scholarly journals Protective Effects of a Novel Lactobacillus brevis Strain with Probiotic Characteristics Against Staphylococcus aureus Lipoteichoic Acid-Induced Intestinal Inflammatory Response

2021 ◽  
Author(s):  
Won-Ju Kim ◽  
Jun-Hyun Hyun ◽  
Na-Kyoung Lee ◽  
Hyun-Dong Paik
Keyword(s):  
Staphylococcus Aureus ◽  
Inflammatory Response ◽  
Lactobacillus Brevis ◽  
Lipoteichoic Acid ◽  
Protective Effects

scholarly journals Molecules from Staphylococcus aureus that bind CD14 and stimulate innate immune responses.

1995 ◽  
Vol 182 (6) ◽  
pp. 1673-1682 ◽  
Author(s):  
T Kusunoki ◽  
E Hailman ◽  
T S Juan ◽  
H S Lichenstein ◽  
S D Wright
Keyword(s):  
Staphylococcus Aureus ◽  
Inflammatory Response ◽  
Minor Component ◽  
Lipoteichoic Acid ◽  
Cell Types ◽  
Abundant Species ◽  
Gram Positive ◽  
Gram Negative ◽  
Free Phenol ◽  
Gram Positive Bacteria

Mammals mount a rapid inflammatory response to gram-negative bacteria by recognizing lipopolysaccharide (LPS, endotoxin). LPS binds to CD14, and the resulting LPS-CD14 complex induces synthesis of cytokines and up-regulation of adhesion molecules in a variety of cell types. Gram-positive bacteria provoke a very similar inflammatory response, but the molecules that provoke innate responses to these bacteria have not been defined. Here we show that protein-free, phenol extracts of Staphylococcus aureus contain a minor component that stimulates adhesion of neutrophils and cytokine production in monocytes and in the astrocytoma cell line, U373. Responses to this component do not absolutely require CD14, but addition of soluble CD14 enhances sensitivity of U373 cells by up to 100-fold, and blocking CD14 on monocytes decreases sensitivity nearly 1,000-fold. Deletion of residues 57-64 of CD14, which are required for responses to LPS, also eliminates CD14-dependent responses to S. aureus molecules. The stimulatory component of S. aureus binds CD14 and blocks binding of radioactive LPS. Unlike LPS, the activity of S. aureus molecules was neither enhanced by LPS binding protein nor inhibited by bactericidal/permeability increasing protein. The active factor in extracts of S. aureus is also structurally and functionally distinct from the abundant species known as lipoteichoic acid (LTA). Cell-stimulating activity fractionates differently from LTA on a reverse-phase column, pure LTA fails to stimulate cells, and LTA antagonizes the action of LPS in assays of IL-6 production. These studies suggest that mammals may use CD14 in innate responses to both gram-negative and gram-positive bacteria, and that gram-positive bacteria may contain an apparently unique, CD14-binding species that initiates cellular responses.

scholarly journals Sodium Phenylbutyrate Ameliorates Inflammatory Response Induced by Staphylococcus aureus Lipoteichoic Acid via Suppressing TLR2/NF-κB/NLRP3 Pathways in MAC-T Cells

Molecules ◽  
2018 ◽  
Vol 23 (12) ◽  
pp. 3056 ◽  
Author(s):  
Xin Wang ◽  
Mengmeng Zhang ◽  
Ning Jiang ◽  
Aizhong Zhang
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Host Defense ◽  
Bovine Mastitis ◽  
Lipoteichoic Acid ◽  
Tnf Α ◽  
Host Defense Peptide ◽  
Sodium Phenylbutyrate

