scholarly journals Systemically Administered Ligands of Toll-Like Receptor 2, -4, and -9 Induce Distinct Inflammatory Responses in the Murine Lung

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
H. Ehrentraut ◽  
R. Meyer ◽  
M. Schwederski ◽  
S. Ehrentraut ◽  
M. Velten ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Pulmonary Inflammation ◽  
Myeloperoxidase Activity ◽  
Cpg Odn ◽  
Toll Like Receptor ◽  
Activity Assay ◽  
Murine Lung ◽  
Expression Activity ◽  
Toll Like Receptor 2

Objective. To determine whether systemically administered TLR ligands differentially modulate pulmonary inflammation.Methods. Equipotent doses of LPS (20 mg/kg), CpG-ODN (1668-thioat 1 nmol/g), or LTA (15 mg/kg) were determined via TNF activity assay. C57BL/6 mice were challenged intraperitoneally. Pulmonary NFκB activation (2 h) and gene expression/activity of key inflammatory mediators (4 h) were monitored.Results. All TLR ligands induced NFκB. LPS increased the expression of TLR2, 6, and the cytokines IL-1αβ, TNF-α, IL-6, and IL-12p35/p40, CpG-ODN raised TLR6, TNF-α, and IL12p40. LTA had no effect. Additionally, LPS increased the chemokines MIP-1α/β, MIP-2, TCA-3, eotaxin, and IP-10, while CpG-ODN and LTA did not. Myeloperoxidase activity was highest after LPS stimulation. MMP1, 3, 8, and 9 were upregulated by LPS, MMP2, 8 by CpG-ODN and MMP2 and 9 by LTA. TIMPs were induced only by LPS. MMP-2/-9 induction correlated with their zymographic activities.Conclusion. Pulmonary susceptibility to systemic inflammation was highest after LPS, intermediate after CpG-ODN, and lowest after LTA challenge.

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.

Curcumin decreases toll-like receptor 2 gene expression and function in human monocytic THP-1 and neutrophilic HL-60 cells

Cytokine ◽  
2009 ◽  
Vol 48 (1-2) ◽  
pp. 57
Author(s):  
Tomomi Ono ◽  
Tsuyoshi Shuto ◽  
Yuko Ohira ◽  
Mary Ann Suico ◽  
Tomoaki Koga ◽  
...  
Keyword(s):  
Gene Expression ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
And Function

scholarly journals Essential Calcium-binding Cluster ofLeptospiraLipL32 Protein for Inflammatory Responses through the Toll-like Receptor 2 Pathway

2013 ◽  
Vol 288 (17) ◽  
pp. 12335-12344 ◽  
Author(s):  
Yueh-Yu Lo ◽  
Shen-Hsing Hsu ◽  
Yi-Ching Ko ◽  
Cheng-Chieh Hung ◽  
Ming-Yang Chang ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Inflammatory Responses ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals A novel role for HMGB1 in TLR9-mediated inflammatory responses to CpG-DNA

Blood ◽  
2007 ◽  
Vol 110 (6) ◽  
pp. 1970-1981 ◽  
Author(s):  
Stanimir Ivanov ◽  
Ana-Maria Dragoi ◽  
Xin Wang ◽  
Corrado Dallacosta ◽  
Jennifer Louten ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Synthetic Analog ◽  
Cpg Odn ◽  
Toll Like Receptor ◽  
Cpg Dna ◽  
Early Endosomes ◽  
Intermediate Compartment ◽  
Tlr9 Activation

AbstractCpG-DNA or its synthetic analog CpG-ODN activates innate immunity through Toll-like receptor 9 (TLR9). However, the mechanism of TLR9 activation by CpG-DNA remains elusive. Here we have identified HMGB1 as a CpG-ODN–binding protein. HMGB1 interacts and preassociates with TLR9 in the endoplasmic reticulum-Golgi intermediate compartment (ERGIC), and hastens TLR9's redistribution to early endosomes in response to CpG-ODN. CpG-ODN stimulates macrophages and dendritic cells to secrete HMGB1; in turn, extracellular HMGB1 accelerates the delivery of CpG-ODNs to its receptor, leading to a TLR9-dependent augmentation of IL-6, IL-12, and TNFα secretion. Loss of HMGB1 leads to a defect in the IL-6, IL-12, TNFα, and iNOS response to CpG-ODN. However, lack of intracellular TLR9-associated HMGB1 can be compensated by extracellular HMGB1. Thus, the DNA-binding protein HMGB1 shuttles in and out of immune cells and regulates inflammatory responses to CpG-DNA.

scholarly journals Leptospira surface adhesin (Lsa21) induces Toll like receptor 2 and 4 mediated inflammatory responses in macrophages

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Syed M. Faisal ◽  
Vivek P. Varma ◽  
M. Subathra ◽  
Sarwar Azam ◽  
Anil K. Sunkara ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

Toll-like receptor 2 gene expression in the nasal and sinonasal mucosa

2016 ◽  
Vol 24 (4) ◽  
pp. 3
Author(s):  
E. V. Tyrnova ◽  
G. M. Aleshina ◽  
Yu. K. Yanov ◽  
V. N. Kokryakov
Keyword(s):  
Gene Expression ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Sinonasal Mucosa

scholarly journals Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages

2001 ◽  
Vol 69 (3) ◽  
pp. 1477-1482 ◽  
Author(s):  
Matthew Hirschfeld ◽  
Janis J. Weis ◽  
Vladimir Toshchakov ◽  
Cindy A. Salkowski ◽  
M. Joshua Cody ◽  
...  
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Periodontal Pathogen ◽  
Agonist Activity ◽  
Toll Like Receptor ◽  
Inflammatory Gene Expression ◽  
Murine Macrophages ◽  
Tlr4 Agonist ◽  
Differential Gene ◽  
Toll Like Receptor 2

ABSTRACT Lipopolysaccharide (LPS) derived from the periodontal pathogenPorphyromonas gingivalis has been reported to differ structurally and functionally from enterobacterial LPS. These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation of P. gingivalis LPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants. More importantly, TLR2 stimulation by this P. gingivalis LPS preparation resulted in differential expression of a panel of genes that are normally induced in murine macrophages by Escherichia coli LPS. These data suggest that (i) P. gingivalis LPS does not signal through TLR4 and (ii) signaling through TLR2 and through TLR4 differs quantitatively and qualitatively. Our data support the hypothesis that the shared signaling pathways elicited by TLR2 and by TLR4 agonists must diverge in order to account for the distinct patterns of inflammatory gene expression.

Sign in / Sign up

Export Citation Format

Share Document