Endotoxin Translocation and Gut Inflammation Are Increased in Broiler Chickens Receiving an Oral Lipopolysaccharide (LPS) Bolus during Heat Stress

Abstract

Lipopolysaccharides (LPS), also termed endotoxins, are the major component of the outer membrane of Gram-negative bacteria. In general, endotoxins in the intestine are considered harmless in healthy animals. However, different stressors, such as heat stress, can lead to a compromised gut barrier, resulting in endotoxin translocation. Chickens are considered to be less sensitive to the effects of LPS compared with other species, for example, humans, pigs, or calves, probably because of the lack of the functional-specific TRAM-TRIF signalling pathway (MyD88-independent). Therefore, six LPS preparations (three different strains with two different preparation methods each) were compared in murine macrophages and characterized according to their MyD88-dependent pathway activation. All tested LPS preparations induced a strong inflammatory response after 4 and 24 h on a murine macrophage cell line. However, there was a similar strong response in the gene expression profile as well as production of nitrite oxide and TNF-alpha from LPS of different strains and preparation methods. On the basis of the results of the in vitro study, one LPS preparation was chosen for the subsequent in vivo study with broilers to assess the effect of an oral LPS bolus (E. coli O55:B5 phenol extracted; 2 mg/kg b.w.) during heat stress conditions (10 h, 36 °C). The most pronounced effects were seen in broilers receiving the oral LPS bolus during heat stress conditions. The endotoxin activity in the intestine as well as the serum concentration of the 3-OH C14 (part of LPS) were increased. In addition, an increased expression of genes related to inflammation and stress response (e.g., IL-6, IL-1beta, HSP70) was observed, whereas the expression of genes associated with gut health (e.g., MUC2, FABP2) was decreased. To conclude, an increase of intestinal LPS combined with heat stress can pose a risk to animal health.

Effect of Lipopolysaccharides (LPS) and Lipoteichoic Acid (LTA) on the Inflammatory Response in Rumen Epithelial Cells (REC) and the Impact of LPS on Claw Explants

“…Of note, we did not see any effect of LPS on the expression of TLR4. This result is supported by previous findings of our research group with other cell types, namely mouse macrophages, after LPS stimulation for 4 and 24 h [29]. We hypothesize that due to the strong upregulation of proinflammatory cytokines already after 1 h of LPS stimulation, the lack of effect on TLR4, MyD88, and TRAF6 might be a consequence of a negative feedback loop as described by Lichte et al [30].…”

New insights into genetics underlying of plumage color

“…2016; Reisinger et al . 2020) and also appears to induce pigmentation in melanocytes through the MAPK signaling pathway and up‐regulation of MITF , which activates the tyrosinase enzyme (Ahn et al . 2008).…”

“…Heat stress in chickens causes endotoxemia owing to lipopolysaccharide (LPS) release from the gut. LSP induces HSF1 (Slawinska et al 2016;Reisinger et al 2020) and also appears to induce pigmentation in melanocytes through the MAPK signaling pathway and up-regulation of MITF, which activates the tyrosinase enzyme (Ahn et al 2008).…”

Novel Models for Chronic Intestinal Inflammation in Chickens: Intestinal Inflammation Pattern and Biomarkers

“…However, no difference between challenge groups and control was found at 14, 28 or 36 days. The measuring of serum LPS in chickens is controversial in the literature and it seems to vary according to the intensity of the challenge to which birds are exposed (60)(61)(62). Ovotransferrin, an acute phase protein mainly produced during inflammation, has been suggested as a fecal biomarker of intestinal inflammation due to its increase in excreta of broilers facing necrotic enteritis and coccidiosis (25), or diet with 52% of rye (13).…”