Lymphocyte-Macrophage Interactions in the Response to Surgical Infections

Christou, Nicolas V.; Mannick, John A.; West, Michael A.; Kasper, Dennis L.

doi:10.1001/archsurg.1987.01400140121017

Cited by 32 publications

(14 citation statements)

References 78 publications

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“…MDP, a known modulator of the hepatic macrophage [18], has been demonstrated to have a nonspecific immunostimulating effect in various pathological conditions such as septic shock and bacterial challenge [33,34]. Moreover MDP is able to elicit, but not to fully activate, macrophages [35]. Pretreatment of rats with 500 g of MDP administered intravenously 5 min prior to the induction of liver ischemia was followed by a significant improvement of phagocytic activity of Kupffer cells.…”

Section: Discussionmentioning

confidence: 99%

Improvement of Normothermic Rat Liver Ischemia/Reperfusion by Muramyl Dipeptide

Cursio¹,

Gugenheim²,

Panaïa‐Ferrari³

et al. 1998

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Improvement of Normothermic Rat Liver Ischemia/Reperfusion by Muramyl Dipeptide

Cursio¹,

Gugenheim²,

Panaïa‐Ferrari³

et al. 1998

Journal of Surgical Research

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“…It has been shown that after he patic ischemia in baboons [22] or in dogs [18], the RES phagocytic dysfunction may contribute to systemic endotoxinemia and death. According to Christou et al [23] resi dent macrophages can be elicited in a first moment and then with more potent stimuli fully activated. The two functions of hepatic macrophages, phagocytic capacity and mono kine release, are related to these different steps of activation.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Prostaglandin E<sub>1</sub>on Normothermic Liver Ischemia

Crafa¹,

Gugenheim²,

Saint–Paul

et al. 1991

Eur Surg Res

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Effects of treatment with prostaglandin E₁ (PgE₁) on normothermic liver ischemia were studied in male Lewis rats. Animals were subjected to 90 min of warm liver ischemia. Two groups of rats were constituted: group A (no treatment) and group B (PgE₁ treatment). PgE₁ (100 µg/kg) was given as a bolus 2 min before induction of ischemia and 2 min before the end of ischemia. Survival rates were assessed and, 6 h after the end of ischemia, serum transaminases, histology of the liver, Kupffer cell activity were evaluated. PgE₁ treatment significantly improved survival rate (80%) in comparison with the nontreated group (40%). A significant reduction in transaminase levels was observed after PgE₁ treatment. The extent of necrosis and congestion was improved by PgE₁ treatment. Sheep red blood cell ⁵¹Cr liver uptake was deeply depressed 6 h after the end of ischemia in group A (6 ± 2.3 %/g tissue), and was significantly higher (p < 0.001) after PgE₁ administration in group B (32.98 ± 11.7 %/g tissue). Our results demonstrate that PgE₁ is able to protect the liver from ischemic insult. The mechanism by which prostaglandins exert this beneficial effect on normothermic liver ischemia may be related to their action on hepatic macrophages.

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“…Using the 72-hour immunostimulatory skin test regimen, we were able to demonstrate a prolonged postoperative im munosuppression in contrast to previous studies using weekly test regimens [19,24], At present, one can merely speculate about the clinical implications of the duration of postoperative immunosuppression. Available data indicate that impaired preoperative and postoperative CMI is an important risk factor and related to postoperative infection and death [6,18,[25][26][27], We failed, however, to show any significant difference in the DTH response between patients with postoperative infectious complications and patients with out.…”

Section: Discussionmentioning

confidence: 85%

“…Several other abnormalities in cellular immune responses have been dem onstrated after surgery or other injuries [5.6. 19-22], The precise mechanism leading to posttraumatic appearance of circulating im munosuppressive substances, as well as com plex lymphocyte-macrophage interactions, have been described [6,22,23]. Hitherto, much effort has been made to prevent or reverse posttraumatic immunosuppression [5.…”

Section: Discussionmentioning

confidence: 99%

Duration of Postoperative Immunosuppression Assessed by Repeated Delayed Type Hypersensitivity Skin Tests

et al. 1992

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The duration of postoperative impairment in cell-mediated immunity was assessed by repeated skin testing with seven delayed type common antigens in 15 patients undergoing major elective abdominal surgery compared to a similar testing regimen in 10 healthy volunteers. All were skin tested four times, with 72-hour intervals, and in the surgical patients the first test was applied 2 days before surgery, followed by tests on postoperative days 1, 4 and 7. The tests were read after 48 h. Postoperatively, the skin test area decreased on day 3 (p < 0.01) and recurred to preoperative levels on day 9. In contrast, the skin test area in the volunteers increased from test to test (p < 0.001) during the study, confirming a previous finding of a vaccination effect. These results suggest that the postoperative immunosuppression is maintained for about 6-9 days.

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Lymphocyte-Macrophage Interactions in the Response to Surgical Infections

Cited by 32 publications

References 78 publications

Improvement of Normothermic Rat Liver Ischemia/Reperfusion by Muramyl Dipeptide

Improvement of Normothermic Rat Liver Ischemia/Reperfusion by Muramyl Dipeptide

Protective Effects of Prostaglandin E<sub>1</sub>on Normothermic Liver Ischemia

Duration of Postoperative Immunosuppression Assessed by Repeated Delayed Type Hypersensitivity Skin Tests

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