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)

In brown chicken with chronic inflammatory processes of the joints amyloid arthropathy easily develops. The amyloid has been shown to be of the AA type which is derived from serum amyloid A (SAA). The aim of the present study was to investigate whether fibroblast-like synoviocytes (FLS) originating from brown chicken and other chicken breeds express SAA mRNA and produce SAA protein. FLS were isolated from the knee joint synovium of healthy brown chickens, white chickens, and broilers. The absence of macrophages in FLS cultures was confirmed by assessment of the phagocytic capability and by immunohistochemistry. Additionally, cultured cells were identified by electron microscopy and immunohistochemical staining. Expression of SAA mRNA in normal and lipopolysaccharide (LPS)-stimulated cells was assessed by in situ hybridization, Northern blot analysis, reverse transcriptase-polymerase chain reaction (RT-PCR), Southern blot analysis and real-time quantitative PCR. SAA protein production was analyzed by Western blotting and ELISA. SAA mRNA was detected in unstimulated FLS isolated from the three different chicken breeds and more abundantly in those stimulated with LPS. However, SAA protein production was only detected in culture medium and cell lysate of LPS-stimulated FLS. Furthermore, FLS produced SAA in a concentration-dependent manner after stimulation with different amounts of LPS. The data suggest that during infection and inflammation chicken FLS may act as a source of articular SAA. This process may enhance development of amyloid from SAA in the joint.
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PMID:Serum amyloid A production by chicken fibroblast-like synoviocytes. 1591 Sep 91

Almost half of all clinical cases of mastitis are caused by Gram-negative bacteria. Among these bacteria, intramammary infection by Pseudomonas aeruginosa remains one of the most refractory to antibiotic therapy. The ability to recognize potentially harmful pathogens whether previously encountered or not, as well as the induction of an initial pro-inflammatory response to these pathogens, are critical components of host innate immunity. Although the innate immune response to another Gram-negative mastitis-causing pathogen, Escherichia coli, has been well-characterized, little is known about the response to other Gram-negative bacteria, including P. aeruginosa. The objective of the current study was to characterize the systemic and localized bovine innate immune response to intramammary infection with P. aeruginosa. The contralateral quarters of ten mid-lactating Holstein cows were challenged with either saline or P. aeruginosa. Following the establishment of infection, milk samples were collected and assayed for changes in cytokine and growth factor concentrations, complement activation, and changes in the levels of soluble CD14 (sCD14) and lipopolysaccharide (LPS)-binding protein (LBP), two accessory molecules involved in host recognition of Gram-negative bacteria. Initial increases in milk somatic cell counts were evident within 12h of experimental challenge and remained elevated for >or=3 weeks. Increased permeability of the mammary gland vasculature, as evidenced by elevated milk levels of BSA, was initially observed 20 h post-infection and persisted for 2 weeks. Within 32 h of challenge, increased levels of IL-8, TNF-alpha, IL-10, and IL-12 were detected, however, the elevated levels of these cytokines were not sustained for longer than a 24h period. In contrast, elevations in IL-1beta, IFN-gamma, TGF-alpha, TGF-beta1, TGF-beta2, sCD14, LBP, and activated complement factor 5 (C5a) were sustained for periods of >48 h. Systemic changes were characterized by elevated body temperature, induction of the acute phase protein synthesis of serum amyloid A and LBP, and a transient decrease in circulating neutrophils and lymphocytes. Together, these data demonstrate the capability of the mammary gland to mount a robust innate immune response to P. aeruginosa that is characterized by the induction of pro-inflammatory cytokines, complement activation, and increased levels of accessory molecules involved in Gram-negative bacterial recognition.
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PMID:The bovine innate immune response during experimentally-induced Pseudomonas aeruginosa mastitis. 1597 Mar 35

