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Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice
Yun-Feng Ni, Jian Wang, Xiao-Long Yan, Feng Tian, Jin-Bo Zhao, Yun-Jie Wang, Tao Jiang
Respiratory Research , 2010, DOI: 10.1186/1465-9921-11-33
Abstract: To investigate the protective effect of butyrate, a HDAC inhibitor, on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.ALI was induced in Balb/c mice by intratracheally instillation of LPS (1 mg/kg). Before 1 hour of LPS administration, the mice received butyrate (10 mg/kg) orally. The animals in each group were sacrificed at different time point after LPS administration. Pulmonary histological changes were evaluated by hematoxylin-eosin stain and lung wet/dry weight ratios were observed. Concentrations of interleukin (IL)-1β and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid (BALF) and concentrations of nitric oxide (NO) and myeloperoxidase (MPO) activity in lung tissue homogenates were measured by enzyme-linked immunosorbent assay (ELISA). Expression of nuclear factor (NF)-κB p65 in cytoplasm and nucleus was determined by Western blot analysis respectively.Pretreatment with butyrate led to significant attenuation of LPS induced evident lung histopathological changes, alveolar hemorrhage, and neutrophils infiltration with evidence of reduced MPO activity. The lung wet/dry weight ratios, as an index of lung edema, were reduced by butyrate administration. Butyrate also repressed the production of TNF-α, IL-1β and NO. Furthermore, the expression of NF-κB p65 in nucleus was markedly suppressed by butyrate pretreatment.Butyrate had a protective effect on LPS-induced ALI, which may be related to its effect on suppression of inflammatory cytokines production and NF-κB activation.Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are well defined and readily recognised clinical disorders caused by many clinical insults to the lung or because of predispositions to lung injury [1]. Sepsis and pneumonia are the main causes of ALI clinically. ALI occurring during gram-negative bacterial pneumonia and sepsis is caused in large part by lipopolysaccharide (LPS), a component of the cell walls of gram-negative bacteria [2]. When t
Butyrate-Induced Transcriptional Changes in Human Colonic Mucosa
Steven A. L. W. Vanhoutvin,Freddy J. Troost,Henrike M. Hamer,Patrick J. Lindsey,Ger H. Koek,Daisy M. A. E. Jonkers,Andrea Kodde,Koen Venema,Robert J. M. Brummer
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0006759
Abstract: Fermentation of dietary fiber in the colon results in the production of short chain fatty acids (mainly propionate, butyrate and acetate). Butyrate modulates a wide range of processes, but its mechanism of action is mostly unknown. This study aimed to determine the effects of butyrate on the transcriptional regulation of human colonic mucosa in vivo.
Peripheral Leukocytapheresis Attenuates Acute Lung Injury Induced by Lipopolysaccharide In Vivo
Zhi-Gao He,Jian Huang,Shun-Gang Zhou,Jing He,Fang-Xiang Chen,Xian-Kai Huang
Mediators of Inflammation , 2012, DOI: 10.1155/2012/694635
Abstract: The mortality of acute lung injury and acute respiratory distress syndrome (ALI/ARDS) remains high and efforts for prevention and treatments have shown little improvement over the past decades. The present study investigated the efficacy and mechanism of leukocytapheresis (LCAP) to partially eliminate peripheral neutrophils and attenuate lipopolysaccharide (LPS)-induced lung injury in dogs. A total of 24 healthy male mongrel dogs were enrolled and randomly divided into LPS, LCAP and LCAP-sham groups. All animals were injected with LPS to induce endotoxemia. The serum levels of leucocytes, neutrophil elastase, arterial blood gas, nuclear factor-kappa B (NF-κB) subunit p65 in lung tissues were measured. The histopathology and parenchyma apoptosis of lung tissues were examined. We found that 7, 3, and 7 animals in the LPS, LCAP, and sham-LCAP groups, respectively, developed ALI 36 h after LPS infusion. The levels of NF-κB p65 in lung tissue, neutrophils and elastase in blood, decreased significantly following LCAP. LCAP also alleviated apoptosis, and NF-κB p65 in lung tissues. Collectively, our results show that partial removal of leucocytes from peripheral blood decreases elastase level in serum. This, in turn, attenuates lung injuries and may potentially decrease the incidence of ALI.
