Inhibition of lipopolysaccharide‐mediated rat alveolar macrophage activation <i>in vitro</i> by antiflammin‐1

Han, Jian; Li, Chen; Liu, Huijun; Fen, Dandan; Hu, Wanxiang; Liu, Yong; Guan, Cha Xiang; Luo, Ziqiang

doi:10.1016/j.cellbi.2008.04.023

Cited by 7 publications

(9 citation statements)

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“…LPS-TLR4 signaling is one of the most important inflammatory response signal pathways (25). As AMs are the major effector cells that participate in the initiation and development of ALI (4,5,26), modulating the excessive inflammatory response to pathogenassociated molecular patterns in AMs during systemic inflammatory response syndrome is a therapeutic target for treating ALI/ARDS. PALM3 is a novel interactive partner of single immunoglobulin IL-1 receptor-related molecule (SIgIRR) and may function as an adaptor in LPS-TLR4 signaling (19).…”

Section: Discussionmentioning

confidence: 99%

“…Rat AMs were routinely grown in ham's F12 medium supplemented with 10% fetal bovine serum and seeded in 6-well plates at a density of 1x10 5 cells/well. After the cell growth reached 50-60% confluence, rat AMs were treated with 0.5 µg/ml LPS (Escherichia coli 0111: B4; Sigma-Aldrich; Merck KGaA, Darmstadt, Germany) as described previously to simulate ALI in an in vitro model (4,5). The total RNA and protein were isolated before the treatment with LPS and at 3, 6, 12, 24 and 48 h following the addition of LPS for the analysis of PALM3 expression.…”

Section: Methodsmentioning

confidence: 99%

“…Alveolar macrophages (AMs) are the most abundant cells in the alveoli, distal airspaces and conducting airways (4). They form the first line of defense against airborne particles and microbes.…”

Section: Paralemmin-3 Contributes To Lipopolysaccharide-induced Inflamentioning

confidence: 99%

“…They form the first line of defense against airborne particles and microbes. AMs account for 90% of the cells in bronchoalveolar lavage fluid; as the main immune cells, they recognize pathogen-associated molecular patterns and trigger innate immunity and host defenses (4,5). Previous studies have demonstrated that macrophages contribute to the modulation of inflammatory responses during ALI/ARDS as well as to the resolution of inflammation and tissue repair in lungs (5,6).…”

Section: Paralemmin-3 Contributes To Lipopolysaccharide-induced Inflamentioning

confidence: 99%

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Paralemmin-3 contributes to lipopolysaccharide-induced inflammatory response and is involved in lipopolysaccharide-Toll-like receptor-4 signaling in alveolar macrophages

Chen

Tang

et al. 2017

Int J Mol Med

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Alveolar macrophages (AMs) are the first line of defense against foreign stimulation in alveoli, and they participate in inflammatory responses during acute lung injury (ALI). Previous studies indicated that paralemmin-3 (PALM3) expression is induced by lipopolysaccharides (LPS) and may be involved in LPS-Toll-like receptor 4 (TLR4) signaling in alveolar epithelial cells. The aim of the present study was to investigate the effect of PALM3 on LPS-induced inflammation and its underlying mechanisms in rat AMs. For this purpose, the authors detected the expression of PALM3 in AMs by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting following LPS stimulation. Following this, a recombinant adenovirus expressing short hairpin RNA (shRNA) for PALM3 was constructed, as well as a recombinant adenovirus carrying the rat PALM3 gene to modulate the expression of PALM3 in rat AMs. At 48 h after transfection, the PALM3 expression in AMs was detected by RT-qPCR and western blotting. The levels of several cytokines and the activity of nuclear factor-κB and interferon regulatory factor 3 in AMs were measured after LPS stimulation. The localization of PALM3 and LPS-TLR4 signaling adaptor molecules in AMs was analyzed by confocal microscopy, and the physical interactions of PALM3 with these adaptors were assessed by co-immunoprecipitation assays. LPS induced PALM3 expression in AMs and that PALM3 expression promoted the LPS-induced inflammatory response, while PALM3 downregulation suppressed the LPS-induced inflammatory response in AMs. In addition, the results demonstrated that PALM3 could interact with TLR4, myeloid differentiation factor 88, interleukin (IL)-1 receptor associated kinase-1, tumor necrosis factor receptor associated factor-6, and Toll-IL-1 receptor containing adapter molecule-2 in AMs after LPS stimulation. These results suggested that PALM3 contributes to the LPS-induced inflammatory response and participates in LPS-TLR4 signaling in AMs. These data may provide the basis for the development of novel targeted therapeutic strategies of treating ALI.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Paralemmin-3 Contributes To Lipopolysaccharide-induced Inflamentioning

confidence: 99%

Section: Paralemmin-3 Contributes To Lipopolysaccharide-induced Inflamentioning

confidence: 99%

See 2 more Smart Citations

Paralemmin-3 contributes to lipopolysaccharide-induced inflammatory response and is involved in lipopolysaccharide-Toll-like receptor-4 signaling in alveolar macrophages

