Effects of Toll-like receptor ligands on RAW 264.7 macrophage morphology and zymosan phagocytosis

Sigola, Lynette B.; Fuentes, Ana-Lucía; Millis, Leonard M.; Vapenik, Jacqueline; Murira, Armstrong

doi:10.1016/j.tice.2016.04.002

Cited by 27 publications

(15 citation statements)

References 38 publications

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“…(28,29) We previously demonstrated intracellular macrophage delivery of GF9, GA31, and GE31 by macrophage-targeted GF9-HDL and GA/E31-HDL, respectively, and hypothesized that the observed macrophage endocytosis of these complexes is SR mediated. (16,17) To further investigate the molecular mechanisms involved in this process, we used J774 macrophages as a model for Kupffer cells and incubated them with rho B-labeled GF9-HDL or GA/ E31-HDL in the presence or absence of cytochalasin D, fucoidan, or BLT-1, which are known to inhibit all SRs, (30) SR-A, (31) or SR-BI, (32) respectively.…”

Section: Quantitatively Similar Macrophage Endocytosis Of Gf9-hdl Andmentioning

confidence: 99%

Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice

et al. 2018

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Alcoholic liver disease (ALD) is characterized by macrophage and neutrophil leukocyte recruitment and activation in the liver. Damage‐ and pathogen‐associated molecular patterns contribute to a self‐perpetuating proinflammatory state in ALD. Triggering receptor expressed on myeloid cells 1 (TREM‐1) is a surface receptor that amplifies inflammation induced by toll‐like receptors (TLRs) and is expressed on neutrophils and monocytes/macrophages. We hypothesized that TREM‐1 signaling contributes to proinflammatory pathway activation in ALD. Using an in vivo ALD model in mice, we tested the effects of ligand‐independent TREM‐1 inhibitory peptides that were formulated into human high‐density lipoprotein (HDL)‐mimicking complexes GF9‐HDL and GA/E31‐HDL. As revealed in vitro, macrophages endocytosed these rationally designed complexes through scavenger receptors. A 5‐week alcohol feeding with the Lieber‐DeCarli diet in mice resulted in increased serum alanine aminotransferase (ALT), liver steatosis, and increased proinflammatory cytokines in the liver. TREM‐1 messenger RNA (mRNA) expression was significantly increased in alcohol‐fed mice, and TREM‐1 inhibitors significantly reduced this increase. TREM‐1 inhibition significantly attenuated alcohol‐induced spleen tyrosine kinase (SYK) activation, an early event in both TLR4 and TREM‐1 signaling. The TREM‐1 inhibitors significantly inhibited macrophage (epidermal growth factor‐like module‐containing mucin‐like hormone receptor‐like 1 [F4/80], clusters of differentiation [CD]68) and neutrophil (lymphocyte antigen 6 complex, locus G [Ly6G] and myeloperoxidase [MPO]) markers and proinflammatory cytokines (monocyte chemoattractant protein 1 [MCP‐1], tumor necrosis factor α [TNF‐α], interleukin‐1β [IL‐1β], macrophage inflammatory protein 1α [MIP‐1α]) at the mRNA level compared to the HDL vehicle. Administration of TREM‐1 inhibitors ameliorated liver steatosis and early fibrosis markers (α‐smooth muscle actin [αSMA] and procollagen1α [Pro‐Col1α]) at the mRNA level in alcohol‐fed mice. However, the HDL vehicle also reduced serum ALT and some cytokine protein levels in alcohol‐fed mice, indicating HDL‐related effects. Conclusion: HDL‐delivered novel TREM‐1 peptide inhibitors ameliorate early phases of inflammation and neutrophil and macrophage recruitment and activation in the liver and attenuate hepatocyte damage and liver steatosis. TREM‐1 inhibition represents a promising therapeutic approach for further investigations in ALD.

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Section: Quantitatively Similar Macrophage Endocytosis Of Gf9-hdl Andmentioning

confidence: 99%

Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice

et al. 2018

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“…It requires recognition through a variety of germ-line encoded pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), that bind to conserved molecular patterns on microbes, referred to as pathogen-associated molecular patterns. Moreover, stimulation of PRRs initiates intracellular signaling pathways and eventually induces the expression of cytokine genes [ 21 , 26 , 27 ].…”

Section: Resultsmentioning

confidence: 99%

Immunomodulatory Activity of Octenyl Succinic Anhydride Modified Porang (Amorphophallus oncophyllus) Glucomannan on Mouse Macrophage-Like J774.1 Cells and Mouse Primary Peritoneal Macrophages

et al. 2017

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Porang is a local plant of Indonesia, which has a high content of glucomannan. In this study, porang glucomannan (PG) was esterified with octenyl succinic anhydride (OSA) to enhance emulsion properties to be widely used in food industry. OSA-modified PG (OSA-PG) enhanced the phagocytosis activity of macrophage-like J774.1 cells and mouse peritoneal macrophages. In addition, OSA-PG increased the production of IL-6 and TNF-α by enhancing their gene expression. Immunoblot analysis displayed that OSA-PG tended to activate both nuclear factor-κB and mitogen-activated protein kinase cascades. Treatment of OSA-PG with polymyxin B revealed that cytokine production induced by OSA-PG was not caused by endotoxin contamination. Our findings also indicated that OSA-PG activates macrophages through not only Toll-like receptor (TLR) 4, but another receptor. Overall findings suggested that OSA-PG has a potential as an immunomodulatory food factor by stimulating macrophages.

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“…Macrophages are derived from monocytes and participate in innate immunity, and the ability to secrete cytokines and chemokines is an important basis for macrophages in immune response and antigen presentation . The TLR4‐mediated reaction to inflammatory stimulation of macrophage is a highly complex cross‐talk pathway.…”

Section: Discussionmentioning

confidence: 99%

Monophosphoryl lipid A alleviated radiation‐induced testicular injury through TLR4‐dependent exosomes

Zhe

Cao

Liao

et al. 2020

J Cellular Molecular Medi

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Radiation protection on male testis is an important task for ionizing radiation‐related workers or people who receive radiotherapy for tumours near the testicle. In recent years, Toll‐like receptors (TLRs), especially TLR4, have been widely studied as a radiation protection target. In this study, we detected that a low‐toxicity TLR4 agonist monophosphoryl lipid A (MPLA) produced obvious radiation protection effects on mice testis. We found that MPLA effectively alleviated testis structure damage and cell apoptosis induced by ionizing radiation (IR). However, as the expression abundance differs a lot in distinct cells and tissues, MPLA seemed not to directly activate TLR4 singling pathway in mice testis. Here, we demonstrated a brand new mechanism for MPLA producing radiation protection effects on testis. We observed a significant activation of TLR4 pathway in macrophages after MPLA stimulation and identified significant changes in macrophage‐derived exosomes protein expression. We proved that after MPLA treatment, macrophage‐derived exosomes played an important role in testis radiation protection, and specially, G‐CSF and MIP‐2 in exosomes are the core molecules in this protection effect.

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Effects of Toll-like receptor ligands on RAW 264.7 macrophage morphology and zymosan phagocytosis

Cited by 27 publications

References 38 publications

Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice

Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice

Immunomodulatory Activity of Octenyl Succinic Anhydride Modified Porang (Amorphophallus oncophyllus) Glucomannan on Mouse Macrophage-Like J774.1 Cells and Mouse Primary Peritoneal Macrophages

Monophosphoryl lipid A alleviated radiation‐induced testicular injury through TLR4‐dependent exosomes

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