This study was conducted to evaluate the response of two dam lines of pigs to acute increases of LPS. Acute-phase proteins were also measured to determine their potential use as biological indicators of the immune response. Thirty-six pigs (initial body weight = 21.3 +/- 0.48 kg) were allotted by dam line (Lines 1 and 2) and sex (castrates and gilts) to one of three LPS dose treatments and penned individually. Treatments were a single i.m. injection of 0 (LPS-0), 25 (LPS-25) or 50 microg LPS/kg body weight (BW) (LPS-50). Acute changes in feed intake were related to a pre-injection baseline intake. Feeders were weighed daily to establish baseline feed intake (average daily feed intake -48 to 0 h prior to injection). The acute feed intake response (AFIR) was computed as the average daily feed intake 0-48 h after injection divided by baseline intake. Serum was harvested at time 0 and 48 h after injection. LPS-0 pigs grew faster and consumed more feed than the LPS-25 or LPS-50 pigs (0.79 kg/d versus 0.51 and 0.50 kg/d; 1.15 kg/d versus 0.96 and 0.89 kg/d, respectively; P<0.001). The AFIR of Line 1 castrates and Line 2 gilts was similar for LPS-25 and LPS-50 treatments, while Line 1 gilts and Line 2 castrates had decreased AFIR with increased LPS dose (sex x line x LPS, P<0.05). Three of 18 castrates died but no gilts died following the LPS challenge (P<0.10). Castrates had higher haptoglobin (Hpt) concentrations than gilts on d 0 (18.1 units of absorption/mg of protein versus 13.1 units of absorption/mg of protein; P<0.03). Line 1 pigs had higher C-reactive protein (CRP) concentrations than Line 2 pigs (P<0.05) on d 0. LPS treatment did not change serum concentrations of CRP, Hpt or ceruloplasmin (Cp). However, the change in serum amyloid A (SAA) concentration decreased quadratically (from 0 to 48 h) with increasing LPS dose (P<0.02). This change in SAA was negatively correlated with the AFIR (r= -0.80; P<0.001). In general, castrates appear to be more sensitive to endotoxin challenges than gilts. Serum amyloid A, but not the other acute-phase proteins evaluated, was a good biological indicator of immune system activation following an acute lipopolysaccharide challenge when compared to the acute change in feed intake.
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PMID:Acute feed intake and acute-phase protein responses following a lipopolysaccharide challenge in pigs from two dam lines. 1598 49

The aim of the study was to determine the intraarticular serum amyloid A (SAA) response pattern in horses with inflammatory arthritis. Inflammatory arthritis was induced by injection of lipopolysaccharide (LPS) into the radiocarpal joint of four horses. Serum and synovial fluid (SF) samples were collected before and at 4, 8, 12, 24, 48, 72, 96, and 144 h after injection. Concentrations of SAA were measured by immunoturbidometry, and expression of SAA isoforms was visualized by denaturing isoelectric focusing and Western blotting. The LPS injection caused systemic and local clinical signs of inflammation. Serum amyloid A appeared in serum and SF within 8h after LPS injection. Isoelectric focusing showed three major SAA bands with apparent isoelectric points (pI) of 7.9, 8.6, and >9.3 in serum and SF. Synovial fluid contained two additional isoforms with highly alkaline apparent pI values (apparent pI value extrapolated from standard curve=10.0 and 10.2), which were not present in any of the serum samples. In conclusion, intraarticular injection of LPS induced systemic and local inflammatory responses in the horses. By demonstrating SF-specific SAA isoforms the results of the present study suggest that SAA is synthesized locally in the equine inflamed joint, similar to what has been demonstrated in humans previously. The marked local SAA synthesis suggests an important pathophysiological role in inflammatory arthritis.
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PMID:Serum amyloid A isoforms in serum and synovial fluid in horses with lipopolysaccharide-induced arthritis. 1633 10

