Macrophage-activating lipopeptide-2 induces cyclooxygenase-2 and prostaglandin E2 via toll-like receptor 2 in human placental trophoblast cells

Mitsunari, Masahiro; Yoshida, Souichi; Shoji, Takako; Tsukihara, Satoru; Iwabe, Tomio; Harada, Tasuku; Terakawa, Naoki

doi:10.1016/j.jri.2006.02.003

Cited by 79 publications

(85 citation statements)

References 24 publications

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“…Particulate Ni and air pollution in the form of diesel exhaust particles (DEP) stimulates COX-2 expression in bronchial epithelial BEAS-2B cells (34,35), which suggests that induction of COX-2 may provide a mechanism whereby air particulate matter pollution stimulates an inflammatory response in pulmonary cells. Microbial stimuli in the form of MALP-2 have also been shown to activate COX-2 (36). It would therefore stand to reason that combined exposures to chemical and microbial stimuli could interact to enhance induction of COX-2 as was observed in the current study.…”

Section: Discussionsupporting

confidence: 57%

“…It has yet to be determined whether Ni and MALP-2 synergistically induce COX-2 mRNA through transcriptional or post-transcriptional mechanisms. Given that NFkB and C/EBP are important signaling pathways in inflammatory responses (37,38), and both MALP-2 and NiSO 4 can activate NFkB (19,39), one possible explanation is that Ni and MALP-2 activate C/EBP in concert with members of the NF-kB/Rel family to induce COX-2 promoter activity. Alternatively, it is also possible that the dramatic increase in COX-2 may be mediated, in part, through enhanced stabilization of COX-2 mRNA levels.…”

Section: Discussionmentioning

confidence: 99%

“…This is of importance as (1) real life exposures are more like to involve mixtures of chemical and microbial agents, and (2) induction of COX-2 plays an important role in the production of immune-modulators and is widely recognized as having an important role in the onset of inflammation in the lung (39,(48)(49)(50). The findings that COX-2 contributes to the synergistic production of CXCL8 and inhibition of CXCL10 in HLF present a potential mechanism whereby exposure to PM-derived metals can exacerbate cellular responses to microbial stimuli and modulate pulmonary inflammation and its consequences such as fibrosis and angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Brant¹,

Fabisiak²

2008

Am J Respir Cell Mol Biol

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Particulate matter air pollution (PM) has been linked with chronic respiratory diseases. Real-life exposures are likely to involve a mixture of chemical and microbial stimuli, yet little attention has been paid to the potential interactions between PM components (e.g., Ni) and microbial agents on the development of inflammatory-like conditions in the lung. Using the Toll-like receptor (TLR)-2 agonist MALP-2 as a lipopeptide relevant to microbial colonization, we hypothesized that nickel sensitizes human lung fibroblasts (HLF) for microbial-driven chemokine release through modulation of TLR signaling pathways. NiSO 4 (200 mM) synergistically enhanced CXCL8, yet antagonized CXCL10 mRNA expression and protein release from HLF in response to MALP-2. RT 2 -PCR pathway-focused array results indicated that NiSO 4 exposure did not alter the expression of TLRs or their downstream signaling mediators, yet significantly increased the expression of cyclooxygenase 2 (COX-2). Moreover, when NiSO 4 was given in combination with MALP-2, there was an amplified induction of COX-2 mRNA and protein along with its metabolic product, PGE2, in HLF. The COX-2 inhibitor, NS-398, attenuated NiSO 4 and MALP-2-induced PGE2 and CXCL8 release and partially reversed the NiSO 4 -dependent inhibition of MALP-2-induced CXCL10 release from HLF. These data indicate that NiSO 4 alters the pattern of TLR-2-dependent chemokine release from HLF via a COX-2-mediated pathway. The quantitative and qualitative effects of NiSO 4 on microbial-driven chemokine release from HLF shed new light on how PM-derived metals can exacerbate respiratory diseases.Keywords: COX-2; nickel; inflammation; chemokines; fibroblasts Particulate matter air pollution (PM) is a contributing risk factor for many adverse health effects, including respiratory diseases (1). Real-life scenarios are likely to involve exposures not only to chemical stresses such as PM, but microbial stimuli as well. While much attention has been paid to microbial-driven inflammation in the lung, limited information is available regarding the potential interactions between PM exposures and microbial stress on respiratory function. There are reports, however, of increased numbers of hospitalizations for respiratory disorders including infections on days of increased levels of PM (2). In support of these epidemiologic findings, several rodent models have shown PM exposure can increase susceptibility to infectious bacteria such as Listeria monocytogenes and Streptococcus pneumoniae (3, 4).Recent evidence suggests that colonization with species originally considered commensal and not causing overt disease (e.g., Mycoplasma fermentans) also has the potential to interact with other stimuli and/or alter biological responses in infected host cells (5, 6). For example, we have previously shown that exposure of human lung fibroblast cells (HLF) to M. fermentans synergistically enhances the release of IL-6 by PM in the form of residual oil fly ash (ROFA) compared to either stimulus alone (7). It is well recognized t...

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Brant¹,

Fabisiak²

2008

Am J Respir Cell Mol Biol

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“…Ten different human TLRs, each responding to a specific set of ligands, have been identified [4]. TLR expression and activation in primary trophoblasts [5][6][7][8][9][10] may contribute substantially to development of inflammatory pregnancy complications such as preeclampsia [11][12][13]. In Tangerås/Stødle et al [7] we demonstrated a broad functional TLR profile in primary first trimester trophoblasts, while the trophoblast cell line BeWo showed no TLR mediated cytokine response.…”

Section: Introductionmentioning

confidence: 93%

“…LPS-induced IL-8 release from HTR-8 cells (the non-immortalized parental cell line of HTR-8/SVneo) has been reported, but only after very high doses of LPS [35]. In this study trophoblast cell lines have been compared to primary trophoblasts from first trimester, but the broad TLR expression profile and cytokine responsiveness has also been reported for primary trophoblasts at later gestations [8][9][10]. Our findings suggest the suitability of SGHPL-5 cells in studying trophoblast responses to infection and tissue damage.…”

Section: Multivariate Analysis Of Tlr Gene Expression and Cytokine Rementioning

confidence: 99%

Toll-like receptor profiling of seven trophoblast cell lines warrants caution for translation to primary trophoblasts

et al. 2015

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Toll-Like Receptors in Stem/Progenitor Cells

Sallustio

Picerno

Tatullo

et al. 2021

Handbook of Experimental Pharmacology

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Macrophage-activating lipopeptide-2 induces cyclooxygenase-2 and prostaglandin E2 via toll-like receptor 2 in human placental trophoblast cells

Cited by 79 publications

References 24 publications

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Toll-like receptor profiling of seven trophoblast cell lines warrants caution for translation to primary trophoblasts

Toll-Like Receptors in Stem/Progenitor Cells

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