Abstract
Total parenteral nutrition (TPN) impairs host immunocompetence, a mechanism possibly underlying the high morbidity of infectious complications in critically ill patients. Our recent study demonstrated TPN to reduce the number and function of hepatic mononuclear cells (MNCs) and to worsen survival after intraportal Pseudomonas challenge in mice. The present study examined the duration of enteral nutrition (EN) needed to reverse TPN-induced changes in hepatic MNCs in a murine model. Male ICR mice (6 weeks) received 5 days of TPN followed by 0 (TPN), 12 (EN12), 24 (EN24), 48 (EN48) or 72 (EN72)h of chow feeding. Control mice (Control) were given chow with intravenous saline infusions for 5 days. After nutritional support, hepatic MNCs were isolated and counted. Lipopolysaccharide (LPS) receptor expressions (CD14 and TLR4/MD2) on Kupffer cells were analyzed by flowcytometry. In addition, TPN, EN12, EN48 and control mice were given intraportal Pseudomonas challenge and survival was monitored. The TPN group was significantly lower in hepatic MNC number and LPS receptor expressions than the Control group. However, EN quickly reversed TPN-induced hepatic impairments in MNC loss within 12h, CD14 expression within 48 h and TLR4/MD2 expression within 24h. Survival of the EN48 group was significantly improved as compared with the TPN and EN12 groups. EN rapidly reverses TPN-induced impairment of hepatic immunity along with increased hepatic MNC numbers and LPS receptor expressions on Kupffer cells.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.