Abstract
Purpose of study: Interleukin-2 (IL-2) is a potent activator of lymphocytes, but its effectiveness as an anticancer agent is compromised by several adverse side effects including pulmonary edema. One explanation for the pulmonary toxicity of IL-2 is that activated lymphocytes directly induce the pulmonary vascular endothelium to become more leaky. Methods: To test this hypothesis the number of total lymphocytes, γδ T cells, and CD2- positive cells (αβ T cells and natural killer cells) in peripheral blood and lung lymph of sheep were compared before and after IL-2 infusion. Hemodynamic and lymph dynamic changes were also evaluated. Results: IL-2 decreased mean aortic pressure, increased cardiac output, lowered systemic vascular resistance, and doubled lung lymph flow (P ≤ 0.05), but had no effect on plasma or lymph oncotic pressure. The lymph protein concentration and the lymph-to-plasma protein concentration ratio were not different after IL-2 infusion. IL-2 had no effect on the number of total lymphocytes, γδ T cells, or CD2-positive cells in the peripheral blood. In contrast, the number of total lymphocytes, γδ T cells, and CD2-positive cells in lung lymph decreased significantly (P ≤ 0.05). Conclusions: The lymphocyte populations decreased more than could be explained by the increase in lymph flow, demonstrating that lung lymphocytes were not reduced simply by dilution. These results imply that the pulmonary edema associated with IL-2 is not caused by activated lymphocytes.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 163-167 |
| Number of pages | 5 |
| Journal | Journal of Surgical Research |
| Volume | 60 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 1 1996 |
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ASJC Scopus subject areas
- Surgery
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Interleukin-2 does not sequester activated lymphocytes into lung lymph of sheep. / Mahvi, David M.; Conhaim, Robert L.; Harms, Bruce A.; Storm, F. Kristian.
In: Journal of Surgical Research, Vol. 60, No. 1, 01.01.1996, p. 163-167.Research output: Contribution to journal › Article
TY - JOUR
T1 - Interleukin-2 does not sequester activated lymphocytes into lung lymph of sheep
AU - Mahvi, David M.
AU - Conhaim, Robert L.
AU - Harms, Bruce A.
AU - Storm, F. Kristian
PY - 1996/1/1
Y1 - 1996/1/1
N2 - Purpose of study: Interleukin-2 (IL-2) is a potent activator of lymphocytes, but its effectiveness as an anticancer agent is compromised by several adverse side effects including pulmonary edema. One explanation for the pulmonary toxicity of IL-2 is that activated lymphocytes directly induce the pulmonary vascular endothelium to become more leaky. Methods: To test this hypothesis the number of total lymphocytes, γδ T cells, and CD2- positive cells (αβ T cells and natural killer cells) in peripheral blood and lung lymph of sheep were compared before and after IL-2 infusion. Hemodynamic and lymph dynamic changes were also evaluated. Results: IL-2 decreased mean aortic pressure, increased cardiac output, lowered systemic vascular resistance, and doubled lung lymph flow (P ≤ 0.05), but had no effect on plasma or lymph oncotic pressure. The lymph protein concentration and the lymph-to-plasma protein concentration ratio were not different after IL-2 infusion. IL-2 had no effect on the number of total lymphocytes, γδ T cells, or CD2-positive cells in the peripheral blood. In contrast, the number of total lymphocytes, γδ T cells, and CD2-positive cells in lung lymph decreased significantly (P ≤ 0.05). Conclusions: The lymphocyte populations decreased more than could be explained by the increase in lymph flow, demonstrating that lung lymphocytes were not reduced simply by dilution. These results imply that the pulmonary edema associated with IL-2 is not caused by activated lymphocytes.
AB - Purpose of study: Interleukin-2 (IL-2) is a potent activator of lymphocytes, but its effectiveness as an anticancer agent is compromised by several adverse side effects including pulmonary edema. One explanation for the pulmonary toxicity of IL-2 is that activated lymphocytes directly induce the pulmonary vascular endothelium to become more leaky. Methods: To test this hypothesis the number of total lymphocytes, γδ T cells, and CD2- positive cells (αβ T cells and natural killer cells) in peripheral blood and lung lymph of sheep were compared before and after IL-2 infusion. Hemodynamic and lymph dynamic changes were also evaluated. Results: IL-2 decreased mean aortic pressure, increased cardiac output, lowered systemic vascular resistance, and doubled lung lymph flow (P ≤ 0.05), but had no effect on plasma or lymph oncotic pressure. The lymph protein concentration and the lymph-to-plasma protein concentration ratio were not different after IL-2 infusion. IL-2 had no effect on the number of total lymphocytes, γδ T cells, or CD2-positive cells in the peripheral blood. In contrast, the number of total lymphocytes, γδ T cells, and CD2-positive cells in lung lymph decreased significantly (P ≤ 0.05). Conclusions: The lymphocyte populations decreased more than could be explained by the increase in lymph flow, demonstrating that lung lymphocytes were not reduced simply by dilution. These results imply that the pulmonary edema associated with IL-2 is not caused by activated lymphocytes.
UR - http://www.scopus.com/inward/record.url?scp=0030027028&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030027028&partnerID=8YFLogxK
U2 - 10.1006/jsre.1996.0026
DO - 10.1006/jsre.1996.0026
M3 - Article
C2 - 8592409
AN - SCOPUS:0030027028
VL - 60
SP - 163
EP - 167
JO - Journal of Surgical Research
JF - Journal of Surgical Research
SN - 0022-4804
IS - 1
ER -