Hydroxytyrosol exerts an anti-inflammatory effect by suppressing Toll-like receptor 2 and TLR 2 downstream pathways in Staphylococcus aureus-induced mastitis in mice

2017 ◽  
Vol 35 ◽  
pp. 595-604 ◽  
Author(s):  
Haichong Wu ◽  
Kangfeng Jiang ◽  
Tao Zhang ◽  
Gan Zhao ◽  
Ganzhen Deng
Keyword(s):  
Staphylococcus Aureus ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Anti Inflammatory ◽  
Inflammatory Effect

scholarly journals Dietary Chitin Particles Called Mimetic Fungi Ameliorate Colitis in Toll-Like Receptor 2/CD14- and Sex-Dependent Manners

2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Patricia Louis ◽  
Brian Mercer ◽  
Aiko M. Cirone ◽  
Christina Johnston ◽  
Zachary J. Lee ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Fungal Cell ◽  
Size Dependent ◽  
Major Structural Component ◽  
Acidic Mammalian Chitinase ◽  
Inflammatory Bowel ◽  
Toll Like Receptor 2 ◽  
Anti Inflammatory ◽  
Inflammatory Effect

ABSTRACTChitin is a naturalN-acetylglucosamine polymer and a major structural component of fungal cell walls. Dietary chitin is mucoadhesive; anti-inflammatory effects of chitin microparticles (CMPs; 1- to 10-μm diameters) have been demonstrated in models of inflammatory bowel disease (IBD). The goals of this study were to assess (i) whether CMPs among various chitin preparations are the most effective against colitis in male and female mice and (ii) whether host chitin-binding Toll-like receptor 2 (TLR2) and CD14 are required for the anti-inflammatory effect of chitin. We found that colitis in male mice was ameliorated by CMPs and large chitin beads (LCBs; 40 to 70 μm) but not by chitosan (deacetylated chitin) microparticles, oligosaccharide chitin, or glucosamine. In fact, LCBs were more effective than CMPs. In female colitis, on the other hand, CMPs and LCBs were equally and highly effective. Neither sex of TLR2-deficient mice showed anti-inflammatory effects when treated with LCBs. No anti-inflammatory effect of LCBs was seen in either CD14-deficient males or females. Furthermore, anin vitrostudy indicated that when LCBs and CMPs were digested with stomach acidic mammalian chitinase (AMC), their size-dependent macrophage activations were modified, at least in part, suggesting reduced particle sizes of dietary chitin in the stomach. Interestingly, stomach AMC activity was greater in males than females. Our results indicated that dietary LCBs were the most effective preparation for treating colitis in both sexes; these anti-inflammatory effects of LCBs were dependent on host TLR2 and CD14.

3,6-Dihydroxyflavone: A Potent Inhibitor with Anti-Inflammatory Activity Targeting Toll-like Receptor 2

2018 ◽  
Vol 40 (1) ◽  
pp. 51-55
Author(s):  
Pavithra K. Balasubramanian ◽  
Jieun Kim ◽  
Kkabi Son ◽  
Prasannavenkatesh Durai ◽  
Yangmee Kim
Keyword(s):  
Potent Inhibitor ◽  
Inflammatory Activity ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Anti Inflammatory

scholarly journals Protective effect of Lactobacillus reuteri DSM 17938 against experimental necrotizing enterocolitis is mediated by Toll-like receptor 2

2018 ◽  
Vol 315 (2) ◽  
pp. G231-G240 ◽  
Author(s):  
Thomas K. Hoang ◽  
Baokun He ◽  
Ting Wang ◽  
Dat Q. Tran ◽  
J. Marc Rhoads ◽  
...  
Keyword(s):  
T Cells ◽  
Necrotizing Enterocolitis ◽  
Immune Modulation ◽  
Lactobacillus Reuteri ◽  
Inflammatory Responses ◽  
Cow Milk ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Anti Inflammatory

Lactobacillus reuteri DSM 17938 (LR 17938) has been shown to reduce the incidence and severity of necrotizing enterocolitis (NEC). It is unclear if preventing NEC by LR 17938 is mediated by Toll-like receptor 2 (TLR2), which is known to mediate proinflammatory responses to bacterial cell wall components. NEC was induced in newborn TLR2−/− or wild-type (WT) mice by the combination of gavage-feeding cow milk-based formula and exposure to hypoxia and cold stress. Treatment groups were administered formula supplemented with LR 17938 or placebo (deMan-Rogosa-Sharpe media). We observed that LR 17938 significantly reduced the incidence of NEC and reduced the percentage of activated effector CD4+T cells, while increasing Foxp3+ regulatory T cells in the intestinal mucosa of WT mice with NEC, but not in TLR2−/− mice. Dendritic cell (DC) activation by LR 17938 was mediated by TLR2. The percentage of tolerogenic DC in the intestine of WT mice was increased by LR 17938 treatment during NEC, a finding not observed in TLR2−/− mice. Furthermore, gut levels of proinflammatory cytokines IL-1β and IFN-γ were decreased after treatment with LR 17938 in WT mice but not in TLR2−/− mice. In conclusion, the combined in vivo and in vitro findings suggest that TLR2 receptors are involved in DC recognition and DC-priming of T cells to protect against NEC after oral administration of LR 17938. Our studies further clarify a major mechanism of probiotic LR 17938 action in preventing NEC by showing that neonatal immune modulation of LR 17938 is mediated by a mechanism requiring TLR2. NEW & NOTEWORTHY Lactobacillus reuteri DSM 17938 (LR 17938) has been shown to protect against necrotizing enterocolitis (NEC) in neonates and in neonatal animal models. The role of Toll-like receptor 2 (TLR2) as a sensor for gram-positive probiotics, activating downstream anti-inflammatory responses is unclear. Our current studies examined TLR2 −/− mice subjected to experimental NEC and demonstrated that the anti-inflammatory effects of LR 17938 are mediated via a mechanism requiring TLR2.

