Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The binding of metal ions to Pseudomonas aeruginosa PAO1 cells attached to a ZnSe surface has been observed in this research through cation exchange experiments using ATR-IR spectroscopy. A biofilm consisting of a single layer of Pseudomonas aeruginosa PAO1 cells was formed on a ZnSe prism by flowing a bacterial suspension in a 0.03 mol L(-)(1) NaNO(3) solution at pH 5.0 across its surface. Exposure of the biofilm to chromium(III) nitrate solution resulted in increases in all band absorbances. This absorbance increase has been attributed to the binding of chromium(III) to the bacterial exopolymers associated with the prism surface. The chromium(III) binding causes the exopolymers to contract and move the bacterial cell closer to the ZnSe surface. Further study of chromium(III) ion exchange using a mutant P. aeruginosa with a truncated lipopolysaccharide (LPS) chain resulted in much smaller absorbance changes. This observation supports the view that the extension of bacterial exopolymers and hence the distance of the bacterial cell from the surface is strongly influenced by environmental factors such as the presence of metal cations. Following chromium(III) cation exchange, the bacterial band absorbances remained constant even when the bacteria were washed with a 0.03 mol L(-)(1) NaNO(3) solution, indicating that the chromium(III) was irreversibly bound. Ion exchange with nickel(II) and cobalt(II) nitrate solutions within identical biofilms showed that these cations caused relatively small increases in absorbances that were reversible, indicating that nickel(II) and cobalt(II) are less strongly bound than chromium(III) within P. aeruginosa biofilms. The absence of discernible IR spectral changes with metal binding appears to indicate a predominantly electrostatic mechanism for binding of Cr(III), Ni(II), and Co(II) ions by bacteria in the early stages of biofilm formation.
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PMID:Monitoring metal ion binding in single-layer Pseudomonas aeruginosa biofilms using ATR-IR spectroscopy. 1637 33

Poor ambient air quality is associated with increased morbidity and mortality, including respiratory infections. However, its effects on various host-defense mechanisms are poorly understood. This study utilized an in vitro model to study the effect of particulate matter (PM(2.5)) on one antimicrobial mechanism of host defense in the airway, beta-defensin-2 and its bovine homologue, tracheal antimicrobial peptide (TAP) induction in response to lipopolysaccharide (LPS) and IL-1beta. Our model utilized cultured primary bovine tracheal epithelial (BTE) cells and the human alveolar type II epithelial cell line, A549, treated with 0-20 microg/cm(2) residual oil fly ash (ROFA) for 6 h. The cells were then washed and stimulated for 18 h with 100 ng/ml LPS or for 6 h with 100 ng/ml IL-1beta. ROFA inhibited the LPS-induced increase in TAP mRNA and protein without inducing significant cytotoxicity. As little as 2.5 microg/cm(2) of ROFA inhibited LPS-induced TAP gene expression by 30%. The inhibitory activity was associated with the soluble fraction and not the washed particle. The activity in the leachate was attributed to vanadium, but not nickel or iron. SiO(2) and TiO(2) were utilized as controls and did not inhibit LPS induction of TAP gene expression in BTE. ROFA also inhibited the increase of IL-1beta-induced human beta-defensin-2, a homologue of TAP, in A549 cells. The results show that ROFA, V(2)O(5), and VOSO(4) inhibit the ability of airway epithelial cells to respond to inflammatory stimuli at low, physiologically relevant doses and suggest that exposure to these agents could result in an impairment of defense against airborne pathogens.
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PMID:Inhibition of beta-defensin gene expression in airway epithelial cells by low doses of residual oil fly ash is mediated by vanadium. 1664 20

Activation of the innate immune system might predispose a host to toxicant-induced inflammation. In vitro macrophage models were employed to investigate the effects of preexposure to Toll-like receptor (TLR) agonists on induction of proinflammatory cytokine gene expression by the trichothecene mycotoxin deoxynivalenol (DON) and other toxicants. Priming of the murine RAW 264.7 macrophage line or peritoneal murine macrophages with the TLR4 agonist lipopolysaccharide (LPS) at 100 ng/ml for 4, 8, and 16 h significantly increased DON-induced IL-1beta, IL-6, and TNF-alpha mRNA expression as compared to LPS or DON alone. The minimum LPS concentration for sensitization of both cell types was 1 ng/ml. LPS priming also potentiated IL-1beta mRNA induction by DON in human whole-blood cultures, suggesting the relevance of the murine findings. As observed for LPS, preexposure to TLR agonists including zymosan (TLR2), poly (I:C) (TLR3), flagellin (TLR5), R848 (TLR7/8), and ODN1826 (TLR9) sensitized RAW 267.4 cells to DON-induced proinflammatory gene expression. Amplified proinflammatory mRNA expression was similarly demonstrated in LPS-sensitized RAW 264.7 cells exposed to the microbial toxins satratoxin G, Shiga toxin, and zearalenone as well as the anthropogenic toxicants nickel chloride, triphenyltin, 2,4-dinitrochlorobenzene, and 2,3,7,8-tetrachlorodibenzodioxin. The results suggest that prior TLR activation might render macrophages highly sensitive to subsequent induction of proinflammatory gene expression by xenobiotics with diverse mechanisms of action.
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PMID:Toll-like receptor priming sensitizes macrophages to proinflammatory cytokine gene induction by deoxynivalenol and other toxicants. 1668 89