This study was designed to determine whether the acute-phase response in aged mice is altered by interleukin (IL) 6 deficiency. Young and aged wild-type (WT) and IL-6 knockout (KO) BALB/C female mice were injected with lipopolysaccharide (LPS; 1.5 microg/g body weight). After 24 h, aged IL-6 KO mice had an improved survival when compared with aged WT mice. Serum levels of IL-6 in aged WT animals given LPS were determined and, as expected, were significantly higher when compared with young LPS-treated WT animals (P<0.05). Serum levels of the acute-phase protein, serum amyloid A, were 50% lower in aged LPS-treated IL-6 KO mice relative to aged WT mice given LPS (P<0.001). In contrast, the induction of LPS-binding protein was not affected by age or IL-6 deficiency in LPS-treated animals. Circulating levels of corticosterone were markedly reduced in aged LPS-treated IL-6 KO mice relative to aged WT mice given LPS. These data indicate that IL-6 is an important contributor to the outcome of the acute-phase response of aged individuals challenged with endotoxin. We conclude that the absence of IL-6, a cytokine that contributes to the elevated basal proinflammatory state observed in aging, can improve the ability of aged mice to withstand an otherwise lethal challenge of bacterial endotoxin.
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PMID:Aberrant acute-phase response in aged interleukin-6 knockout mice. 1672 Dec 65

Septicemia and endotoxemia initiated by bacterial lipopolysaccharide (LPS) are relatively common in suckling and weaned piglets. Maternal milk is a source of both nutrition and immune protection for piglets. Passive transfer of colostral antibodies is necessary for protection of neonatal piglets against diseases, but the concentration of immunoglobulins in milk rapidly declines during the 1st wk of lactation in all mammals. We hypothesized, therefore, that nonimmunoglobulin substances in milk contribute to the innate protection of neonates against septicemia during the suckling period. Using LPS-affinity chromatography for isolation of LPS-binding proteins and liquid chromatography-mass spectrometry for their identification, we identified in porcine milk the following proteins with LPS-binding capacity: lactoferrin, soluble CD14, serum amyloid A, alpha-S1 casein, beta-casein, and kappa-casein. For lactoferrin, alpha-S1 casein, and kappa-casein, in vitro pepsin digestion did not inhibit LPS-binding activity, whereas combined digestion with pepsin and pancreatin abolished it. The biologic functions of these LPS-binding proteins and peptides were not determined.
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PMID:Identification of lipopolysaccharide-binding proteins in porcine milk. 1704 75

Binge ethanol (EtOH) consumption suppresses inflammatory responses and resistance to infection, but paradoxically it is associated with increased levels of acute phase proteins (which are indicators of inflammation) and an increased risk of inflammation-mediated pathologies such as cardiovascular disease and cirrhosis of the liver. The latter effect may be mediated by increased translocation of bacteria leading to activation of toll-like receptor 4 (TLR4). In this study, the dose-response and time course of the effects of EtOH alone or EtOH in conjunction with a TLR4 agonist (lipopolysaccharide [LPS]) were evaluated in mice. EtOH alone at a dosage of 6 g/kg induced an acute phase response (as indicated by enzyme-linked immunosorbent assay for serum amyloid A and serum amyloid P) that was maximal 24 h after dosing. Lower dosages of EtOH did not have this effect but did suppress the acute phase response to LPS and the production of interleukin-6 up to 3 h after dosing. EtOH at 6 g/kg did not induce an acute phase response in C3H/HeJ (TLR4 mutant) mice, indicating that this response is mediated through TLR4. These results provide a resolution for the apparently paradoxical pro- and anti-inflammatory actions of EtOH with regard to acute phase responses.
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PMID:An explanation for the paradoxical induction and suppression of an acute phase response by ethanol. 1713 63

