Induction of Cyclooxygenase-2 Signaling by <i>Stomatococcus mucilaginosus</i> Highlights the Pathogenic Potential of an Oral Commensal

Yuan, Zhujun; Panchal, Dipti; Syed, Mansoor Ali; Mehta, Hiren J.; Joo, Myungsoo; Hadid, Walid; Sadikot, Ruxana T.

doi:10.4049/jimmunol.1300883

Cited by 15 publications

(18 citation statements)

References 62 publications

(91 reference statements)

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“…In a previous study, we demonstrated that activation of the signaling pathway of MyD88, an adaptor molecule of all TLRs, except TLR3, inhibited I/R injury in the small intestine via induction of COX-2 expression and PGE 2 synthesis [37] . Although some reports indicated involvement of the TLR2/MyD88-dependent signaling pathway in the induction of COX-2 [38] , [39] , [40] , we found that TLR2 deficiency did not affect COX-2 expression and PGE 2 synthesis in the small intestine during the development of intestinal I/R injury. Several lines of evidence demonstrated that the TLR4/MyD88-dependent pathway induced COX-2 expression, leading to prevention of damage and maintenance of mucosal integrity in the gastrointestinal tract [41] , [42] , [43] .…”

Section: Discussioncontrasting

confidence: 87%

Toll-Like Receptor 2 Mediates Ischemia-Reperfusion Injury of the Small Intestine in Adult Mice

et al. 2014

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Toll-like receptor 2 (TLR2) recognizes conserved molecular patterns associated with both gram-negative and gram-positive bacteria, and detects some endogenous ligands. Previous studies demonstrated that in ischemia-reperfusion (I/R) injury of the small intestine, the TLR2-dependent signaling exerted preventive effects on the damage in young mice, but did not have a significant effect in neonatal mice. We investigated the role of TLR2 in adult ischemia-reperfusion injury in the small intestine. Wild-type and TLR2 knockout mice at 16 weeks of age were subjected to intestinal I/R injury. Some wild-type mice received anti-Ly-6G antibodies to deplete circulating neutrophils. In wild-type mice, I/R induced severe small intestinal injury characterized by infiltration by inflammatory cells, disruption of the mucosal epithelium, and mucosal bleeding. Compared to wild-type mice, TLR2 knockout mice exhibited less severe mucosal injury induced by I/R, with a 35%, 33%, and 43% reduction in histological grading score and luminal concentration of hemoglobin, and the numbers of apoptotic epithelial cells, respectively. The I/R increased the activity of myeloperoxidase (MPO), a marker of neutrophil infiltration, and the levels of mRNA expression of tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and cyclooxygenase-2 (COX-2) in the small intestine of the wild-type mice by 3.3-, 3.2-, and 13.0-fold, respectively. TLR2 deficiency significantly inhibited the I/R-induced increase in MPO activity and the expression of mRNAs for TNF-α and ICAM-1, but did not affect the expression of COX-2 mRNA. I/R also enhanced TLR2 mRNA expression by 2.9-fold. TLR2 proteins were found to be expressed in the epithelial cells, inflammatory cells, and endothelial cells. Neutrophil depletion prevented intestinal I/R injury in wild-type mice. These findings suggest that TLR2 may mediate I/R injury of the small intestine in adult mice via induction of inflammatory mediators such as TNF-α and ICAM-1.

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Section: Discussioncontrasting

confidence: 87%

Toll-Like Receptor 2 Mediates Ischemia-Reperfusion Injury of the Small Intestine in Adult Mice

et al. 2014

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“…Samples were prepared in RIPA buffer containing proteinase and phosphatase inhibitors according to instructions (Sigma Aldrich, USA). Western blotting was performed as described previously 53 , appropriate primary antibodies and horseradish peroxidase-conjugated secondary antibodies were used prior to visualization via chemiluminescence (Amersham Biosciences, USA).…”

Section: Methodsmentioning

confidence: 99%

HIV-related proteins prolong macrophage survival through induction of Triggering receptor expressed on myeloid cells-1