This study aimed to investigate the anti-inflammatory properties of sodium phenylbutyrate (SPB) against Staphylococcus aureus (S. aureus) lipoteichoic acid (LTA)-stimulated bovine mammary alveolar (MAC-T) cells. Quantitative PCR was performed to examine the effect of SPB on inflammatory cytokines and host defense peptide (HDP) gene expression. Western blot wanalysis was used to detect the effect of SPB on the TLR2/NF-κB/NLRP3 signaling pathway. The results showed that SPB significantly suppressed the expression of TNF-α, IL-1β, IL-6; meanwhile, the markedly decreased expression of LTA-stimulated TLR2, NLRP3, ASC, caspase-1, and IL-1β, and the inhibited IkBα and p65 phosphorylation were also observed. However, increased TAP and Bac5 expression in LTA-stimulated MAC-T cells was further detected. In summary, these results suggest that SPB ameliorates the inflammatory response induced by S. aureus LTA via suppressing the TLR2/NF-κB/NLRP3 signaling pathway, which indicates that SPB may be a potential agent for the treatment of bovine mastitis.

scholarly journals Heterozygous Toll-Like Receptor 2 Polymorphism Does Not Affect Lipoteichoic Acid-Induced Chemokine and Inflammatory Responses

2004 ◽  
Vol 72 (3) ◽  
pp. 1828-1831 ◽  
Author(s):  
Sonja von Aulock ◽  
Nicolas W. J. Schröder ◽  
Stephanie Traub ◽  
Katja Gueinzius ◽  
Eva Lorenz ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Lipoteichoic Acid ◽  
Cytokine Response ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Functional Allele ◽  
Polymorphic Gene ◽  
Toll Like Receptor 2

ABSTRACT While transfection of tlr2 conveyed responsiveness to lipoteichoic acid (LTA), the Arg753Gln polymorphic gene could not. LTA induced a stronger chemokine and anti-inflammatory response than lipopolysaccharides did. Blood from heterozygous polymorphic and wild-type donors reacted uniformly to LTA and Staphylococcus aureus. Thus, one functional allele for Toll-like receptor 2 suffices for full cytokine response.

scholarly journals Comparing the protective effects of resveratrol, curcumin and sulforaphane against LPS/IFN-γ-mediated inflammation in doxorubicin-treated macrophages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haidy A. Saleh ◽  
Eman Ramdan ◽  
Mohey M. Elmazar ◽  
Hassan M. E. Azzazy ◽  
Anwar Abdelnaser
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Raw 264.7 Cells ◽  
Inos Mrna ◽  
No Production ◽  
Raw 264.7 ◽  
Mrna Levels ◽  
Protective Effects ◽  
Tnf Α ◽  
Ifn Γ

AbstractDoxorubicin (DOX) chemotherapy is associated with the release of inflammatory cytokines from macrophages. This has been suggested to be, in part, due to DOX-mediated leakage of endotoxins from gut microflora, which activate Toll-like receptor 4 (TLR4) signaling in macrophages, causing severe inflammation. However, the direct function of DOX on macrophages is still unknown. In the present study, we tested the hypothesis that DOX alone is incapable of stimulating inflammatory response in macrophages. Then, we compared the anti-inflammatory effects of curcumin (CUR), resveratrol (RES) and sulforaphane (SFN) against lipopolysaccharide/interferon-gamma (LPS/IFN-γ)-mediated inflammation in the absence or presence of DOX. For this purpose, RAW 264.7 cells were stimulated with LPS/IFN-γ (10 ng/mL/10 U/mL) in the absence or presence of DOX (0.1 µM). Our results showed that DOX alone is incapable of stimulating an inflammatory response in RAW 264.7 macrophages. Furthermore, after 24 h of incubation with LPS/IFN-γ, a significant increase in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) mRNA levels was observed. Similarly, nitric oxide (NO) production and TNF-α and IL-6 protein levels were significantly upregulated. Moreover, in LPS/IFN-γ-treated macrophages, the microRNAs (miRNAs) miR-146a, miR-155, and miR-21 were significantly overexpressed. Interestingly, upon testing CUR, RES, and SFN against LPS/IFN-γ-mediated inflammation, only SFN was able to significantly reverse the LPS/IFN-γ-mediated induction of iNOS, TNF-α and IL-6 and attenuate miR-146a and miR-155 levels. In conclusion, SFN, at the transcriptional and posttranscriptional levels, exhibits potent immunomodulatory action against LPS/IFN-γ-stimulated macrophages, which may indicate SFN as a potential treatment for DOX-associated inflammation.

