A Grain-Based Subacute Ruminal Acidosis Challenge Causes Translocation of Lipopolysaccharide and Triggers Inflammation

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E. Khafipour, D. O. Krause, and J. C. Plaizier
Department of Animal Science, University of Manitoba, Winnipeg, MB, Canada

INTRODUCTION

Grain-based subacute ruminal acidosis (SARA) challenge increases the concentrations of the acute phase proteins serum amyloid A (SAA) and haptoglobin (Hp) in peripheral blood of cattle (Gozho et al., 2007; Emmanuel et al., 2008; Plaizier et al., 2008). These increases in acute phase proteins, which are part of the acute phase response, indicate that SARA causes inflammation (Horadagoda et al., 1999). This inflammation could be initiated by dietary-induced damage to the gut mucosa or by translocation of immunogenic compounds into circulation, such as free LPS (Horadagoda et al., 1999).

There is substantial evidence that grain-based SARA challenge increases the content of free LPS in the rumen due to the increase in lysis of gram-negative bacteria (Gozho et al., 2007; Nagaraja and Lechtenberg, 2007; Plaizier et al., 2008). This increase in luminal LPS could increase permeability of the gut for LPS (Chin et al., 2006). Also, the barrier function of rumen epithelium may be compromised by the parakeratosis, rumenitis, and abscesses of the rumen wall that result from high rumen acidity (Kleen et al., 2003). Additionally, the high rumen osmolality that is seen during SARA can cause swelling and rupture of ruminal papillae, which will also reduce the barrier function of the rumen. Despite this, no evidence of LPS in the peripheral circulation during SARA has been found (Gozho et al., 2007). There is also inconsistency in detection of LPS in peripheral blood during experimentally induced acute ruminal acidosis (Dougherty et al., 1975; Andersen and Jarlov, 1990; Andersen et al., 1994b). In recent years, the sensitivity and accuracy of bioassays used to detect LPS in low concentrations have been substantially improved, which makes the conclusion of previous studies regarding the absence of LPS in peripheral circulation questionable. The increases in the concentrations of the acute phase proteins SAA and Hp in peripheral blood do not prove translocation of LPS, as these concentrations can increase due to other inflammatory stimuli. However, because LPS interacts with a specific acute phase protein, LPS binding protein (LBP), an increase in LBP in peripheral circulation will provide evidence of the translocation of LPS (Sriskandan and Altmann, 2008).

The main objective of this study was to determine if a grain-based SARA challenge causes translocation of LPS from the gut into peripheral circulation. This was achieved by measuring plasma LPS using a high-sensitivity assay and by monitoring LBP levels in peripheral plasma and milk. The effects of the grain-based SARA challenge on feed intake, milk production and composition, blood metabolites, and SAA and Hp in peripheral blood were also determined.