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T-lymphocytes contribute to hepatic leukostasis and hypoxic stress induced by gut ischemia-reperfusion.
Microcirculation. 1999 Dec; 6(4):267-80.M

Abstract

Although neutrophils have been implicated in the hepatic injury elicited by gut ischemia/reperfusion (I/R), the contribution of other leukocyte populations to this injury process remains unclear. The objective of this study was to determine whether lymphocytes contribute to gut I/R-induced microvascular dysfunction and inflammatory responses in the liver. Intravital videomicroscopy was used to monitor leukocyte recruitment, the number of nonperfused sinusoids and pyridine nucleotide (NADH) autofluorescence in livers of wild-type, SCID, and interferon-gamma (IFN-gamma) knockout mice exposed to 15 min of gut ischemia and 1 h of reperfusion. In wild-type mice, gut I/R elicited significant increases in the number of stationary leukocytes, nonperfused sinusoids, NADH autofluorescence (indicating hypoxia), and elevated plasma alanine aminotransferase (ALT) and TNF-alpha levels. All of these responses were profoundly attenuated in SCID mice, while only some of the responses (in the midzonal region) were blunted in IFN-gamma knockout mice. Reconstitution (24 h before ischemia) of the circulating lymphocyte pool with T-cell enriched splenocytes, but not T cell deficient (from nude mice), CD4+ T-cell depleted splenocytes or splenocytes derived from IFN-gamma knockout mice, allowed the SCID mice to respond to gut I/R in a manner similar to wild-type mice. Some of the responses were restored following reconstitution with CD8+ T-cell depleted splenocytes. These findings implicate CD4+ T-lymphocytes and IFN-gamma in the hepatic microvascular dysfunction and inflammatory cell accumulation elicited by gut I/R.

Authors+Show Affiliations

Department of Molecular and Cellular Physiology, LSU Medical Center, Shreveport 71130-3932, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10654278

Citation

Horie, Y, et al. "T-lymphocytes Contribute to Hepatic Leukostasis and Hypoxic Stress Induced By Gut Ischemia-reperfusion." Microcirculation (New York, N.Y. : 1994), vol. 6, no. 4, 1999, pp. 267-80.
Horie Y, Wolf R, Chervenak RP, et al. T-lymphocytes contribute to hepatic leukostasis and hypoxic stress induced by gut ischemia-reperfusion. Microcirculation. 1999;6(4):267-80.
Horie, Y., Wolf, R., Chervenak, R. P., Jennings, S. R., & Granger, D. N. (1999). T-lymphocytes contribute to hepatic leukostasis and hypoxic stress induced by gut ischemia-reperfusion. Microcirculation (New York, N.Y. : 1994), 6(4), 267-80.
Horie Y, et al. T-lymphocytes Contribute to Hepatic Leukostasis and Hypoxic Stress Induced By Gut Ischemia-reperfusion. Microcirculation. 1999;6(4):267-80. PubMed PMID: 10654278.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - T-lymphocytes contribute to hepatic leukostasis and hypoxic stress induced by gut ischemia-reperfusion. AU - Horie,Y, AU - Wolf,R, AU - Chervenak,R P, AU - Jennings,S R, AU - Granger,D N, PY - 2000/2/2/pubmed PY - 2000/2/19/medline PY - 2000/2/2/entrez SP - 267 EP - 80 JF - Microcirculation (New York, N.Y. : 1994) JO - Microcirculation VL - 6 IS - 4 N2 - Although neutrophils have been implicated in the hepatic injury elicited by gut ischemia/reperfusion (I/R), the contribution of other leukocyte populations to this injury process remains unclear. The objective of this study was to determine whether lymphocytes contribute to gut I/R-induced microvascular dysfunction and inflammatory responses in the liver. Intravital videomicroscopy was used to monitor leukocyte recruitment, the number of nonperfused sinusoids and pyridine nucleotide (NADH) autofluorescence in livers of wild-type, SCID, and interferon-gamma (IFN-gamma) knockout mice exposed to 15 min of gut ischemia and 1 h of reperfusion. In wild-type mice, gut I/R elicited significant increases in the number of stationary leukocytes, nonperfused sinusoids, NADH autofluorescence (indicating hypoxia), and elevated plasma alanine aminotransferase (ALT) and TNF-alpha levels. All of these responses were profoundly attenuated in SCID mice, while only some of the responses (in the midzonal region) were blunted in IFN-gamma knockout mice. Reconstitution (24 h before ischemia) of the circulating lymphocyte pool with T-cell enriched splenocytes, but not T cell deficient (from nude mice), CD4+ T-cell depleted splenocytes or splenocytes derived from IFN-gamma knockout mice, allowed the SCID mice to respond to gut I/R in a manner similar to wild-type mice. Some of the responses were restored following reconstitution with CD8+ T-cell depleted splenocytes. These findings implicate CD4+ T-lymphocytes and IFN-gamma in the hepatic microvascular dysfunction and inflammatory cell accumulation elicited by gut I/R. SN - 1073-9688 UR - https://www.unboundmedicine.com/medline/citation/10654278/T_lymphocytes_contribute_to_hepatic_leukostasis_and_hypoxic_stress_induced_by_gut_ischemia_reperfusion_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1073-9688&date=1999&volume=6&issue=4&spage=267 DB - PRIME DP - Unbound Medicine ER -