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.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) improves the innate immune response and enhances survival in murine polymicrobial sepsis

2010 ◽  
Vol 38 (11) ◽  
pp. 2169-2174 ◽  
Author(s):  
Katharina Cziupka ◽  
Alexandra Busemann ◽  
Lars Ivo Partecke ◽  
Christian Pötschke ◽  
Matthias Rath ◽  
...  
Keyword(s):  
Immune Response ◽  
Tumor Necrosis Factor ◽  
Innate Immune Response ◽  
Tumor Necrosis ◽  
Innate Immune ◽  
Polymicrobial Sepsis ◽  
Necrosis Factor

scholarly journals Cytokine secretion requires phosphatidylcholine synthesis

2008 ◽  
Vol 181 (6) ◽  
pp. 945-957 ◽  
Author(s):  
Yong Tian ◽  
Caroline Pate ◽  
Alberto Andreolotti ◽  
Limin Wang ◽  
Elaine Tuomanen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Golgi Complex ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cytokine Secretion ◽  
Wild Type ◽  
Factor Α ◽  
Phosphatidylcholine Synthesis ◽  
Necrosis Factor

Choline cytidylyltransferase (CCT) is the rate-limiting enzyme in the phosphatidylcholine biosynthetic pathway. Here, we demonstrate that CCTα-mediated phosphatidylcholine synthesis is required to maintain normal Golgi structure and function as well as cytokine secretion from the Golgi complex. CCTα is localized to the trans-Golgi region and its expression is increased in lipopolysaccharide (LPS)-stimulated wild-type macrophages. Although LPS triggers transient reorganization of Golgi morphology in wild-type macrophages, similar structural alterations persist in CCTα-deficient cells. Pro–tumor necrosis factor α and interleukin-6 remain lodged in the secretory compartment of CCTα-deficient macrophages after LPS stimulation. However, the lysosomal-mediated secretion pathways for interleukin-1β secretion and constitutive apolipoprotein E secretion are unaltered. Exogenous lysophosphatidylcholine restores LPS-stimulated secretion from CCTα-deficient cells, and elevated diacylglycerol levels alone do not impede secretion of pro–tumor necrosis factor α or interleukin-6. These results identify CCTα as a key component in membrane biogenesis during LPS-stimulated cytokine secretion from the Golgi complex.

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.

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