Hypercapnia attenuates the endotoxin-induced tissue metabolic acidosis in esophageal mucosa
M Ponichter, H Billert, J Jastrzebski
Critical Care , 2003, DOI: 10.1186/cc1904
Abstract: Prospective, controlled experimental study.University laboratory.Thirty-six rabbits of both sexes, anesthetized with pentobarbital and ventilated mechanically (normoventilation).Animals were assigned to one of four groups: a) endotoxemic control group (n = 9), receiving intravenous Escherichia coli endotoxin (20 mg/kg bolus) via a peripheral vein; b) hypercapnia control group (n = 9), receiving exogenous carbon dioxide to achieve mild hypercapnia 60–90 mmHg; c) hypercapnia treated group (n = 9), treated identically to endotoxemic controls, and additionally receiving exogenous carbon dioxide to achieve mild hypercapnia 60–90 mmHg; d) control group (n = 9), receiving neither endotoxin nor carbon dioxide.We compared hemodynamics, blood gases, WBC, rectal temperature and tonometric findings in esophageal mucosa obtained in each group. Endotoxin injection decreased mean arterial pressure from 79 ± 9 to 54 ± 17.5 mmHg, decreased bicarbonate level from 21.6 ± 3 to 17.6 ± 4 mmHg, decreased WBC from 7.9 ± 2 to 1.9 ± 0.7 G/l, increased rectal temperature from 37.7 ± 1 to 39.9 ± 1.5°C, and caused a marked, continuous decrease in regional pH (pHi) from 7.40 ± 0.08 to 7.12 ± 0.11 at the end of the experiment. Hypercapnia alone had a minimal effect on the parameters and findings. Both hypercapnia and endotoxemia had no significant effect on regional CO2 (PrCO2) compared with controls, indicating lack of significant mucosal blood flow abnormalities throughout the experiment. In the hypercapnia treated group we observed an initial decrease in regional pH (pHi) from 7.42 ± 0.13 to 7.13 ± 0.08, but the value of this parameter remained stable (7.07 ± 0.05 at the end of the experiment) and the statistical difference compared with hypercapnia controls was nonsignificant (P > 0.05).1. Endotoxin injection caused marked tissue acidosis without disturbing esophageal mucosal blood flow, which indicates a metabolic character of acidosis and underlines the significance of intracellular abnorma
Synthetic RGDS peptide attenuates lipopolysaccharide-induced pulmonary inflammation by inhibiting integrin signaled MAP kinase pathways
Changsuk Moon, Jeong Han, Hyun-Jung Park, Jong Hah, Jihee Kang
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-18
Abstract: Saline or LPS (1.5 mg/kg) was administered i.t. with or without a single dose of RGDS (1, 2.5, or 5 mg/kg, i.p.), anti-αv or anti-β3 mAb (5 mg/kg, i.p.). Mice were sacrificed 4 or 24 h post-LPS.A pretreatment with RGDS inhibited LPS-induced increases in neutrophil and macrophage numbers, total protein levels and TNF-α and MIP-2 levels, and matrix metalloproteinase-9 activity in bronchoalveolar lavage (BAL) fluid at 4 or 24 h post-LPS treatment. RGDS inhibited LPS-induced phosphorylation of focal adhesion kinase and MAP kinases, including ERK, JNK, and p38 MAP kinase, in lung tissue. Importantly, the inhibition of the inflammatory responses and the kinase pathways were still evident when this peptide was administered 2 h after LPS treatment. Similarly, a blocking antibody against integrin αv significantly inhibited LPS-induced inflammatory cell migration into the lung, protein accumulation and proinflammatory mediator production in BAL fluid, at 4 or 24 h post-LPS. Anti-β3 also inhibited all LPS-induced inflammatory responses, except the accumulation of BAL protein at 24 h post-LPS.These results suggest that RGDS with high specificity for αvintegrins attenuates inflammatory cascade during LPS-induced development of acute lung injury.Acute lung injury is characterized by an intense pulmonary inflammatory response, with neutrophil recruitment, interstitial edema, disruption of epithelial integrity, and parenchymal injury [1]. The migration of leukocytes to inflamed sites depends on the interactions of various integrins expressed on leukocytes with the Ig superfamily of cell adhesion molecules (ICAM-1 and ICAM-2) present on the endothelium and with the extracellular matrix ligands. Multiple integrins participate in neutrophil migration into the lung during LPS-induced lung injury. In addition to β2 integrin (CD18), α4β1 and α5β1 integrins also contribute to β2-independent neutrophil migration during pulmonary inflammation [2]. However, neither β2 blockade nor α4 plus α5