Yuan

Fan

Staitieh

et al. 2017

Sci Rep

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Triggering receptor expressed on myeloid cells-1(TREM-1) is a member of the superimmunoglobulin receptor family. We have previously shown that TREM-1 prolongs survival of macrophages treated with lipoolysaccharide through Egr2-Bcl2 signaling. Recent studies suggest a role for TREM-1 in viral immunity. Human immunodeficiency virus-1 (HIV) targets the monocyte/macrophage lineage at varying stages of infection. Emerging data suggest that macrophages are key reservoirs for latent HIV even in individuals on antiretroviral therapy. Here, we investigated the potential role of TREM-1 in HIV latency in macrophages. Our data show that human macrophages infected with HIV show an increased expression of TREM-1. In parallel, direct exposure to the HIV-related proteins Tat or gp120 induces TREM-1 expression in macrophages and confers anti-apoptotic attributes.NF-κB p65 silencing identified that these proteins induce TREM-1 in p65-dependent manner. TREM-1 silencing in macrophages exposed to HIV-related proteins led to increased caspase 3 activation and reduced Bcl-2 expression, rendering them susceptible to apotosis. These novel data reveal that TREM-1 may play a critical role in establishing HIV reservoir in macrophages by inhibiting apoptosis. Therefore, targeting TREM-1 could be a novel therapeutic approach to enhance clearance of the HIV reservoir, at least within the macrophage pools.

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“…Lung samples were placed in 50 mmol/l K 2HPO4 buffer (pH 6.0) containing 0.5% hexadecyl trimethyl ammonium bromide and stored at Ϫ80°C until used. Myeloperoxidase (MPO) activity was measured as described previously (41,51).…”

Section: Methodsmentioning

confidence: 99%

TREM-1-accentuated lung injury via miR-155 is inhibited by LP17 nanomedicine

Yuan

Syed

Panchal

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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Triggering receptors expressed on myeloid cell-1 (TREM-1) is a superimmunoglobulin receptor expressed on myeloid cells. Synergy between TREM-1 and Toll-like receptor amplifies the inflammatory response; however, the mechanisms by which TREM-1 accentuates inflammation are not fully understood. In this study, we investigated the role of TREM-1 in a model of LPS-induced lung injury and neutrophilic inflammation. We show that TREM-1 is induced in lungs of mice with LPS-induced acute neutrophilic inflammation. TREM-1 knockout mice showed an improved survival after lethal doses of LPS with an attenuated inflammatory response in the lungs. Deletion of TREM-1 gene resulted in significantly reduced neutrophils and proinflammatory cytokines and chemokines, particularly IL-1β, TNF-α, and IL-6. Physiologically deletion of TREM-1 conferred an immunometabolic advantage with low oxygen consumption rate (OCR) sparing the respiratory capacity of macrophages challenged with LPS. Furthermore, we show that TREM-1 deletion results in significant attenuation of expression of miR-155 in macrophages and lungs of mice treated with LPS. Experiments with antagomir-155 confirmed that TREM-1-mediated changes were indeed dependent on miR-155 and are mediated by downregulation of suppressor of cytokine signaling-1 (SOCS-1) a key miR-155 target. These data for the first time show that TREM-1 accentuates inflammatory response by inducing the expression of miR-155 in macrophages and suggest a novel mechanism by which TREM-1 signaling contributes to lung injury. Inhibition of TREM-1 using a nanomicellar approach resulted in ablation of neutrophilic inflammation suggesting that TREM-1 inhibition is a potential therapeutic target for neutrophilic lung inflammation and acute respiratory distress syndrome (ARDS).

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Induction of Cyclooxygenase-2 Signaling by Stomatococcus mucilaginosus Highlights the Pathogenic Potential of an Oral Commensal

Cited by 15 publications

References 62 publications

Toll-Like Receptor 2 Mediates Ischemia-Reperfusion Injury of the Small Intestine in Adult Mice

Toll-Like Receptor 2 Mediates Ischemia-Reperfusion Injury of the Small Intestine in Adult Mice

HIV-related proteins prolong macrophage survival through induction of Triggering receptor expressed on myeloid cells-1

TREM-1-accentuated lung injury via miR-155 is inhibited by LP17 nanomedicine

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