scholarly journals Toll-Like Receptor 2 Release by Macrophages: An Anti-inflammatory Program Induced by Glucocorticoids and Lipopolysaccharide

2019 ◽  
Vol 10 ◽  
Author(s):  
Jessica Hoppstädter ◽  
Anna Dembek ◽  
Rebecca Linnenberger ◽  
Charlotte Dahlem ◽  
Ahmad Barghash ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Anti Inflammatory

scholarly journals Uncoupling of Pro- and Anti-Inflammatory Properties of Staphylococcus aureus

2015 ◽  
Vol 83 (4) ◽  
pp. 1587-1597 ◽  
Author(s):  
Adam G. Peres ◽  
Camille Stegen ◽  
Junbin Li ◽  
An Qi Xu ◽  
Benoit Levast ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Inflammatory Responses ◽  
Proinflammatory Response ◽  
Healthy Human ◽  
Content Type ◽  
Cell Immunity ◽  
Extracellular Signal ◽  
Severe Infections ◽  
Toll Like Receptor 2 ◽  
Anti Inflammatory

Staphylococcus aureusis a Gram-positive bacterium that is carried by a quarter of the healthy human population and that can cause severe infections. This pathobiosis has been linked to a balance between Toll-like receptor 2 (TLR2)-dependent pro- and anti-inflammatory responses. The relationship between these two types of responses is unknown. Analysis of 16 nasal isolates ofS. aureusshowed heterogeneity in their capacity to induce pro- and anti-inflammatory responses, suggesting that these two responses are independent of each other. Uncoupling of these responses was corroborated by selective signaling through phosphoinositol 3-kinase (PI3K)-Akt-mTOR and extracellular signal-regulated kinase (ERK) for the anti-inflammatory response and through p38 for the proinflammatory response. Uncoupling was also observed at the level of phagocytosis and phagosomal processing ofS. aureus, which were required solely for the proinflammatory response. Importantly, the anti-inflammatory properties of anS. aureusisolate correlated with its ability to modulate T cell immunity. Our results suggest the presence of anti-inflammatory TLR2 ligands in the staphylococcal cell wall, whose identification may provide templates for novel immunomodulatory drugs.

scholarly journals Staphylococcus aureus Releases Proinflammatory Membrane Vesicles To Resist Antimicrobial Fatty Acids

mSphere ◽  
2020 ◽  
Vol 5 (5) ◽  
Author(s):  
Arnaud Kengmo Tchoupa ◽  
Andreas Peschel
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Content Type ◽  
Healthy Humans ◽  
Toll Like Receptor 2

ABSTRACT Staphylococcus aureus is a major pathogen, which colonizes one in three otherwise healthy humans. This significant spread of S. aureus is largely due to its ability to circumvent innate immune responses, including antimicrobial fatty acids (AFAs) on the skin and in nasal secretions. In response to AFAs, S. aureus swiftly induces resistance mechanisms, which have yet to be completely elucidated. Here, we identify membrane vesicle (MV) release as a resistance strategy used by S. aureus to sequester host-specific AFAs. MVs protect S. aureus against a wide array of AFAs. Strikingly, beside MV production, S. aureus modulates MV composition upon exposure to AFAs. MVs purified from bacteria grown in the presence of linoleic acid display a distinct protein content and are enriched in lipoproteins, which strongly activate Toll-like receptor 2 (TLR2). Cumulatively, our findings reveal the protective capacities of MVs against AFAs, which are counteracted by an increased TLR2-mediated innate immune response. IMPORTANCE The nares of one in three humans are colonized by Staphylococcus aureus. In these environments, and arguably on all mucosal surfaces, bacteria encounter fatty acids with antimicrobial properties. Our study uncovers that S. aureus releases membrane vesicles (MVs) that act as decoys to protect the bacterium against antimicrobial fatty acids (AFAs). The AFA-neutralizing effects of MVs were neither strain specific nor restricted to one particular AFA. Hence, MVs may represent “public goods” playing an overlooked role in shaping bacterial communities in AFA-rich environments such as the skin and nose. Intriguingly, in addition to MV biogenesis, S. aureus modulates MV composition in response to exposure to AFAs, including an increased release of lipoproteins. These MVs strongly stimulate the innate immunity via Toll-like receptor 2 (TLR2). TLR2-mediated inflammation, which helps to fight infections, may exacerbate inflammatory disorders like atopic dermatitis. Our study highlights intricate immune responses preventing infections from colonizing bacteria.

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