scholarly journals Effect of Lipopolysaccharides (LPS) and Lipoteichoic acid (LTA) on the Inflammatory Response in Rumen Epithelial Cells (REC) and the Impact of LPS on Claw Explants

Animals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 2058
Author(s):  
Nicole Reisinger ◽  
Dominik Wendner ◽  
Nora Schauerhuber ◽  
Elisabeth Mayer
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Structural Integrity ◽  
Animal Health ◽  
Lipoteichoic Acid ◽  
Local Inflammatory Response ◽  
Tissue Integrity ◽  
Separation Force ◽  
The Impact ◽  
Rumen Epithelial Cells

Endotoxins play a crucial role in ruminant health due to their deleterious effects on animal health. The study aimed to evaluate whether LPS and LTA can induce an inflammatory response in rumen epithelial cells. For this purpose, epithelial cells isolated from rumen tissue (RECs) were stimulated with LPS and LTA for 1, 2, 4, and 24 h. Thereafter, the expression of selected genes of the LPS and LTA pathway and inflammatory response were evaluated. Furthermore, it was assessed whether LPS affects inflammatory response and structural integrity of claw explants. Therefore, claw explants were incubated with LPS for 4 h to assess the expression of selected genes and for 24 h to evaluate tissue integrity via separation force. LPS strongly affected the expression of genes related to inflammation (NFkB, TNF-α, IL1B, IL6, CXCL8, MMP9) in RECs. LTA induced a delayed and weaker inflammatory response than LPS. In claw explants, LPS affected tissue integrity, as there was a concentration-dependent decrease of separation force. Incubation time had a strong effect on inflammatory genes in claw explants. Our data suggest that endotoxins can induce a local inflammatory response in the rumen epithelium. Furthermore, translocation of LPS might negatively impact claw health.

scholarly journals Up-regulation of long non-coding RNA CYTOR induced by icariin promotes the viability and inhibits the apoptosis of chondrocytes

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guoyou Wang ◽  
Lei Zhang ◽  
Huarui Shen ◽  
Qi Hao ◽  
Shijie Fu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Loss Of Function ◽  
Protective Function ◽  
Non Coding Rna ◽  
Effective Component ◽  
Short Hairpin Rnas ◽  
Function Models

Abstract Background Icariin (ICAR) is the main effective component extracted from epimedium, and is reported to have the potential to treat osteoarthritis (OA). However, its pharmacological function on chondrocytes has not been fully clarified. Methods Different doses of ICAR were used to treat chondrocyte cell lines, including CHON-001 and ATDC5. Then the expressions of different lncRNAs were measured by qRT-PCR. Interleukin-1β (IL-1β) was used to simulate the inflammatory response environment of chondrocytes. Overexpression plasmids and short hairpin RNAs of lncRNA CYTOR were used to construct gain-of-function and loss of function models. CCK-8 was conducted to determine the cell viability. Flow cytometry was used to detect the apoptosis of chondrocytes. Enzyme-linked immunosorbent assay (ELISA) was adopted to measure the contents of inflammatory factors (IL-6, IL-8, TNF-α) in the supernatant of the chondrocytes. Results Compared with other lncRNAs, CYTOR was changed most significantly in both CHON-001 and ATDC5 cells after treatment with ICAR. ICAR promotes the viability and inhibits the apoptosis of CHON-001 and ATDC5 cells induced by IL-1β, accompanied with reduced levels of inflammatory factors. Overexpression of CYTOR facilitated the viability of chondrocytes, while repressed their apoptosis and inflammatory response. What’s more, knockdown of CYTOR reversed the protective effects of ICAR on chondrocytes. Conclusion CYTOR was a pivotal lncRNA involved in the protective function of ICAR on chondrocytes.

Sign in / Sign up

Export Citation Format

Share Document