Effects of intravenous lipopolysaccharide administration on feed intake, ruminal forage degradability, and liquid parameters and physiological responses in beef cattle

Abstract

This experiment compared DMI, ruminal forage degradability, and liquid parameters as well as physiological responses in beef cattle receiving a lipopolysaccharide (LPS) challenge or not. Eight ruminally cannulated Angus × Hereford steers (485 ± 16 kg BW) were housed in individual pens on d -7, ranked by BW, and allocated to 1 of 2 treatments administered on d 0: 1) an intravenous (i.v.) bolus dose (0.5 μg/kg of BW, diluted in 5 mL of 0.9% sterile saline) of bacterial LPS ( 0111:B4) or 2) a 5-mL i.v. injection of 0.9% sterile saline (CON). Steers had free-choice access to mixed alfalfa-grass hay, water, and a commercial vitamin + mineral mix during the experiment (d -7 to 6). Hay DMI was evaluated daily from d -5 to 6. Immediately prior to treatment administration (h 0), polyester bags containing 4 g of ground dietary hay (DM basis) were immersed into the rumen of each steer and incubated for 0, 4, 8, 12, 24, 36, and 48 h for DM and NDF degradability evaluation. Steers were also intraruminally pulse-dosed with 5 g of Co-EDTA immediately prior to treatment administration, and rumen fluid samples were collected at 0, 2, 4, 6, 8, 12, 16, and 24 h for ruminal liquid volume and dilution rate calculations. Blood was collected every 2 h from -2 to 8 h, every 4 h from 8 to 16 h, every 12 h from 24 to 72 h, and every 24 h from 96 to 144 h relative to treatment administration. Values obtained before treatment administration were used as a covariate within each respective analysis. Steers receiving LPS had less ( ≤ 0.03) DMI on d 0 and 1 compared with CON steers. Steers receiving LPS had reduced ( ≤ 0.05) rumen liquid volume and dilution rate as well as ruminal disappearance rate and effective degradability of DM and NDF compared with CON steers. Steers receiving LPS had greater ( ≤ 0.05) plasma tumor necrosis factor α at 2 h, greater plasma haptoglobin from 24 to 72 h, greater plasma cortisol from 12 to 16 h, greater serum NEFA from 6 to 48 h, greater plasma insulin and glucose at 2 h, reduced plasma glucose from 4 to 12 h, greater plasma cholecystokinin at 16 h, and greater plasma leptin concentrations at 8, 12, 16, 36, 48, and 60 h after treatment administration compared with CON steers. Hence, LPS administration transiently reduced DMI in steers via physiological reactions that modulate gastrointestinal motility and satiety centers in the central nervous system, in addition to potential host-microbiome endocrine interactions that impaired ruminal hay DM and NDF degradability.

Lipopolysaccharide Alters Thermogenic and Inflammatory Genes in White Adipose Tissue in Mice Fed Diets with Distinct 18‐Carbon Fatty‐Acid Composition

“…Although HFD‐induced weight gain did not lead to a difference in serum metabolites between the different diet groups, the LPS‐treated mice had higher serum insulin concentration despite having lower serum glucose concentration than vehicle‐treated mice. LPS is known to impair insulin signaling through activation of nuclear factor‐κB (NF‐κB) signaling (Birnbaum, ; Song et al, ), and this is in accordance with similar reports of dysregulation of insulin and glucose concentrations in ewes (Yates et al, ) and cattle (Lippolis et al, ).…”

Impacts of stress-induced inflammation on feed intake of beef cattle

“…Moreover, increased circulating proinflammatory cytokines elicits the hepatic synthesis of APP, including haptoglobin (Carroll and Forsberg, 2007;Carroll et al, 2009). All these inflammation responses have been associated with reduced feed intake in animals and humans (Kapaś and Krueger, 1992;Fantino and Wieteska, 1993;Sonti et al, 1996;Rodrigues et al, 2015;Lippolis et al, 2017) and will be covered in the next section of this review. It is important to highlight that stress and inflammation are two separate physiological events that often, but not always, occur simultaneously, and the LPS-induced inflammation may not necessarily represent all forms of stress-induced inflammation.…”

“…Therefore, the stress-induced response might result in lessened sensitization of satiety signals increasing appetite in humans (Adam and Epel, 2007). Nonetheless, a reduction in feed intake might also occur during acute and chronic inflammatory reactions in humans and livestock species (Gautron, 2009;Rodrigues et al, 2015;Lippolis et al, 2017). It is widely known that the administration of proinflammatory cytokines such as LPS, tumor necrosis factor-alpha (TNF-a), IL-6, and IL-8 reduces feed intake (Kapaś and Krueger, 1992;Fantino and Wieteska, 1993;Sonti et al, 1996;Rodrigues et al, 2015;Lippolis et al, 2017).…”

“…Nonetheless, a reduction in feed intake might also occur during acute and chronic inflammatory reactions in humans and livestock species (Gautron, 2009;Rodrigues et al, 2015;Lippolis et al, 2017). It is widely known that the administration of proinflammatory cytokines such as LPS, tumor necrosis factor-alpha (TNF-a), IL-6, and IL-8 reduces feed intake (Kapaś and Krueger, 1992;Fantino and Wieteska, 1993;Sonti et al, 1996;Rodrigues et al, 2015;Lippolis et al, 2017). Upon a pathogenic stimulus, the innate immune system elicits several responses, including the synthesis of proinflammatory cytokines (i.e., TNF-a) from leukocytes, with the intent of attenuating or eliminating the infection (Carroll and Forsberg, 2007;Carroll et al, 2009;Rodrigues et al, 2015).…”

“…Other studies suggest that these cytokines can regulate feed intake by stimulating adipocytes to synthesize leptin (Grunfeld et al, 1996). For instance, circulating TNF-a levels were previously reported as a feed intake reducer by modulating the central nervous and endocrine system and disrupting gastrointestinal function (Klasing and Korver, 1997;Lippolis et al, 2017). Gautron and Layé (2010) reported that feed intake reduction during an acute and chronic inflammatory state results from the action of proinflammatory cytokines and prostaglandins E 2 on the nervous system.…”