scholarly journals Lipoteichoic acid from Staphylococcus aureus Activates the Complement System via C3 Induction and CD55 Inhibition

2021 ◽  
Vol 9 (6) ◽  
pp. 1135
Author(s):  
Bong Jun Jung ◽  
Hangeun Kim ◽  
Kyoung Ok Jang ◽  
Seongjae Kim ◽  
Dae Kyun Chung
Keyword(s):  
Staphylococcus Aureus ◽  
Hepg2 Cells ◽  
Protein Production ◽  
Interleukin 1 ◽  
Membrane Attack Complex ◽  
Lipoteichoic Acid ◽  
Underlying Mechanism ◽  
Toll Like Receptor ◽  
A Cell ◽  
The Complement System

Staphylococcus aureus inhibits complement activity by secreting a variety of toxins. However, the underlying mechanism of complement component regulation by lipoteichoic acid (LTA), a cell wall component of S. aureus, has not been elucidated. In this study, we observed that aLTA (LTA of S. aureus) increased C3 expression in THP-1 cells. The mechanism of aLTA-mediated C3 induction includes an aLTA-toll-like receptor (TLR) 2 interaction, interleukin 1 receptor associated kinase (IRAK) 2 recruitment, and nuclear factor kappa B (NF-kB) activation. In HepG2 cells, C3 protein production begins to increase from 3 h and increases steadily until 48 h. On the other hand, CD55 levels increased up to 6 h after aLTA treatment and started to decrease after 24 h and levels were decreased at 48 h by more than 50% compared to untreated cells. The expression of CD55 in HepG2 cells was shown to be regulated by IRAK-M induced by aLTA. Serum C3 levels increased in mice injected with aLTA, which resulted in an increase in the amount and activity of the membrane attack complex (MAC). We also observed that CD55 mRNA was increased in the liver 24 h after aLTA injection, but was decreased 48 h after injection. These results suggest that aLTA increases complement levels via induction of C3 and inhibition of CD55, which may cause associated MAC-mediated liver damage.

scholarly journals Repression of Acetaminophen-Induced Hepatotoxicity in HepG2 Cells by Polyphenolic Compounds from Lauridia tetragona (L.f.) R.H. Archer

Molecules ◽  
2019 ◽  
Vol 24 (11) ◽  
pp. 2118 ◽  
Author(s):  
Samuel Odeyemi ◽  
John Dewar
Keyword(s):  
Hepg2 Cells ◽  
Antioxidant Properties ◽  
Reducing Power ◽  
Underlying Mechanism ◽  
Hepatoprotective Activity ◽  
Polyphenolic Compounds ◽  
Hepatocellular Injury ◽  
Liver Glutathione ◽  
Total Antioxidant ◽  
A Cell

Lauridia tetragona (L.f) R.H. Archer is routinely used in traditional medicine; however, its hepatoprotective property is yet to be scientifically proven. To this effect, the hepatoprotective activity of the polyphenolic-rich fractions (PPRFs) was investigated against acetaminophen (APAP) injured HepG2 cells. The ability of the PPRF to scavenge free radicals was tested against 2,2-diphenyl-1-picrylhydrazyl (DPPH), and [2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonicacid)] (ABTS). The ferric ion reducing power (FRAP) was also evaluated as a cell-free antioxidant assay. The hepatoprotective activity was then investigated by observing the effect of PPRFs against APAP-induced reduction in cell viability of HepG2 cells. The concentrations of alanine aminotransferase (AST), aspartate aminotransferase (ALT) and lactate dehydrogenase (LDH) released into the medium were evaluated while the underlying mechanism was further explored through western blot analysis. Thereafter, the isolated PPRFs were identified using UHPLC-QToF-MS. All six fractions of the PPRFs isolated showed significant antioxidant properties that were evident by the effective scavenging of DPPH, ABTS, and higher FRAP. The results indicated that PPRF pretreatments ameliorated APAP-induced hepatocellular injury by significantly inhibiting the leakage of AST, ALT, and LDH into the medium. The most active fractions for hepatoprotection were PPRF4 and PPRF6 with IC50 of 50.243 ± 8.03 and 154.59 ± 1.9 μg/mL, respectively. PPRFs markedly increased activities of liver superoxide dismutase, total antioxidant capacity, and liver glutathione concentration. Both PPRF4 and PPRF6 significantly increased the expression of Nrf2 and translocation. The LC-MS analysis revealed the presence of a wide variety of polyphenolics such as coumarin, ferulic acid, and caffeine among the dominant constituents. In conclusion, this study demonstrates that the isolated PPRFs have potential hepatoprotective activity that may be due to the increased expression of antioxidative genes dependent on Nrf2.

scholarly journals Response to Staphylococcus aureus requires CD36-mediated phagocytosis triggered by the COOH-terminal cytoplasmic domain