The effects of grain-induced subacute ruminal acidosis (SARA) in lactating dairy cows on free ruminal lipopolysaccharide (LPS) and indicators of inflammation were determined. Four mid lactation dairy cows were divided into 2 groups of 2 cows and used in a repeated switchover design. During each period, SARA was induced in 2 animals for 5 subsequent days by replacing 25% of their total mixed ration (dry matter basis) with a concentrate made of 50% wheat and 50% barley. The other 2 cows acted as controls and were fed a total mixed ration diet in which 44% of dry matter was concentrate. On average, inducing SARA did not affect milk composition, increased the duration of rumen pH below 5.6 from 187 to 309 min/d, and increased free ruminal LPS concentration from 24,547 endotoxin units (EU)/mL to 128,825 EU/mL. Averaged across treatments, milk fat yield and milk protein yield were 0.66 and 1.00 kg/d, respectively. Rumen pH and milk fat data suggest that control cows also experienced ruminal acidosis, albeit a milder form of this disease than SARA cows. Serum LPS concentration in both control and SARA cows was less than the detection limit of <0.01 EU/mL for the assay. Induction of SARA elevated serum amyloid A concentration from 286.8 to 498.8 mug/mL, but did not affect other markers of inflammation including haptoglobin, fibrinogen, serum copper, or white blood cells. These results suggest that grain-induced SARA in mid lactation dairy cows increases the lysis of gram-negative bacteria and activates an inflammatory response.
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PMID:Ruminal lipopolysaccharide concentration and inflammatory response during grain-induced subacute ruminal acidosis in dairy cows. 1723 62

Systemic inflammatory stimuli, such as infection, increase the risk of stroke and are associated with poorer clinical outcome. The mechanisms underlying the impact of systemic inflammatory stimuli on stroke are not well defined. We investigated the impact of systemic inflammation on experimental stroke and potential mechanisms involved. Focal cerebral ischemia was induced by intraluminal filament occlusion of the middle cerebral artery (MCAo). Brain damage and neurological deficit 24 h after MCAo were exacerbated by systemic lipopolysaccharide (LPS) administration. This exacerbation was critically dependent on interleukin (IL)-1, because coadministration of IL-1 receptor antagonist abolished the effect of LPS on brain damage. Systemic administration of IL-1 increased ischemic damage to a similar extent as LPS and also exacerbated brain edema. IL-1 markedly potentiated circulating levels of the acute phase proteins, serum amyloid A and IL-6, and the neutrophil-selective CXC chemokines, KC and macrophage inflammatory protein-2. Neutrophil mobilization and cortical neutrophil infiltration were aggravated by IL-1 before changes in ischemic damage. Neutropenia abolished the damaging effects of systemic IL-1. These data show for the first time that an acute systemic inflammatory stimulus is detrimental to outcome after experimental stroke and highlight IL-1 as a critical mediator in this paradigm. Our data suggest IL-1-induced potentiation of neutrophil mobilization via CXC chemokine induction is a putative mechanism underlying this effect. Our results may help to explain the poorer outcome in stroke patients presenting with infection and may have implications for neurodegenerative diseases involving neurovascular alterations, such as Alzheimer's disease, in which systemic inflammation can modulate disease progression.
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PMID:Systemic inflammatory stimulus potentiates the acute phase and CXC chemokine responses to experimental stroke and exacerbates brain damage via interleukin-1- and neutrophil-dependent mechanisms. 1744 25

In mammary gland infections, the contribution of NF-kappaB is not well defined, and was therefore investigated following intramammary inoculation of Escherichia coli. Non-invasive real-time in vivo imaging of the transcription factor activation was performed in mammary glands of transgenic mice expressing luciferase under the control of NF-kappaB. Bacterial inoculation resulted in a major increase in luminescence as compared with control glands. This activation was confirmed by immunohistochemical nuclear staining of the NF-kappaB p65 subunit in mammary epithelium of infected glands, while nuclear p50 was not detected. The systemic response to the intramammary inoculation of Escherichia coli was also studied. NF-kappaB activation in the liver increased over time, and a relatively mild but longer-lasting response was observed as compared with the acute hepatic response of mice receiving lipopolysaccharide. This systemic reaction was confirmed by increased circulating levels of the acute phase protein serum amyloid A, tumour necrosis factor-alpha and interleukin-6. In addition, high concentrations of both cytokines in the mammary gland inoculated with bacteria showed that the infection was also well established at the local level. These results indicate that in vivo monitoring of NF-kappaB activation is an attractive novel approach to study mammary gland inflammation, and that this transcription factor is imperative in the early stages of the host immune response towards coliform intramammary infections, both at the local and systemic level.
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PMID:In vivo imaging of NF-kappaB activity during Escherichia coli-induced mammary gland infection. 1824 Dec 10


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