Nickel is a component of biomedical alloys that is released during corrosion and causes inflammation in tissues by as yet unknown mechanisms. Recent data show that Ni(II) at concentrations of 10-50 microM amplifies lipopolysaccharide-triggered, NFkappaB-mediated cytokine secretion from monocytes. In the current study, we tested the hypothesis that Ni(II) amplifies cytokine secretion by activating the Nrf2 antioxidant pathway rather than by enhancing activity of the NFkappaB signaling pathway. Human THP1 monocytes were exposed to Ni(II) concentrations of 10-30 microM for 6-72 h, then immunoblots of whole-cell lysates or cytosolic and nuclear proteins were used to detect changes in Nrf2 or NFkappaB signaling. Our results show that Ni(II) increased (by 1-2 fold) whole-cell Nrf2 levels and nuclear translocation of Nrf2, and amplified lipopolysaccharide (LPS)-induction of Nrf2 (by 3-5 fold), but had no detectable effect on the initial activation or nuclear translocation of NFkappaB. Because Nrf2 target gene products are known regulators of NFkappaB nuclear activity, our results suggest that Ni(II) may affect cytokine secretion indirectly via modulation of the Nrf2 pathway.
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PMID:Ni(II) activates the Nrf2 signaling pathway in human monocytic cells. 1680 55

Type 1 and type 2 cytokines are primary mediators in contact allergy and aeroallergen-mediated disorders, respectively. For both types of disease, dendritic cells (DCs) are pivotal in initiating immune hyperresponsiveness. We studied whether contact and respiratory allergens possess intrinsic capacities to polarize DC towards DC1 and DC2 functions, independent of environmental factors. Human monocyte-derived DCs were exposed to the positive controls [type 1: lipopolysaccharide (LPS) + interferon-gamma; type 2: LPS + prostaglandin E(2)], contact allergens [2,4-dinitrochlorobenzene (DNCB), oxazolone (OXA), and nickel sulfate (NiSO(4))], and respiratory allergens [trimellitic anhydride (TMA) and the protein allergen derived from Dermatophagoides pteronyssinus (Der p1)]. The polarizing potentials of the allergens on DCs were determined by the secretion of type 1 [tumour necrosis factor-alpha (TNF-alpha), CXCL10, and interleukin (IL)-12p70] and type 2 (IL-10) cytokines. The contact allergens, DNCB and OXA, induced strict type 1 DC polarization, whereas the respiratory allergens, TMA and Der p1, showed strict type 2 DC polarization. The contact allergen, NiSO(4), induced both DC1 (TNF-alpha and CXCL10 production) and DC2 (decreased IL-12p70/IL-10 ratio) features. These results support the view that allergens have an intrinsic capacity to skew immune responses at the DC level, irrespective of local factors such as those determined by cutaneous or mucosal epithelial microenvironments.
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PMID:Intrinsic characteristics of contact and respiratory allergens influence production of polarizing cytokines by dendritic cells. 1695 23

Two mononuclear nickel(II) complexes with Schiff-base ligands derived from the epimeric sugars glucosamine and mannosamine have been synthesized. The X-ray crystal structure reveals a distorted octahedral geometry at the nickel(II) ions with an N4O2 donor set and the rare 2,3-chelation of the donor atoms of the carbohydrate backbone. Upon complexation only the glucopyranose ring maintains the 4C1 chair conformation, whereas the mannopyranose ring adopts the OS5 screw-boat conformation. Dimeric units of complex cations are formed by intermolecular hydrogen bonding which are further assembled by pi-stacking affording one-dimensional chains with a twofold screw symmetry.
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PMID:Nickel(II) complexes with Schiff-base ligands derived from epimeric pyranose backbones as 2,3-chelators: modeling the coordination chemistry of chitosan. 1835 96