Artemisinin Attenuates Lipopolysaccharide-Stimulated Proinflammatory Responses by Inhibiting NF-κB Pathway in Microglia Cells  [PDF]
Cansheng Zhu, Zhaojun Xiong, Xiaohong Chen, Fuhua Peng, Xueqiang Hu, Yanming Chen, Qing Wang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035125
Abstract: Microglial activation plays an important role in neuroinflammation, which contributes to neuronal damage, and inhibition of microglial activation may have therapeutic benefits that could alleviate the progression of neurodegeneration. Recent studies have indicated that the antimalarial agent artemisinin has the ability to inhibit NF-κB activation. In this study, the inhibitory effects of artemisinin on the production of proinflammatory mediators were investigated in lipopolysaccharide (LPS)-stimulated primary microglia. Our results show that artemisinin significantly inhibited LPS-induced production of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1) and nitric oxide (NO). Artemisinin significantly decreased both the mRNA and the protein levels of these pro-inflammatory cytokines and inducible nitric oxide synthase (iNOS) and increased the protein levels of IκB-α, which forms a cytoplasmic inactive complex with the p65-p50 heterodimeric complex. Artemisinin treatment significantly inhibited basal and LPS-induced migration of BV-2 microglia. Electrophoretic mobility shift assays revealed increased NF-κB binding activity in LPS-stimulated primary microglia, and this increase could be prevented by artemisinin. The inhibitory effects of artemisinin on LPS-stimulated microglia were blocked after IκB-α was silenced with IκB-α siRNA. Our results suggest that artemisinin is able to inhibit neuroinflammation by interfering with NF-κB signaling. The data provide direct evidence of the potential application of artemisinin for the treatment of neuroinflammatory diseases.
Treatment with TNF-α or bacterial lipopolysaccharide attenuates endocardial endothelial cell-mediated stimulation of cardiac fibroblasts
Leena Kuruvilla, Cheranellore Kartha
Journal of Biomedical Science , 2009, DOI: 10.1186/1423-0127-16-21
Abstract: We investigated whether the stimulatory effect of EE on cardiac fibroblasts would be altered when EECs are activated by the cytokine tumor necrosis factor-α (TNF-α) or the endotoxin bacterial lipopolysaccharide (LPS). Both TNF-α and LPS were found to independently attenuate the stimulatory effect of EE on cardiac fibroblasts. These agents lowered the synthesis or release of ET-1 and increased the secretion of TGF-β and NO.The findings of this study using endocardial endothelial cells (EECs) and neonatal cardiac fibroblasts demonstrate that pro-inflammatory cytokines cause altered secretion of paracrine factors by EECs and inhibit proliferation and lower collagen synthesis in fibroblasts. These changes may influence fibroblast response and extra cellular matrix remodeling in pathological conditions of the heart.The endocardial endothelium (EE) that lines the inner cavity of the heart is distinct from the microvascular endothelial cells in terms of embryological origin, cytoskeletal organization, receptor – mediated functions, electrophysiological properties, release of prostanoids and growth characteristics in culture [1]. The EE is strategically situated between the circulating blood and the cardiac muscle and it modulates cardiac muscle performance exactly as the vascular endothelium modulates vascular structure and vasomotor tone. Brutsaert et al [2] have demonstrated that EE is an important modulator of subjacent cardiac muscle performance. Dysfunction of this interface could be a critical factor in various pathological conditions of the heart. Evidence of physiologically significant paracrine interactions between the endocardial cell populations and muscle cells of the heart accrued from studies on factors of endothelial origin such as endothelins, angiotensin II, nitric oxide (NO), natriuretic peptides, bradykinin prostaglandins, adenylpurines, myofilament desensitizing element and enzymes such as angiotensin converting enzyme and kininase. Importantly, an imba
