scholarly journals The Respiratory Commensal Bacterium Dolosigranulum pigrum 040417 Improves the Innate Immune Response to Streptococcus pneumoniae

2021 ◽  
Vol 9 (6) ◽  
pp. 1324
Author(s):  
Fernanda Raya Tonetti ◽  
Mikado Tomokiyo ◽  
Ramiro Ortiz Moyano ◽  
Sandra Quilodrán-Vega ◽  
Hikari Yamamuro ◽  
...  
Keyword(s):  
Immune Response ◽  
Streptococcus Pneumoniae ◽  
Innate Immune Response ◽  
Pneumococcal Infection ◽  
Innate Immune ◽  
Nasal Administration ◽  
Commensal Bacterium ◽  
Beneficial Effects ◽  
Immunological Mechanisms ◽  
Immunomodulatory Properties

Previously, we demonstrated that the nasal administration of Dolosigranulum pigrum 040417 differentially modulated the respiratory innate immune response triggered by the activation of Toll-like receptor 2 in infant mice. In this work, we aimed to evaluate the beneficial effects of D. pigrum 040417 in the context of Streptococcus pneumoniae infection and characterize the role of alveolar macrophages (AMs) in the immunomodulatory properties of this respiratory commensal bacterium. The nasal administration of D. pigrum 040417 to infant mice significantly increased their resistance to pneumococcal infection, differentially modulated respiratory cytokines production, and reduced lung injuries. These effects were associated to the ability of the 040417 strain to modulate AMs function. Depletion of AMs significantly reduced the capacity of the 040417 strain to improve both the reduction of pathogen loads and the protection against lung tissue damage. We also demonstrated that the immunomodulatory properties of D. pigrum are strain-specific, as D. pigrum 030918 was not able to modulate respiratory immunity or to increase the resistance of mice to an S. pneumoniae infection. These findings enhanced our knowledge regarding the immunological mechanisms involved in modulation of respiratory immunity induced by beneficial respiratory commensal bacteria and suggested that particular strains could be used as next-generation probiotics.

scholarly journals Innate Immune Response as a New Challenge in Periodontal Inflammation

2021 ◽  
Author(s):  
Ana Marina Andrei ◽  
Elena Cristina Andrei ◽  
Elena Camelia Stănciulescu ◽  
Mihaela Cezarina Mehedinți ◽  
Mihaela Jana Țuculină ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Periodontal Diseases ◽  
Bacterial Species ◽  
Innate Immune ◽  
Beneficial Effects ◽  
Periodontal Tissues ◽  
Periodontal Inflammation ◽  
Genetic And Environmental Factors ◽  
Tlr Signalling

Gingivitis and periodontitis are induced by numerous pathogenic microbiota hosted in the subgingival biofilm that first trigger the innate immune response. Innate immune response is part of a homeostatic system which is the first line defence and defines the host inherited resistance to infection. Both genetic and environmental factors are involved in variable individual susceptibility to inflammation of periodontal tissues. That is why, although more than 600 bacterial species have been detected in the periodontal plaque, the type of bacteria incriminated in the development of the inflammation is still unclear. Moreover, in the last decade gene polymorphisms have been largely recognised as important conditions associated with increased susceptibility to periodontal diseases. Manipulating the immune response by the development of drugs that inhibit adverse host reactions and promote beneficial effects might be of therapeutic or prophylactic importance. This work intends to assess the importance of Toll-like receptors as main effectors of the innate immune response in the triggering, maintenance and progression of periodontal inflammation, as well as of the involvement of synthetic molecules targeting TLR signalling pathways in treating periodontal diseases.

scholarly journals The Exopolysaccharide of Lactobacillus fermentum UCO-979C Is Partially Involved in Its Immunomodulatory Effect and Its Ability to Improve the Resistance against Helicobacter pylori Infection

2020 ◽  
Vol 8 (4) ◽  
pp. 479
Author(s):  
Valeria Garcia-Castillo ◽  
Guillermo Marcial ◽  
Leonardo Albarracín ◽  
Mikado Tomokiyo ◽  
Patricia Clua ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Helicobacter Pylori Infection ◽  
Beneficial Effects ◽  
Ifn Γ ◽  
H Pylori

Lactobacillus fermentum UCO-979C (Lf979C) beneficially modulates the cytokine response of gastric epithelial cells and macrophages after Helicobacter pylori infection in vitro. Nevertheless, no in vivo studies were performed with this strain to confirm its beneficial immunomodulatory effects. This work evaluated whether Lf979C improves protection against H. pylori infection in mice by modulating the innate immune response. In addition, we evaluated whether its exopolysaccharide (EPS) was involved in its beneficial effects. Lf979C significantly reduced TNF-α, IL-8, and MCP-1 and augmented IFN-γ and IL-10 in the gastric mucosa of H. pylori-infected mice. The differential cytokine profile induced by Lf979C in H. pylori-infected mice correlated with an improved reduction in the pathogen gastric colonization and protection against inflammatory damage. The purified EPS of Lf979C reduced IL-8 and enhanced IL-10 levels in the gastric mucosa of infected mice, while no effect was observed for IFN-γ. This work demonstrates for the first time the in vivo ability of Lf979C to increase resistance against H. pylori infection by modulating the gastric innate immune response. In addition, we advanced knowledge of the mechanisms involved in the beneficial effects of Lf979C by demonstrating that its EPS is partially responsible for its immunomodulatory effect.

