scholarly journals Aspergeillus Fumigatus: The Effects of Adiponectin on Inflammatory Cytokine Production

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Rick Foust ◽  
Robert Templeton
Keyword(s):  
Cytokine Production ◽  
Cytokine Secretion ◽  
Rt Pcr ◽  
Macrophage Cell ◽  
Experimental Conditions ◽  
Inflammatory Cytokine Production ◽  
Cytokine Tumor Necrosis Factor ◽  
Immune Pathology ◽  
Necrosis Factor ◽  
Wild Type Control

Background and Hypothesis: Although inflammatory cytokines are important for antifungal defenses, excessive production significantly increases host immune pathology. It is therefore important to identify host pathways that limit detrimental inflammation in invasive fungal infection. Our prior results showed that mice with invasive aspergillosis (IA) that were deficient in the metabolic cytokine production produced more of the cytokine Tumor Necrosis Factor (TNF) than alveolar in wild-type control mice.  Therefore, we hypothesize that adiponectin inhibits antifungal cytokine secretion in alveolar macrophages.   Experimental Design or Project Methods: To test this hypothesis, the commonly used A. fumigatus strain Af293 was purchased from the Fungal Genetics Stock Center and grown on and harvested from agar. The alveolar macrophage cell line MH-S and cytokine ELISA kits was obtained from MilliporeSigma and ThermoFisher, respectively. MH-S cells were stimulated with swollen, fixed Af293 conidia for 24 hours in the presence or absence of recombinant mouse adiponectin. After 24 hours, supernatants and cells was were collected and assayed for ILs 1a, 6, and TNF protein and mRNA , by ELISA and quantitative RT-PCR, respectively.  Results: Although our preliminary results suggest possible inhibition of cytokine secretion by adiponectin in response to A. fumigatus, significant differences have thus far not been observed.   Conclusion and Potential Impact: We are therefore currently optimizing our experimental conditions to improve antifungal cytokine secretion. These studies may ultimately assist in the discovery of novel therapeutic targets and improve the prognosis of A. fumigatus infections 

scholarly journals Fosfomycin Alters Lipopolysaccharide-Induced Inflammatory Cytokine Production in Mice

1999 ◽  
Vol 43 (3) ◽  
pp. 697-698 ◽  
Author(s):  
Tetsuya Matsumoto ◽  
Kazuhiro Tateda ◽  
Shuichi Miyazaki ◽  
Nobuhiko Furuya ◽  
Akira Ohno ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Serum Levels ◽  
Necrosis Factor Alpha ◽  
Inflammatory Cytokine Production ◽  
Factor Alpha ◽  
Lps Treatment ◽  
Necrosis Factor

ABSTRACT To determine the mechanisms of immunomodulating action of fosfomycin (FOF), we examined its effect on the production of inflammatory cytokines in mice injected with lipopolysaccharide (LPS). Treatment with FOF significantly lowered the peak serum levels of tumor necrosis factor alpha and interleukin-1β, indicating that FOF alters inflammatory cytokine production after LPS stimulation.

Induction of Mn SOD in human monocytes without inflammatory cytokine production by a mutant endotoxin

1998 ◽  
Vol 275 (3) ◽  
pp. C740-C747 ◽  
Author(s):  
Licheng Tian ◽  
Julie E. White ◽  
Hung-Yun Lin ◽  
Visa S. Haran ◽  
Joseph Sacco ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Lipid A ◽  
Cytokine Production ◽  
Mitogen Activated Protein Kinase ◽  
Wild Type ◽  
Inflammatory Cytokine Production ◽  
Mitogen Activated Protein ◽  
Factor Α ◽  
Necrosis Factor

Endotoxin selectively induces monocyte Mn superoxide dismutase (SOD) without affecting levels of Cu,Zn SOD, catalase, or glutathione peroxidase. However, little is known about the structure-activity relationship and the mechanism by which endotoxin induces Mn SOD. In this study we demonstrated that a mutant Escherichia coli endotoxin lacking myristoyl fatty acid at the 3′ R-3-hydroxymyristate position of the lipid A moiety retained its full capacity to coagulate Limulus amoebocyte lysate compared with the wild-type E. coli endotoxin and markedly stimulated the activation of human monocyte nuclear factor-κB and the induction of Mn SOD mRNA and enzyme activity. However, in contrast to the wild-type endotoxin, it failed to induce significant production of tumor necrosis factor-α and macrophage inflammatory protein-1α by monocytes and did not induce the phosphorylation and nuclear translocation of mitogen-activated protein kinase. These results suggest that 1) lipid A myristoyl fatty acid, although it is important for the induction of inflammatory cytokine production by human monocytes, is not necessary for the induction of Mn SOD, 2) endotoxin-mediated induction of Mn SOD and inflammatory cytokines are regulated, at least in part, through different signal transduction pathways, and 3) failure of the mutant endotoxin to induce tumor necrosis factor-α production is, at least in part, due to its inability to activate mitogen-activated protein kinase.

scholarly journals Poxvirus-encoded TNF receptor homolog dampens inflammation and protects the host from uncontrolled lung pathology and death during respiratory infection