Nickel-containing alloys are used in dentistry because of their low cost, but poor corrosion behavior increases their risk of causing adverse biological responses. Intraorally, nickel-containing alloys accumulate bacterial plaque that triggers periodontal inflammation via toxins such as lipopolysaccharide (LPS). Recent evidence suggests that in monocytes, Ni(II) amplifies LPS-induced secretion of several cytokines that mediate periodontal destruction. Thus, we investigated the effects of Ni(II), with or without LPS, on the secretion of a broader array of cytokines from monocytes. We then measured monocytic expression of two proteins, Nrf2 and thioredoxin-1 (Trx1), that influence the regulation of cytokine secretion. Cytokine arrays were used to measure the effects of 0-50 microM Ni(II) on cytokine secretion from human THP1 monocytes, with or without LPS activation. Immunoblots were used to estimate Nrf2 and Trx1 levels. Our results indicate that both Ni(II) alone and Ni(II) with LPS have broad-based effects on cytokine secretion. Ni(II) increased Nrf2 levels by threefold, and LPS amplified the effects of Ni(II) by 10-fold. Trx1 levels did not change under any condition tested. Our results suggest that Ni(II)-induced changes in cytokine secretion by monocytes are diverse and may be influenced by Nrf2 but are not likely influenced by changes in whole-cell Trx1 levels.
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PMID:Ni(II) ions dysregulate cytokine secretion from human monocytes. 1843 99

Biomedical alloys may release nickel ions during corrosion phenomena and, in addition to their interaction with oral tissues, these ions may also influence characteristic properties of the immune system cells. The aim of this study was to evaluate the effect of nickel chloride on the expression of functionally distinct surface antigens in murine RAW macrophages. The expression of the surface antigens CD14, CD40, MHC class I, MHC class II, CD80, CD86, CD54 was analyzed by flow cytometry. The bacterial endotoxin lipopolysaccharide (LPS) was used as a positive control to induce antigen expression. Cells were stimulated with NiCl(2) (0.1 and 0.5mm) in the presence and absence of LPS (0.1 or 25 microg/ml). After exposure periods of 6, 24 and 48 h, LPS caused a time- and dose-dependent increase in the expression of all surface antigens. CD14 expression was up-regulated by 0.1 microg/ml LPS by about 10-fold after 24h and 100-fold after 48 h. After 48 h, NiCl(2) alone up-regulated the expression of all surface antigens between 2- and 4-fold, while in cells stimulated by LPS, 0.1mm NiCl(2) was effective only on CD14, CD40 and MHC class I. Moreover, 0.5mm NiCl(2) even inhibited the LPS-induced expression of all surface antigens, except for CD54, which was still significantly up-regulated. These results show that nickel chloride is able to induce an up-regulation of surface antigen expression, but a high concentration may impair essential functions of macrophages stimulated by LPS.
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PMID:The influence of Ni(II) on surface antigen expression in murine macrophages. 1912 40

Biotin, a water-soluble B complex vitamin, is possibly involved in chronic inflammatory diseases, although the detailed mechanisms are unclear. In this study, we investigated the effects of biotin status on nickel (Ni) allergy in mice. Mice were fed a basal or biotin-deficient (BD) diet for 8 wk and sensitized with an intraperitoneal injection of NiCl(2) and lipopolysaccharide. Ten days after sensitization, NiCl(2) was intradermally injected into pinnas and ear swelling was measured. For in vitro analysis, we cultured a murine macrophage cell line, J774.1, under a biotin-sufficient (C, meaning control) or BD condition for 4 wk and analyzed interleukin (IL)-1 production. Significantly higher ear swelling was induced in BD mice than C mice. Adaptive transfer of splenocytes from both C and BD mice induced Ni allergy in unsensitized mice. Regardless of donor mice, ear swelling was significantly higher in BD recipient mice than C recipient mice. Ni allergy was not induced in either C or BD IL-1(-/-) mice. Splenocytes from BD mice produced a significantly higher amount of IL-1beta than those from C mice. Production and mRNA expression of IL-1beta were significantly higher in BD J774.1 cells than in C cells. Biotin supplementation inhibited the augmentation of IL-1beta production in vitro. In vivo supplementation of biotin in drinking water dose-dependently decreased ear swelling in C and BD mice. These results indicate that biotin status affects Ni allergy in the elicitation phase via the upregulation of IL-1beta production in mice, suggesting that biotin supplementation may have therapeutic effects on human metal allergy.
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PMID:Biotin status affects nickel allergy via regulation of interleukin-1beta production in mice. 1926 31

A knowledge of the acute systemic effects of materials that come into contact with body tissues and fluids is necessary to assess their clinical safety. Here we describe the use of bioradiotelemetry to record the heart rate, body temperature, and motor activity of freely behaving rats in conjunction with weight gain, food, and water consumption after administration of the bacterial endotoxin lipopolysaccharide and the heavy metal nickel chloride. The results of our study reveal that body temperature change was the more sensitive index of the two physiological parameters tested. Core body temperature can be monitored diurnally or nocturnally depending on whether a hyper- or hypothermic response, respectively, to the test solution is anticipated. Weight gain was the most sensitive index of all parameters monitored, but its use as an index requires that the test substance be administered nocturnally. Monitoring physiological parameters offers a complementary assessment of a systemic response, but these markers are not superior to conventional indices such as reduced weight gain. The use of two diverse toxic substances in the present study illustrates that test conditions are dictated by the nature of the systemic response induced by the substance tested.
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PMID:A combined and comparative study of physiologic and behavioral parameters in a systemic toxicity test. 1975 23


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