinetics of inflammatory cells and cytokines in mice after IFV challenge. In our experimental model, we observed increased levels of respiratory TNF-α, IL-6, neutrophils, and macrophages in CRL1505-treated mice early after the challenge with IFV.…”

Section: Beneficial Effects Of Immunobiotics On Ifv Infectionmentioning

confidence: 97%

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Respiratory Antiviral Immunity and Immunobiotics: Beneficial Effects on Inflammation-Coagulation Interaction during Influenza Virus Infection

et al. 2016

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Influenza virus (IFV) is a major respiratory pathogen of global importance, and the cause of a high degree of morbidity and mortality, especially in high-risk populations such as infants, elderly, and immunocompromised hosts. Given its high capacity to change antigenically, acquired immunity is often not effective to limit IFV infection and therefore vaccination must be constantly redesigned to achieve effective protection. Improvement of respiratory and systemic innate immune mechanisms has been proposed to reduce the incidence and severity of IFV disease. In the last decade, several research works have demonstrated that microbes with the capacity to modulate the mucosal immune system (immunobiotics) are a potential alternative to beneficially modulate the outcome of IFV infection. This review provides an update of the current status on the modulation of respiratory immunity by orally and nasally administered immunobiotics, and their beneficial impact on IFV clearance and inflammatory-mediated lung tissue damage. In particular, we describe the research of our group that investigated the influence of immunobiotics on inflammation–coagulation interactions during IFV infection. Studies have clearly demonstrated that hostile inflammation is accompanied by dysfunctional coagulation in respiratory IFV disease, and our investigations have proved that some immunobiotic strains are able to reduce viral disease severity through their capacity to modulate the immune-coagulative responses in the respiratory tract.

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Section: Beneficial Effects Of Immunobiotics On Ifv Infectionmentioning

confidence: 80%

Section: Beneficial Effects Of Immunobiotics On Ifv Infectionmentioning

confidence: 97%

Respiratory Antiviral Immunity and Immunobiotics: Beneficial Effects on Inflammation-Coagulation Interaction during Influenza Virus Infection

et al. 2016

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“…An aberrant pro-coagulant response has been previously described to contribute to IAV pathogenesis [15,16]. To determine if an IAV infection in epithelial cells was sufficient to induce a pro-coagulant state in the adjacent endothelial cells, we measured the time to thrombin generation by incubating human plasma with either IAV-or mock-infected co-cultures.…”

Section: Iav Infection Of Epithelial Cells Results In a Pro-coagulantmentioning

confidence: 99%

“…The inflammatory response to IAV may also result in the upregulation of tissue factor, which can be expressed on both endothelial cells and leukocytes. Increased expression of tissue factor on endothelial cells during IAV infection can result in an aberrant pro-coagulant state, leading to the consumption of coagulation factors, microvascular leak and pulmonary haemorrhage [15][16][17]. Furthermore, a pro-coagulant state induces the release of cytokines such as interleukin (IL)-6 and IL-8 [18], which may further enhance the severity of an IAV-induced cytokine storm and any associated barrier damage.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, a pro-coagulant state induces the release of cytokines such as interleukin (IL)-6 and IL-8 [18], which may further enhance the severity of an IAV-induced cytokine storm and any associated barrier damage. Accordingly, a reduction of the pro-coagulant state of IAV-infected mice is associated with reduced lung injury and improved survival rates [15]. Finally, several in vitro studies have suggested that, like epithelial cells, endothelial cells can be infected by IAV [8,[19][20][21][22], resulting in cell apoptosis and degradation of the AJC.…”

Section: Introductionmentioning

confidence: 99%

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Influenza virus damages the alveolar barrier by disrupting epithelial cell tight junctions

Short

Kasper

Aa³

et al. 2016

Eur Respir J

185

158

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A major cause of respiratory failure during influenza A virus (IAV) infection is damage to the epithelial-endothelial barrier of the pulmonary alveolus. Damage to this barrier results in flooding of the alveolar lumen with proteinaceous oedema fluid, erythrocytes and inflammatory cells. To date, the exact roles of pulmonary epithelial and endothelial cells in this process remain unclear.Here, we used an in vitro co-culture model to understand how IAV damages the pulmonary epithelialendothelial barrier. Human epithelial cells were seeded on the upper half of a transwell membrane while human endothelial cells were seeded on the lower half. These cells were then grown in co-culture and IAV was added to the upper chamber.We showed that the addition of IAV (H1N1 and H5N1 subtypes) resulted in significant barrier damage. Interestingly, we found that, while endothelial cells mounted a pro-inflammatory/pro-coagulant response to a viral infection in the adjacent epithelial cells, damage to the alveolar epithelial-endothelial barrier occurred independently of endothelial cells. Rather, barrier damage was associated with disruption of tight junctions amongst epithelial cells, and specifically with loss of tight junction protein claudin-4.Taken together, these data suggest that maintaining epithelial cell integrity is key in reducing pulmonary oedema during IAV infection. @ERSpublications Influenza A virus damages tight junctions, and specifically claudin-4, of respiratory epithelial cells

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Respiratory syndrome coronavirus‐2 response: Microbiota as lactobacilli could make the difference

Zrelli

Amairia

Zrelli

2020

Journal of Medical Virology

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Coronavirus disease 2019 (COVID‐19) is caused by respiratory syndrome coronavirus qualified as SARS‐CoV‐2. Viral penetration requires binding of the viral spike (S) protein to a specific cellular receptor (ACE2) highly expressed in a nasal goblet and ciliated cells. In several countries, the COVID‐19 evolution was relatively benign compared to others and despite noncompliance with health recommendations on several occasions. In this overview, we attempt to define the criteria that could explain such a difference. Among these criteria, the specificity of Lactobacillus genus strains, as a part of nasal microbiota, could play a role of a barrier against viral penetration and could strengthen the host's immune system in some populations rather than others. In fact, several studies have shown the role of lactic acid bacteria, including lactobacilli, in the prevention of viral respiratory infections. This could provide important information on a possible mechanism of the virus spreading.

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Nasal priming with immunobiotic Lactobacillus rhamnosus modulates inflammation–coagulation interactions and reduces influenza virus-associated pulmonary damage

Cited by 63 publications

References 44 publications

Respiratory Antiviral Immunity and Immunobiotics: Beneficial Effects on Inflammation-Coagulation Interaction during Influenza Virus Infection

Respiratory Antiviral Immunity and Immunobiotics: Beneficial Effects on Inflammation-Coagulation Interaction during Influenza Virus Infection

Influenza virus damages the alveolar barrier by disrupting epithelial cell tight junctions

Respiratory syndrome coronavirus‐2 response: Microbiota as lactobacilli could make the difference

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