2005 ◽  
Vol 170 (3) ◽  
pp. 477-485 ◽  
Author(s):  
Lynda M. Stuart ◽  
Jiusheng Deng ◽  
Jessica M. Silver ◽  
Kazue Takahashi ◽  
Anita A. Tseng ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mutational Analysis ◽  
Scavenger Receptor ◽  
Lipoteichoic Acid ◽  
Cytoplasmic Domain ◽  
Toll Like Receptor ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

Phagocyte recognition and clearance of bacteria play essential roles in the host response to infection. In an on-going forward genetic screen, we identify the Drosophila melanogaster scavenger receptor Croquemort as a receptor for Staphylococcus aureus, implicating for the first time the CD36 family as phagocytic receptors for bacteria. In transfection assays, the mammalian Croquemort paralogue CD36 confers binding and internalization of Gram-positive and, to a lesser extent, Gram-negative bacteria. By mutational analysis, we show that internalization of S. aureus and its component lipoteichoic acid requires the COOH-terminal cytoplasmic portion of CD36, specifically Y463 and C464, which activates Toll-like receptor (TLR) 2/6 signaling. Macrophages lacking CD36 demonstrate reduced internalization of S. aureus and its component lipoteichoic acid, accompanied by a marked defect in tumor necrosis factor-α and IL-12 production. As a result, Cd36−/− mice fail to efficiently clear S. aureus in vivo resulting in profound bacteraemia. Thus, response to S. aureus requires CD36-mediated phagocytosis triggered by the COOH-terminal cytoplasmic domain, which initiates TLR2/6 signaling.

Microglia digest Staphylococcus aureus into low molecular weight biologically active compounds

1996 ◽  
Vol 271 (1) ◽  
pp. R149-R156
Author(s):  
E. F. Fincher ◽  
L. Johannsen ◽  
L. Kapas ◽  
S. Takahashi ◽  
J. M. Krueger
Keyword(s):  
Molecular Weight ◽  
Staphylococcus Aureus ◽  
Cytokine Production ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Primary Cultures ◽  
Biologically Active ◽  
Low Molecular Weight ◽  
Specific Marker ◽  
A Cell

Excess sleep and fever are central nervous system (CNS) facets of the acute phase response; these responses are induced by microbial products, such as muramyl peptides, via their ability to enhance cytokine production. Although peripheral macrophages are known to digest bacteria, thereby releasing muramyl peptides that, in turn, stimulate cytokine production, it was unknown whether CNS phagocytes such as microglia also had this capacity. Primary cultures of microglia were allowed to phagocytize and digest Staphylococcus aureus radiolabeled with a cell wall-specific marker. Radiolabeled low molecular weight substances released into the culture medium were partially purified and tested for the ability to induce excess sleep, fever, and cytokine production. These substances increased non-rapid eye movement sleep, electroencephalographic slow-wave activity, and brain temperature after intracerebroventricular injection into rabbits. They also induced interleukin-1, tumor necrosis factor, and the interleukin-1 receptor antagonist production in human monocytes. Results suggest that microglia perform fundamental macrophage functions and further implicate microglia as resident immunocompetent cells.

scholarly journals Staphylococcus aureus –derived lipoteichoic acid induces temporary T-cell paralysis independent of Toll-like receptor 2

2016 ◽  
Vol 138 (3) ◽  
pp. 780-790.e6 ◽  
Author(s):  
Susanne Kaesler ◽  
Yuliya Skabytska ◽  
Ko-Ming Chen ◽  
Wolfgang E. Kempf ◽  
Thomas Volz ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cell ◽  
Lipoteichoic Acid ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Staphylococcus aureus Peptidoglycan Is a Toll-Like Receptor 2 Activator: a Reevaluation

2005 ◽  
Vol 73 (8) ◽  
pp. 5212-5216 ◽  
Author(s):  
Roman Dziarski ◽  
Dipika Gupta
Keyword(s):  
Staphylococcus Aureus ◽  
Sodium Dodecyl ◽  
Lipoteichoic Acid ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Phenol Extraction ◽  
Tlr2 Activation ◽  
Toll Like Receptor 2 ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Since the ability of peptidoglycan (PGN) to activate Toll-like receptor 2 (TLR2) was recently questioned, we reevaluated activation of TLR2 by PGN. Polymeric soluble or insoluble Staphylococcus aureus PGN, repurified by sodium dodecyl sulfate or phenol extraction, activated TLR2 at 0.1 to 1 or 10 μg/ml, respectively, and induced tumor necrosis factor alpha production. The TLR2 activation by PGN, but not by lipoteichoic acid, was abolished by muramidase digestion. We conclude that polymeric S. aureus PGN is a TLR2 activator.

scholarly journals Divergent roles of Toll-like receptor 2 in response to lipoteichoic acid and Staphylococcus aureus in vivo

2010 ◽  
Vol 40 (6) ◽  
pp. 1639-1650 ◽  
Author(s):  
Mark R. Gillrie ◽  
Lori Zbytnuik ◽  
Erin McAvoy ◽  
Roxna Kapadia ◽  
Kristine Lee ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Lipoteichoic Acid ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
And Staphylococcus Aureus

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.

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