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Our objective was to develop a lipopolysaccharide (LPS) inflammation model in calves to evaluate the acute-phase response with respect to the release of pro-inflammatory cytokines and acute-phase proteins, fever development and sickness behaviour. Fourteen 4-week-old male Holstein Friesian calves were included and randomly assigned to a negative control group (n=3) and an LPS-challenged group (n=11). The latter received an intravenous bolus injection of 0.5 μg of LPS/kg body weight. Blood collection and clinical scoring were performed at 0, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 5, 6, 8, 12, 18, 24, 28, 32, 48, 54 and 72 h post LPS administration (p.a.). In the LPS group, the following clinical signs were observed successively: tachypnoea (on average 18 min p.a.), decubitus (29 min p.a.), general depression (1.75 h p.a.), fever (5h p.a.) and tachycardia (5h p.a.). Subsequent to the recovery from respiratory distress, general depression was prominent, which deteriorated when fever increased. One animal did not survive LPS administration, whereas the other animals recovered on average within 6.1h p.a. Moreover, the challenge significantly increased plasma concentrations of tumour necrosis factor-α, interleukin 6, serum amyloid A and haptoglobin, with peaking levels at 1, 3.5, 24 and 18 h p.a., respectively. The present LPS model was practical and reproducible, caused obvious clinical signs related to endotoxemia and a marked change in the studied inflammatory mediators, making it a suitable model to study the immunomodulatory properties of drugs in future research., (Copyright © 2014 Elsevier B.V. All rights reserved.)

The objective of the present study was to evaluate the potential effects of dietary L-carnitine supplementation on acute phase protein response upon a lipopolysaccharide (LPS) challenge of male broiler chickens receiving a commercial broiler diet supplemented with 15 or 100 mg L-carnitine/kg or an unsupplemented (control) diet from 14 days of age onwards. At 28 days of age, eight chickens per dietary treatment were weighed and subcutaneously injected with 300 microg LPS from E. coli (100 microg LPS/ml saline) or 3 ml saline (unsupplemented group only). During the next 10 days, blood samples were taken repeatedly and analysed for their hemopexin (HX) and alpha-1 acid glycoprotein (AGP) levels. Extra dietary L-carnitine did not affect broiler performance. At day 1 postinjection, plasma HX and AGP levels were significantly increased in all treatment groups. However, the elevations in circulating HX and AGP levels were more pronounced in the L-carnitine supplemented chickens, especially in the 100mg L-carnitine group. It is concluded that extra L-carnitine in the diet of broiler chickens enhances or advances the acute phase protein response. The exact mode of action needs to be elucidated but seems to be consistent with a glucocorticoid mimicking effect.

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.

Following tissue injury or infection, the concentrations of several plasma proteins are altered substantially. The characteristic pattern of this change is termed the acute phase response, and can be observed in many different inflammatory situations, including surgical trauma, injury, infections, tissue infarction and several immunologically mediated states such as temporalis arteritis, polymyalgia rheumatica and rheumatoid arthritis. It is often of great clinical value to monitor the acute phase response in humans but the assays used to measure the acute response in man (e.g., erythrocyte sedimentation rate and C-reactive protein) is less well suited for experimental studies in the rat. We have instead developed a nephelometric assay for determination of fibrinogen as a marker of the inflammatory response in rats. The assay was used to monitor the inflammatory response in type II collagen arthritis in rats. This model involves the induction of severe polyarthritis and is a widely used animal model for rheumatoid arthritis (RA). Fibrinogen concentrations increased from 3.1 g/l before immunization to 10.5 g/l 2 weeks after the immunization, after which they gradually declined towards normal levels. This pattern of fibrinogen alterations correlated well with the inflammatory phase of the arthritic response. Plasma fibrinogen may thus represent a rapid and sensitive marker of the acute phase response in the rat.