Effects of pentoxifylline and polymyxin B on the acute‐phase‐response to <i>Escherichia coli</i> endotoxin in dwarf goats

Miert, A. S. J. P. A. M. van; Duin, C. T. M. van; Wensing, Th.

doi:10.1046/j.1365-2885.1997.00041.x

Cited by 26 publications

(11 citation statements)

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“…In the present study, we demonstrate that LPS from intestinal Gram‐negative bacteria may play a role in the activation of joint inflammation in which immune responses to pathological antigens are involved because oral administration of the endotoxin from E. coli , after AIA had been subsided, reactivated the joint inflammation. The reactivation of AIA was blocked by PMB that neutralized the endotoxin [15]. The role of LPS given p.o.…”

Section: Discussionmentioning

confidence: 99%

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Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

et al. 2005

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We examined whether oral administration of lipopolysaccharide (LPS) from Escherichia coli reactivated antigen-induced arthritis (AIA) in mice that is one of models of human rheumatoid arthritis. To induce AIA, mice were immunized by subcutaneous injection of ovalbumin (OVA) emulsified with complete Freund's adjuvant into the base of the tail (day 0) followed by intraarticular injection of OVA on day 21. To investigate the ability of LPS to reactivate AIA, varying doses of LPS were p.o. administered 48 h after the challenge injection. The results showed that administration of LPS was followed by reactivation of AIA in a dose-related fashion. The reactivation of AIA by LPS was associated with increases in interferon-g, interleukin-1b and tumour necrosis factor-a. Polymyxin B sulfate given immediately before administration of LPS suppressed the reactivation of AIA. These findings suggest that LPS from intestinal bacteria may play a role in the reactivation of joint inflammation in which immune responses to pathogenic antigens are involved.

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Section: Discussionmentioning

confidence: 99%

“…To investigate whether PMB that neutralizes LPS [15] can suppress the reactivation of AIA by the endotoxin, we gave the antibiotic orally immediately before administration of LPS. As shown in Fig.…”

Section: The Effect Of Pmb On the Reactivation Of Aia By Oral Adminismentioning

confidence: 99%

Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

et al. 2005

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“…The LPS active site lipid A was also effective in stimulating the existing joint inflammation. The reactivation of CIA by LPS and lipid A was blocked by PMB that neutralized these Gram negative bacterial cell wall components (van Miert et al ., 1987), supporting the role of LPS and lipid A in the recurrence of joint inflammation. The reactivation of CIA by LPS was also confirmed by histologic changes in joints of LPS‐treated mice showing marked oedema of synovium which had proliferated by the day of the endotoxin challenge, new formation of fibrin, and infiltration of many neutrophils accompanied with mononuclear cells, while control untreated animals failed to have such histologically acute inflammatory features.…”

Section: Discussionmentioning

confidence: 99%

The role of lipopolysaccharide injected systemically in the reactivation of collagen‐induced arthritis in mice

Yoshino¹,

Ohsawa

2000

British J Pharmacology

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1 We investigated the role of bacterial lipopolysaccharide (LPS) in the reactivation of autoimmune disease by using collagen-induced arthritis (CIA) in mice in which autoimmunity to the joint cartilage component type II collagen (CII) was involved. 2 CIA was induced by immunization with CII emulsi®ed with complete Freund's adjuvant at the base of the tail (day 0) followed by a booster injection on day 21. Varying doses of LPS from E. coli were i.p. injected on day 50. 3 Arthritis began to develop on day 25 after immunization with CII and reached a peak on day 35. Thereafter, arthritis subsided gradually but moderate joint in¯ammation was still observed on day 50. An i.p. injection of LPS on day 50 markedly reactivated arthritis on a dose-related fashion. Histologically, on day 55, there were marked oedema of synovium which had proliferated by the day of LPS injection, new formation of ®brin, and intense in®ltration of neutrophils accompanied with a large number of mononuclear cells. The reactivation of CIA by LPS was associated with increases in anti-CII IgG and IgG2a antibodies as well as various cytokines including IL-12, IFN-g, IL-1b, and TNF-a. LPS from S. enteritidis, S. typhimurium, and K. neumoniae and its component, lipid A from E. coli also reactivated the disease. Polymyxin B sulphate suppressed LPS-or lipid A-induced reactivation of CIA. 4 These results suggest that LPS may play an important role in the reactivation of autoimmune joint in¯ammatory diseases such as rheumatoid arthritis in humans.

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“…Treatment with polymyxin B to attenuate clinical endotoxaemia is frequently used in adult horses for conditions such as strangulating intestinal lesions, pleuropneumonia, and postpartum metritis, with beneficial effects (34). The effects of intravenous applications of pentoxifylline and polymyxin B on the acute-phase-response to Escherichia coli endotoxin in dwarf goats have been evaluated (29). However, no study has been carried out on the clinical impact and anti-inflammatory effects of polymyxin B alone on endotoxaemia in sheep.…”

Section: Introductionmentioning

confidence: 99%

Effects of polymyxin B on clinical signs, serum TNF-α, haptoglobin and plasma lactate concentrations in experimental endotoxaemia in sheep

Hajimohammadi

Badiei

Kheibari

et al. 2018

Journal of Veterinary Research

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IntroductionThe experiment evaluated the effects of intravenous administration of polymyxin B on experimental endotoxaemia in sheep.Material and MethodsTwenty clinically healthy fat-tailed sheep were randomly divided into: a group treated with 6,000 U/kg of polymyxin B, a group at 12,000 U/kg, and positive and negative controls. Endotoxaemia was induced by intravenous administration of lipopolysaccharide (LPS) from E. coli serotype O55:B5 at 0.5 μg/kg. polymyxin was infused intravenously along with 2.5 L of isotonic intravenous fluids at 20 mL/kg/h. The positive control group received LPS and 2.5 L of isotonic fluids, the negatives receiving just 2.5 L of isotonic fluids. Clinical signs were evaluated before and at 1.5, 3, 4.5, 6, 24, and 48 h after LPS administration. Blood was also sampled at the denoted hours and serum haptoglobin, tumour necrosis factor-α (TNF-α), and plasma lactate concentrations were assayed.ResultsThe serum concentration of TNF-α in the positive control group increased significantly up to 48 h after LPS administration. The concentration of TNF-α was significantly different from those of the polymyxin B and positive control groups from 3 to 48 h; also, the concentrations of haptoglobin at different times in the polymyxin groups were lower than those of the positive control group and were significant at hours 3 to 48 (P < 0.05). Following the LPS administration, haptoglobin and TNF-α concentrations changed without significant difference between the two polymyxin B groups.ConclusionPolymyxin B (6,000 U/kg) restrained blood lactate concentrations. Furthermore, it significantly improved the clinical signs in endotoxaemic animals, including rectal temperature and heart and respiratory rates. Polymyxin B may be an antiendotoxic in fat-tailed sheep.

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Effects of pentoxifylline and polymyxin B on the acute‐phase‐response to Escherichia coli endotoxin in dwarf goats

Cited by 26 publications

References 12 publications

Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

Reactivation of Antigen‐Induced Arthritis in Mice by Oral Administration of Lipopolysaccharide

The role of lipopolysaccharide injected systemically in the reactivation of collagen‐induced arthritis in mice

Effects of polymyxin B on clinical signs, serum TNF-α, haptoglobin and plasma lactate concentrations in experimental endotoxaemia in sheep

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