Bupleurum Polysaccharides Attenuates Lipopolysaccharide-Induced Inflammation via Modulating Toll-Like Receptor 4 Signaling  [PDF]
Jian Wu, Yun-Yi Zhang, Li Guo, Hong Li, Dao-Feng Chen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0078051
Abstract: Background Bupleurum polysaccharides (BPs), isolated from Bupleurum smithii var. parvifolium, possesses immunomodulatory activity, particularly on inflammation. Bacterial endotoxin lipopolysaccharide (LPS) triggers innate immune responses through Toll-like receptor 4 (TLR4) on host cell membrane. The present study was performed to evaluate whether the therapeutic efficacy of BPs on suppression of LPS’s pathogenecity could be associated with the modulating of TLR4 signaling pathway. Methodology/Principal Findings LPS stimulated expression and activation of factors in the TLR4 signaling system, including TLR4, CD14, IRAK4, TRAF6, NF-κB, and JNK, determined using immunocytochemical and/or Western blot assays. BPs significantly inhibited these effects of LPS. LPS increased pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-12p40, and IFN-β) and NO production, evaluated using ELISA and Griess reaction assays, respectively. BPs antagonized these effects of LPS. Interestingly, BPs alone augmented secretion of some pro-inflammatory cytokines of non-LPS stimulated macrophages and enhanced phagocytic activity towards fluorescent E.coli bioparticles. In a rat model of acute lung injury (ALI) with pulmonary hemorrhage and inflammation, BPs ameliorated lung injuries and suppressed TLR4 expression. Significance The therapeutic properties of BPs in alleviating inflammatory diseases could be attributed to its inhibitory effect on LPS-mediated TLR4 signaling.
18β-Glycyrrhetinic Acid Delivered Orally Induces Isolated Lymphoid Follicle Maturation at the Intestinal Mucosa and Attenuates Rotavirus Shedding  [PDF]
Jay M. Hendricks, Carol Hoffman, David W. Pascual, Michele E. Hardy
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0049491
Abstract: Glycyrrhizin, an abundant bioactive component of the medicinal licorice root is rapidly metabolized by gut commensal bacteria into 18β-glycyrrhetinic acid (GRA). Either or both of these compounds have been shown to have antiviral, anti-hepatotoxic, anti-ulcerative, anti-tumor, anti-allergenic and anti-inflammatory activity in vitro or in vivo. In this study, the ability of GRA to modulate immune responses at the small intestinal mucosa when delivered orally was investigated. Analysis of cytokine transcription in duodenal and ileal tissue in response to GRA treatment revealed a pattern of chemokine and chemokine receptor gene expression predictive of B cell recruitment to the gut. Consistent with this finding, GRA induced increases in CD19+ B cells in the lamina propria and B220+ B cell aggregates framed by CD11c+ dendritic cells in structures resembling isolated lymphoid follicles (ILF). Using a mouse model of rotavirus infection, GRA reduced the duration of viral antigen shedding, and endpoint serum antibody titers were higher in GRA-treated animals. Together the data suggest GRA delivered orally augments lymphocyte recruitment to the intestinal mucosa and induces maturation of B cell-rich ILF independently of ectopic antigenic stimulus. These results provide further support a role for dietary ligands in modulation of dynamic intestinal lymphoid tissue.
Activated Protein C Induces Endoplasmic Reticulum Stress and Attenuates Lipopolysaccharide-Induced Apoptosis Mediated by Glycogen Synthase Kinase-3β
Liang Luo,Tangfeng Lv,Qian Wang,Ting Zhang,Xiaoling Gu,Feng Xu,Yong Song
Mediators of Inflammation , 2012, DOI: 10.1155/2012/485279
Abstract: This study investigated the relationship between antiapoptotic activities induced by activated protein C and endoplasmic reticulum stress. In this study, it was observed that activated protein C elicited a rise in glucose-regulated protein 78 and glycogen synthase kinase-3β and inhibited apoptosis in human umbilical vein endothelial cells induced by lipopolysaccharide. Calcium inhibition did not alter the antiapoptotic effect of activated protein C. The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA. In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β.
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