scholarly journals The Lectin Pathway of Complement Activation Is a Critical Component of the Innate Immune Response to Pneumococcal Infection

2012 ◽  
Vol 8 (7) ◽  
pp. e1002793 ◽  
Author(s):  
Youssif M. Ali ◽  
Nicholas J. Lynch ◽  
Kashif S. Haleem ◽  
Teizo Fujita ◽  
Yuichi Endo ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Complement Activation ◽  
Pneumococcal Infection ◽  
Innate Immune ◽  
Lectin Pathway ◽  
Critical Component

scholarly journals Lack of Proinflammatory Cytokine Interleukin-6 or Tumor Necrosis Factor Receptor-1 Results in a Failure of the Innate Immune Response after Bacterial Meningitis

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Lea-Jessica Albrecht ◽  
Simone C. Tauber ◽  
Julika Merres ◽  
Eugenia Kress ◽  
Matthias B. Stope ◽  
...  
Keyword(s):  
Immune Response ◽  
Streptococcus Pneumoniae ◽  
Tumor Necrosis Factor ◽  
Bacterial Meningitis ◽  
Innate Immune Response ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Innate Immune ◽  
Wild Type ◽  
Necrosis Factor

The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacteriumStreptococcus pneumoniae. By entering the brain, host cells will be activated and proinflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) are released. The goal of the current study was to examine the interaction between IL-6 and TNFR1 as receptor for TNF-αand the innate immune response in vivo in a model ofStreptococcus pneumoniae-induced meningitis. For the experiments IL-6−/−, TNFR1−/−, and TNFR1-IL-6−/−KO mice were used. Our results revealed higher mortality rates and bacterial burden after infection in TNFR1−/−, IL-6−/−, and TNFR1-IL-6−/−mice and a decreased immune response including lower neutrophil infiltration in the meninges of TNFR1−/−and TNFR1-IL-6−/−mice in contrast to IL-6−/−and wild type mice. Furthermore, the increased mortality of TNFR1−/−and TNFR1-IL-6−/−mice correlated with decreased glial cell activation compared to IL-6−/−or wild type mice after pneumococcal meningitis. Altogether, the results show the importance of TNFR1 and IL-6 in the regulation of the innate immune response. The lack of TNFR1 and IL-6 results in higher mortality by weakened immune defence, whereas the lack of TNFR1 results in more severe impairment of the innate immune response than the lack of IL-6 alone.

Potential utility of melatonin in deadly infectious diseases related to the overreaction of innate immune response and destructive inflammation: focus on COVID-19

2020 ◽  
Vol 3 (1) ◽  
pp. 120-143 ◽  
Author(s):  
Dunxian X Tan ◽  
Ruegiger Hardeland
Keyword(s):  
Immune Response ◽  
Infectious Diseases ◽  
Innate Immune Response ◽  
Safety Margin ◽  
Adaptive Immune System ◽  
Innate Immune ◽  
Viral Diseases ◽  
Beneficial Effects ◽  
Adaptive Immune ◽  
Destructive Inflammation

The high mortality of deadly virus infectious diseases including SARS, MERS, COVID-19, and avian flu is often caused by the uncontrolled innate immune response and destructive inflammation. The majority of viral diseases are self-limiting under the help of the activated adaptive immune system. This activity is cell proliferation dependent and thus, it requires several weeks to develop. Patients are vulnerable and mortality usually occurs during this window period. To control the innate immune response and reduce the inflammation during this period will increase the tolerance of patients and lowers the mortality in the deadly virus infection. Melatonin is a molecule that displays respective properties, since it downregulates the overreaction of the innate immune response and overshooting inflammation, but also promotes the adaptive immune activity. Many studies have reported the beneficial effects of melatonin on deadly virus infections in different animal models and its therapeutic efficacy in septic shock patients. Furthermore, melatonin has a great safety margin without serious adverse effects. We suggest the use of melatonin as an adjunctive or even regular therapy for deadly viral diseases, especially if no efficient direct anti-viral treatment is available.

scholarly journals The C-Type Lectin Receptor Mincle Binds to Streptococcus pneumoniae but Plays a Limited Role in the Anti-Pneumococcal Innate Immune Response

PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0117022 ◽  
Author(s):  
Anne Rabes ◽  
Stephanie Zimmermann ◽  
Katrin Reppe ◽  
Roland Lang ◽  
Peter H. Seeberger ◽  
...  
Keyword(s):  
Immune Response ◽  
Streptococcus Pneumoniae ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Lectin Receptor ◽  
Limited Role
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