Abstract
Enterotoxigenic E. coli infection is a major cause of post-weaning diarrhea in pigs and is associated with systemic inflammation and oxidative stress. This study aimed to characterize temporal changes in biomarkers of inflammation and oxidative stress in response to an E. coli lipopolysaccharide (LPS) challenge, providing insights into host immune responses. Ten female pigs (27.9 kg BW; ∼3 months old) were infused with LPS derived from E. coli O111:B4 at LOW (0.75 µg LPS/kg BW) or MODERATE (1.50 µg LPS/kg BW) dosages. Thirteen blood samples were collected via venous catheter at 0 (pre-infusion), and from 0.5 to 72 h post LPS infusion. Rectal temperature, blood cytokines, acute-phase proteins, and oxidative stress markers were measured. A semi-targeted metabolomics approach was applied to investigate oxidative stress markers, including 8-iso-prostaglandin F₂α (8-iso-PGF₂α). Rectal temperature peaked at 3 h and returned to pre-infusion levels by 8 h. Plasma C-reactive protein (CRP) peaked at 12 h, while haptoglobin peaked at 24 h after LPS infusion. Pig major acute-phase protein (Pig-MAP) peaked at 24 h (LOW) and 36 h (MODERATE). Malondialdehyde (MDA) peaked between 0.5 and 1 h and returned to pre-infusion levels within 12 h. The cytokines IL-6, IFN-γ, IL-10 and IL-1β peaked between 1 and 3 h post-infusion. Moreover, cortisol increased rapidly, peaking at 2 h post LPS infusion. These findings indicate distinct temporal responses of inflammatory and oxidative stress markers following LPS challenge, supporting their use as potential biomarkers for evaluating interventions modulating infection-induced oxidative stress in pigs.
| Original language | English |
|---|---|
| Article number | 111004 |
| Journal | Veterinary Immunology and Immunopathology |
| Volume | 288 |
| Number of pages | 12 |
| ISSN | 0165-2427 |
| DOIs | |
| Publication status | Published - 2025 |
Bibliographical note
Publisher Copyright:© 2025 The Authors
Keywords
- Biomarkers
- E. coli infection
- LPS infusion
- Oxidative stress
- Systemic inflammation
Cite this
- APA
- Standard
- Harvard
- Vancouver
- Author
- BIBTEX
- RIS