Relationships between body temperatures and inflammation indicators under physiological and pathophysiological conditions in pigs exposed to systemic lipopolysaccharide and dietary deoxynivalenol

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In healthy conditions, living vertebrates are situated in homoeostasis while keeping their vital functions, such as body core temperature, and different blood parameters stable within physiological limits. This balance is maintained against a large range of intrinsic and extrinsic influences by self‐regulatory mechanisms of the organism ensuring an adequate supply and function of all organs and tissues.
In pathophysiological conditions, such as lipopolysaccharide (LPS)‐induced acute endotoxaemia or chronic mycotoxin exposure, the organism initiates an immune response. To eliminate the pathogenic agents rapidly, self‐regulatory mechanisms get impaired causing a dysregulation of homoeostasis in several body functions, for example body temperature, white blood cell counts (WBC counts) and blood gases, (Bannert et al., 2015; Tesch et al., 2015). While acute internal restoration processes to LPS are accompanied by clinically observable indicators of an immune response, such as the cardinal symptom fever, immune responses to chronic mycotoxin deoxynivalenol (DON) often comprise slowly initiated and less obvious modifications in different parameters, such as leucocyte counts (Tesch et al., 2015).
The endotoxin LPS is a component of the outer cell membrane of Gram‐negative bacteria and has a high stimulatory potential for the innate and acquired immune response characterised by its interaction with different types of leucocytes and their subsequent biosynthesis of various effector molecules, such as tumour necrosis factor alpha (TNF‐α), one of the major fever inducing and amino acid metabolism altering cytokines in mammals (Reid & Li, 2001; Roth & Blatteis, 2014; Spate & Schulze, 2004) . For instance, TNF‐α as well as endotoxin LPS are capable to initiate the degradation of tryptophan (Trp), an essential amino acid, to its metabolite kynurenine (Kyn) and the neurotransmitter serotonin. The catabolism is catalysed by the hepatic enzyme tryptophan 2,3‐dioxygenase (TDO) and the enzyme indoleamine 2,3‐dioxygenase (IDO), that is strongly upregulated in different types of immune cells and tissues, for example lung and spleen, during acute and chronic immune responses (Moffett & Namboodiri, 2003; Schrocksnadel, Wirleitner, Winkler, & Fuchs, 2006). The activity of IDO can be characterised by the kynurenine‐to‐tryptophan ratio (Kyn–Trp ratio) which correlates with concentrations of immune activation markers; thus, it is an important parameter for the activation of the immune system (Moffett & Namboodiri, 2003; Schrocksnadel et al., 2006).
In addition, the mycotoxin DON stimulates the immune system when provided in a chronic manner, as proven by increased leucocyte counts, and alters the organism's acute immune response to LPS‐induced endotoxaemia, mirrored in modifications of clinical symptoms (Tesch et al., 2015). However, continuous measurement of WBC counts is not always routine; thus, chronic DON exposure often remains undetected although this provokes economic losses (e.g., reduced weight gain) in pigs. DON, mainly produced by the fungi Fusarium graminearum and F. culmorum, is often detected in wheat and maize. Both types of grain are major components of porcine diets that frequently expose pigs, as the most DON‐sensitive species (Roth & Blatteis, 2014; Spate & Schulze, 2004), to toxicologically relevant DON levels. For that reason, it can be assumed that a large proportion of commercially used swine may suffer from chronic dietary DON exposure during their lifetime, which can be co‐exposed to LPS‐releasing Enterobacteriaceae species such as Salmonella, Campylobacter and Escherichia coli (E.coli) depending on modern husbandry conditions (Berends, Urlings, Snijders, & Van Knapen, 1996; Smith & Halls, 1968).
In veterinary practice, the clinical examination and especially the rectal temperature measurement of pigs can be distorted by a large range of intrinsic stress factors caused by the activation of the immune response on the one hand and the unfamiliar handling with humans during clinical examination on the other hand.
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