Acute phase response in lactating dairy cows during hyperinsulinemic hypoglycaemic and hyperinsulinemic euglycaemic clamps and after intramammary LPS challenge

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Medzhitov (2008) clearly demonstrated that inflammation can be stimulated by infectious and non‐infectious inducers. Among the latter, Egger and Dixon (2010) observed that an excess in energy intake in mammals can serve as a signal for metabolic and inflammatory changes. In humans, this excess causes a cluster of adverse conditions (e.g. increased glycaemia, obesity, insulin resistance), which leads to the development of the metabolic syndrome. This syndrome seems to be the consequence of a low grade of inflammation, characterized by the excessive and continuous release of pro‐inflammatory cytokines (PIC) such as tumour necrosis factor‐alpha (TNF‐α), interleukin‐1β (IL‐1β) and interleukin‐6 (IL‐6), promoted either from the immune system (e.g. polymorphonucleates, monocytes) or from the adipose tissue (Coppack, 2001 and Gerner et al., 2013).
The detection of the variations of PIC in plasma remains very difficult, and it is easier to analyse some of their consequences during the inflammatory response (Galic et al., 2010; Kabara et al., 2014). Indeed, PIC induce the typical acute phase response in the liver (Fleck, 1989), which cause the increase of the synthesis of positive (pos; i.e. haptoglobin) and the reduction of the synthesis of negative (neg; i.e. albumin, binding proteins of vitamins and hormones, lipoproteins) acute phase proteins (APP). The changes in negAPP can be useful variables to assess inflammatory conditions (Bertoni and Trevisi, 2013). In ruminants, the relationship between the inflammatory response to high and continued energy intake, the consequences at metabolic level and in the adipose tissue are not well known. The adipose tissue provides substrates (e.g. fatty acids, glycerol) to other organs and releases adipokines (e.g. leptin, adiponectin, TNF‐α, IL‐6) with a different profile according to energy balance. This suggests a role during the transition period of dairy cows. Indeed, the attempt to reduce the energy shortage around calving (Grummer, 1995) with an increase in energy density (i.e. overfeeding in late pregnancy) caused negative results: an increase in negative energy balance and health disorders in early lactation (Drackley et al., 2010; Janovick et al., 2011) and more frequent non‐specific inflammation as suggested by the higher concentration of posAPP or increased expression of IL‐1β mRNA in liver tissue (Janovick et al., 2011; Loor et al., 2013). This situation could explain many of the stressful events in the transition period including the reduction of immunocompetence, severe lipomobilization, inadequate feed intake, a marked inflammatory response and a status of oxidative stress (Van Knegsel et al., 2014; Bradford et al., 2015). In early lactation, insulin resistance may modify the activity of adipose and muscle tissues (De Koster and Opsomer, 2013). Nevertheless, the relationship between high energy availability and the inflammatory response in the transition period is complex, because too many factors can interfere with the cow's responses. Therefore, it is desirable to evaluate this relationship in simplified models, such as the hyperinsulinemic hypoglycaemic (HypoG) clamp and the hyperinsulinemic euglycaemic (EuG) clamp, which mimic different metabolic conditions in animals and ensure energy balance close to equilibrium.
Thus, the aim of this study has been to assess the effects of two extreme metabolic conditions (HypoG and EuG clamps) on the inflammatory response measured as changes in posAPP and negAPP, in mid‐lactating dairy cows. Moreover, as dairy cows often experience infection during their lifetime, a second objective of the experiment has been the assessment of the effects of 48 h of HypoG and EuG clamps on the early inflammatory response measured by changes in TNF‐α, IL‐6 and APP in subjects under lipopolysaccharide (LPS) intramammary challenge.
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