Normal mesenteric lymph blunts the pulmonary inflammatory response to endotoxin.

Abstract

BACKGROUND:

Mesenteric lymph may provide the mechanistic link between gut ischemia and acute lung injury after hemorrhagic shock (HS). Studies have focused on the toxic mediators that develop in the post-shock mesenteric lymph (PSML). However, a complementary possibility is that there is loss of protective mediators found in pre-shock normal mesenteric lymph (NML) after HS. We hypothesize that NML protects against inflammatory insults to the pulmonary endothelium and that this effect is lost in PSML.

MATERIALS AND METHODS:

Primary human pulmonary endothelial cells (HMVECs) were incubated with NML or PSML collected from rats subjected to HS and resuscitation and then stimulated with 20 ng/mL LPS. ICAM-1 surface expression was measured by flow cytometry. In subsequent experiments, lipoproteins were extracted from NML before incubation and LPS-induced ICAM-1 expression determined.

RESULTS:

Mean fluorescent intensity (MFI) of LPS-induced ICAM-1 in NML and PSML treated HMVECs were 10.1 +/- 2.3 versus 27.7 +/- 0.83, respectively (P < 0.05). This represented at 71% decrease in ICAM-1 expression by NML compared to ICAM-1 expression in LPS-induced controls (MFI: 34.6 +/- 6.9). Lipoprotein extraction from NML abolished this protective effect (MFI: 31.2 +/- 5.3 versus Control + LPS: 33.5 +/- 3.6, P > 0.05). Baseline ICAM-1 levels were not significantly different among control, NML, and PSML groups.

CONCLUSION:

Lipoproteins in NML contain anti-inflammatory properties that decrease ICAM-1 expression induced by LPS in pulmonary endothelium. Decreased protective lipoproteins after HS and resuscitation may contribute to the toxicity associated with PSML from the ischemic gut.

• Authors: Aaron M Cheng, Ernest E Moore, Tomohiko Masuno, Guillermo A Escobar, Eric L Sarin, Jeffrey L Johnson, Phillip Eckels, Anirban Banerjee
• Journal: The Journal of surgical research (J Surg Res) Vol. 136 Issue 2 Pg. 166-71 (Dec 2006) ISSN: 0022-4804 [Print] United States
• PMID: 17059833 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)

Chemical References

• Albumins
• Lipopolysaccharides
• Lipoproteins
• Triglycerides
• Intercellular Adhesion Molecule-1
• Cholesterol

Topics

• Albumins (metabolism)
• Animals
• Cells, Cultured
• Cholesterol (metabolism)
• Endothelial Cells (cytology)
• Endotoxemia (immunology, metabolism)
• Humans
• Intercellular Adhesion Molecule-1 (metabolism)
• Ischemia (chemically induced, immunology, metabolism)
• Lipopolysaccharides (pharmacology)
• Lipoproteins (metabolism)
• Lymphatic System (immunology, metabolism)
• Male
• Mesentery
• Neutrophils (cytology, immunology)
• Pneumonia (chemically induced, immunology, metabolism)
• Rats
• Rats, Sprague-Dawley
• Shock, Hemorrhagic (chemically induced, immunology, metabolism)
• Triglycerides (metabolism)