Abstract

BackgroundRespiratory infections challenge the swine industry, despite common medicinal practices. The dual signaling nature of PGE2 (supporting both inflammation and resolution) makes it a potent regulator of immune cell function. Therefore, the use of dietary long chain n-6 PUFA to enhance PGE2 effects merits investigation.MethodsDay-old pigs (n = 60) were allotted to one of three dietary groups for 21 d (n = 20/diet), and received either a control diet (CON, arachidonate = 0.5% of total fatty acids), an arachidonate (ARA)-enriched diet (LC n-6, ARA = 2.2%), or an eicosapentaenoic (EPA)-enriched diet (LC n-3, EPA = 3.0%). Alveolar macrophages and lung parenchymal tissue were collected for fatty acid analysis. Isolated alveolar macrophages were stimulated with LPS in situ for 24 h, and mRNA was isolated to assess markers associated with inflammation and eicosanoid production. Culture media were collected to assess PGE2 secretion. Oxidative burst in macrophages was measured by: 1) oxygen consumption and extracellular acidification (via Seahorse), 2) cytoplasmic oxidation and 3) nitric oxide production following 4, 18, and 24 h of LPS stimulation.ResultsConcentration of ARA (% of fatty acids, w/w) in macrophages from pigs fed LC n-6 was 86% higher than CON and 18% lower in pigs fed LC n-3 (P < 0.01). Following LPS stimulation, abundance of COX-2 and TNF-α mRNA (P < 0.0001), and PGE2 secretion (P < 0. 01) were higher in LC n-6 PAM vs. CON. However, ALOX5 abundance was 1.6-fold lower than CON. Macrophages from CON and LC n-6 groups were 4-fold higher in ALOX12/15 abundance (P < 0.0001) compared to LC n-3. Oxygen consumption and extracellular acidification rates increased over 4 h following LPS stimulation (P < 0.05) regardless of treatment. Similarly, increases in cytoplasmic oxidation (P < 0.001) and nitric oxide production (P < 0.002) were observed after 18 h of LPS stimulation but were unaffected by diet.ConclusionsWe infer that enriching diets with arachidonic acid may be an effective means to enhance a stronger innate immunologic response to respiratory challenges in neonatal pigs. However, further work is needed to examine long-term safety, clinical efficacy and economic viability.

Highlights

  • Respiratory infections challenge the swine industry, despite common medicinal practices

  • Serum concentrations of urea nitrogen, cholesterol and mean corpuscular volume were lower in Long chain (LC) n-3 fed pigs (P < 0.05), while albumin was elevated (P < 0.001) compared to contained 0.5% ARA (CON) and LC n-6 fed pigs

  • Increasing dietary long chain n-6 Polyunsaturated Fatty Acids (PUFA) resulted in Arachidonic acid (ARA) enrichment being 2-fold higher in Porcine alveolar macrophages (PAM) compared to CON

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Summary

Introduction

Respiratory infections challenge the swine industry, despite common medicinal practices. Respiratory infections in swine result in severe economic loss despite the wide spread use of vaccines and antibiotics [1]. Vaccines and antibiotics are routine practice the type of bacteria and timing of treatment can impact use and efficacy [1, 3]. Early life protection stems partially from passive immunity through the sow’s colostrum the transfer of maternal antibodies can be limiting. Antibodies against certain Gram-negative bacteria can deplete in piglets within 1–4 weeks of life [3, 4]. Neonates are at a much higher risk for infection During this critical time, it is imperative to explore alternative means to enhance a stronger, well-balanced immunological response to respiratory infections

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