Chen

Tang

et al. 2017

Int J Mol Med

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“…In the present study, continuous treatment with AF-1 (2 mg · kg -1 ) starting on Day 0 significantly alleviated the inflammation on Day 7 and the collagen deposition on Day 28 in the bleomycin-induced model of lung injury (Figures 2 and 3). The anti-inflammatory activity of AF-1 in this model may be due to its blockade of neutrophil trafficking, suppression of the activation of macrophages and reduction of the production and release of inflammatory mediators [11,12]. …”

Section: Discussionmentioning

confidence: 99%

Antiflammin-1 attenuates bleomycin-induced pulmonary fibrosis in mice

et al. 2013

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BackgroundAntiflammin-1 (AF-1), a derivative of uteroglobin (UG), is a synthetic nonapeptide with diverse biological functions. In the present study, we investigated whether AF-1 has a protective effect against bleomycin-induced pulmonary fibrosis.MethodsC57BL/6 mice were injected with bleomycin intratracheally to create an animal model of bleomycin-induced pulmonary fibrosis. On Day 7 and Day 28, we examined the anti-inflammatory effect and antifibrotic effect, respectively, of AF-1 on the bleomycin-treated mice. The effects of AF-1 on the transforming growth factor-beta 1 (TGF-β1)-induced proliferation of murine lung fibroblasts (NIH3T3) were examined by a bromodeoxycytidine (BrdU) incorporation assay and cell cycle analysis.ResultsSevere lung inflammation and fibrosis were observed in the bleomycin-treated mice on Day 7 and Day 28, respectively. Administration of AF-1 significantly reduced the number of neutrophils in the bronchoalveolar lavage fluid (BALF) and the levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) in the lung homogenates on Day 7. Histological examination revealed that AF-1 markedly reduced the number of infiltrating cells on Day 7 and attenuated the collagen deposition and destruction of lung architecture on Day 28. The hydroxyproline (HYP) content was significantly decreased in the AF-1-treated mice. In vitro, AF-1 inhibited the TGF-β1-induced proliferation of NIH3T3 cells, which was mediated by the UG receptor.ConclusionsAF-1 has anti-inflammatory and antifibrotic actions in bleomycin-induced lung injury. We propose that the antifibrotic effect of AF-1 might be related to its suppression of fibroblast growth in bleomycin-treated lungs and that AF-1 has potential as a new therapeutic tool for pulmonary fibrosis.

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Anti‐Inflammatory Peptide‐Conjugated Silk Fibroin/Cryogel Hybrid Dual Fiber Scaffold with Hierarchical Structure Promotes Healing of Chronic Wounds

Fan,

Zhao,

et al. 2024

Advanced Materials

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Chronic wounds resulting from diabetes, pressure, radiation therapy, and other factors continue to pose significant challenges in wound healing. To address this, our study introduces a novel hybrid fibroin fibrous scaffold (FFS) comprising randomly arranged fibroin fibers and vertically aligned cryogel fibers (CF). The fibroin scaffold was efficiently degummed at room temperature and simultaneously formed a porous structure. The aligned cryogel fibers were produced via directional freeze‐drying, achieved by controlling solution concentration and freezing polymerization temperature. The incorporation of aligned cryogel fibers into the expanded fibroin fiber scaffold led to enhanced cell infiltration both in vitro and in vivo, further elevating the hybrid scaffold's tissue compatibility. We also conjugated the anti‐inflammatory peptide 1 (AP‐1) to the hybrid fibrous scaffold, effectively transforming the inflammatory status of chronic wounds from pro‐inflammatory to pro‐reparative. Consequently, the FFS‐AP1+CF group demonstrated superior granulation tissue formation, angiogenesis, collagen deposition, and re‐epithelialization during the proliferative phase compared to the commercial product PELNAC. Moreover, the FFS‐AP1+CF group displayed epidermis thickness, numbers of regenerated hair follicles, and collagen density closer to normal skin tissue. Our findings highlight the potential of random fibroin fibers/aligned cryogel fibers hybrid fibrous scaffold as a promising approach for skin tissue filling and tissue regeneration.This article is protected by copyright. All rights reserved

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Inhibition of lipopolysaccharide‐mediated rat alveolar macrophage activation in vitro by antiflammin‐1

Cited by 7 publications

References 40 publications

Paralemmin-3 contributes to lipopolysaccharide-induced inflammatory response and is involved in lipopolysaccharide-Toll-like receptor-4 signaling in alveolar macrophages

Paralemmin-3 contributes to lipopolysaccharide-induced inflammatory response and is involved in lipopolysaccharide-Toll-like receptor-4 signaling in alveolar macrophages

Antiflammin-1 attenuates bleomycin-induced pulmonary fibrosis in mice

Anti‐Inflammatory Peptide‐Conjugated Silk Fibroin/Cryogel Hybrid Dual Fiber Scaffold with Hierarchical Structure Promotes Healing of Chronic Wounds

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