2020 ◽  
Author(s):  
Zahrah Al Rumaih ◽  
Ma. Junaliah Tuazon Kels ◽  
Esther Ng ◽  
Pratikshya Pandey ◽  
Sergio M. Pontejo ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Tumor Necrosis Factor Receptor ◽  
Binding Domain ◽  
Lung Pathology ◽  
Tnf Receptor ◽  
Response Modifier ◽  
Inflammatory Cytokine Production ◽  
Lethal Infection ◽  
Ifn Γ ◽  
Necrosis Factor

AbstractEctromelia virus (ECTV) causes mousepox, a surrogate mouse model for smallpox caused by variola virus in humans. Both viruses encode tumor necrosis factor receptor (TNFR) homologs termed cytokine response modifier (Crm) proteins, containing a TNF-binding domain and a chemokine-binding domain termed smallpox virus-encoded chemokine receptor (SECRET) domain. Infection of ECTV-resistant C57BL/6 mice with an ECTV CrmD deletion mutant resulted in uniform mortality due to excessive TNF secretion and dysregulated inflammatory cytokine production but viral load was not affected. CrmD dampened lung pathology, leukocyte recruitment and inflammatory cytokines including TNF, IL-6, IL-10 and IFN-γ. Blockade of IL-6, IL-10R or TNF function with monoclonal antibodies reduced lung pathology and provided 60-100% protection from an otherwise lethal infection. IFN-γ caused lung pathology only when both the TNF-binding and SECRET domains were deleted but it was neither necessary nor sufficient to cause pathology when only the CrmD SECRET domain was expressed by virus.

scholarly journals TNF deficiency dysregulates inflammatory cytokine production leading to lung pathology and death during respiratory poxvirus infection

2019 ◽  
Author(s):  
Ma. Junaliah Tuazon Kels ◽  
Esther Ng ◽  
Zahrah Al Rumaih ◽  
Pratikshya Pandey ◽  
Sigrid R. Ruuls ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Cytokine Signaling ◽  
Lung Pathology ◽  
Suppressor Of Cytokine Signaling ◽  
Inflammatory Cytokine Production ◽  
Significant Pathology ◽  
Ifn Γ ◽  
Necrosis Factor ◽  
Severe Lung

AbstractExcessive tumor necrosis factor (TNF) is known to cause significant pathology. Paradoxically, deficiency in TNF (TNF-/-) also caused significant pathology during respiratory ectromelia virus (ECTV) infection, a surrogate mouse model for smallpox. TNF-/- mice succumbed to fulminant disease whereas wild-type mice, and those expressing only transmembrane TNF, recovered. TNF deficiency did not affect viral load or leukocyte recruitment but caused severe lung pathology and excessive production of the cytokines IL-6, IL-10, TGF-β, and IFN-γ. Blockade of these cytokines reduced lung pathology concomitant with induction of protein inhibitor of activated STAT3 (PIAS3) and/or suppressor of cytokine signaling 3 (SOCS3), factors that inhibit STAT3 activation. Short-term inhibition of STAT3 activation in ECTV-infected TNF-/- mice with an inhibitor reduced lung pathology. TNF is essential for regulating inflammation and its deficiency exacerbates ECTV infection as a consequence of significant lung pathology caused by dysregulation of inflammatory cytokine production, in part via overactivation of STAT3.

scholarly journals Sorghum [Sorghum bicolor(L.) Moench] Genotypes with Contrasting Polyphenol Compositions Differentially Modulate Inflammatory Cytokines in Mouse Macrophages

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Davina H. Rhodes ◽  
Stephen Kresovich
Keyword(s):  
Cytokine Production ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Inflammatory Cytokine Production ◽  
Mouse Macrophages ◽  
Health Promoting ◽  
Sorghum Genotypes ◽  
Ethanol Extracts ◽  
Sorghum Grain ◽  
Necrosis Factor

This study sought to characterize and compare anti-inflammatory effects of twenty sorghum accessions with contrasting grain polyphenol concentrations but similar genetic backgrounds (based on a genomewide estimate of relatedness). Cell viability, tumor necrosis factor- (TNF-)α, and interleukin- (IL-) 6 were measured in RAW 264.7 macrophages treated with increasing doses (0, 15, 30, and 60 μg/mL) of sorghum ethanol extracts and stimulated with lipopolysaccharide (LPS). Extract dose had a significant effect on TNF-αand IL-6, with a trend of cytokines decreasing between 0 μg/mL and 15 μg/mL of sorghum extract. Genotype also had a significant effect on the cytokines, with extracts from four accessions significantly decreasing TNF-αand/or IL-6. Cells treated with 3-deoxyanthocyanidin-containing accessions had less cytokine production than non-3-deoxyanthocyanidin accessions, whereas cells treated with proanthocyanidin-containing accessions had more cytokine production than cells treated with nonproanthocyanidin accessions. Additionally, there was a significant effect of theTannin1allele on TNF-αand IL-6. Our results demonstrate that sorghum genotypes differentially modulate induction of inflammatory cytokine production in RAW 264.7 macrophages and that specialty grain has the potential to be tailored by controlling traits at the nucleotide level. This study adds to our knowledge of sorghum health effects and contributes to efforts aimed at developing health-promoting sorghum grain.

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