Corticosteroids increase blood interleukin-10 levels during cardiopulmonary bypass in men

Tabardel, Y; Duchateau, Jean; Schmartz, Denis; Marécaux, Gaëtan; Shahla, M.; Barvais, Luc; Leclerc, Jean Louis; Vincent, Jean‐Louis

doi:10.1016/s0039-6060(96)80217-0

Cited by 161 publications

(73 citation statements)

References 17 publications

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“…The levels of IL-10 mRNA in PBMC increased during the first month of treatment, although prednisolone treatment did not affect the IL-10 plasma levels or the potential of PBMC to produce IL-10 in response to MLSA. Similar conflicting data for the effect of GCs on IL-10 have been obtained for other diseases and experimental models (8,12,14,44). Consistent with our findings, Atkinson et al (2) showed that prednisolone treatment reduced production of IL-10 in skin lesions in patients with T1R, and Moraes et al (31) found that IL-10 mRNA expression in skin lesions in patients with T1R is insensitive to prednisolone treatment.…”

Section: Discussionsupporting

confidence: 91%

Effects of Prednisolone Treatment on Cytokine Expression in Patients with Leprosy Type 1 Reactions

et al. 2005

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Leprosy type 1 reactions (T1R) are due to increased cell-mediated immunity and result in localized tissue damage. The anti-inflammatory drug prednisolone is used for treatment, but there is little good in vivo data on the molecular actions of prednisolone. We investigated the effect of prednisolone treatment on tumor necrosis factor alpha (TNF-␣), interleukin-1␤ (IL-1␤), IL-10, and transforming growth factor ␤1 (TGF-␤1) mRNA and protein expression in blood and skin biopsies from 30 patients with T1R in India. After 1 month of prednisolone treatment the sizes of the skin granulomas were reduced, as were the grades of cells positive for TNF-␣ and IL-10 in skin lesions. Increased production of TGF-␤1 was seen in skin lesions after 6 months of prednisolone treatment. Expression of mRNA for TNF-␣, IL-1␤, and TGF-␤1 was reduced, whereas no change in IL-10 mRNA expression was detected during treatment. The circulating cytokine profiles were similar in patients with and without T1R, and prednisolone treatment had no detectable effects on cytokine expression in the blood. The data emphasize the compartmentalization of pathology in T1R and the importance of the immune response in the skin. Clinical improvement and cytokine expression were compared. Surprisingly, patients with improved skin and nerve function and patients with nonimproved skin and nerve function had similar cytokine profiles, suggesting that clinical improvement is not directly mediated by the cytokines studied here. This in vivo well-controlled study of the immunosuppressive effects of prednisolone showed that the drug does not switch off cytokine responses effectively.

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Section: Discussionsupporting

confidence: 91%

Effects of Prednisolone Treatment on Cytokine Expression in Patients with Leprosy Type 1 Reactions

et al. 2005

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“…Rezende et al (64) suggested that immunocomplexes from patients with chronic intestinal schistosomiasis are able to modulate granulomatous hypersensitivity to S. mansoni eggs by inducing prostaglandin E production that augments the IL-10 level. A rise in IL-10 levels in response to dexamethasone treatment was also described for several in vivo and in vitro models (19,31,68).…”

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confidence: 64%

Dexamethasone, a Drug for Attenuation ofSchistosoma mansoniInfection Morbidity

Pyrrho

Ramos²,

Neto³

et al. 2002

Antimicrob Agents Chemother

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To investigate the possible use of immunomodulators as coadjuvants in the treatment of chronic schistosomiasis, the study described in the present report evaluated the effects of dexamethasone on several parameters which reflect disease severity and morbidity. Parasitological, immunological, and histological parameters were analyzed in animals treated from the first day of infection or after 35 days of infection. In both situations, dexamethasone had no effect on the parasite burden but altered the egg distribution in tissue, indicating that under the schedule used it did not interfere with the development of adult worms or oviposition. Treated mice showed a decrease in the number of eggs in hepatic tissue, reduced granuloma sizes, reduced levels of granuloma maturation, and reduced collagen contents. Dexamethasone-treated mice also had decreased gamma interferon, interleukin-12 (IL-12), and IL-4 levels in serum and increased IL-10 levels in serum. Taken together, these data suggested a decrease in the severity of murine schistosomiasis and point to dexamethasone as a convenient and promising coadjuvant agent in the therapy of this infection.

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“…Steroids may in fact have other important effects in the immature heart and after CPB/DHCA, including increasing L-type calcium current (28,29) or through antiinflammatory properties (9,10). Nevertheless, there is significant evidence that calpain activation and TnI degradation are sufficient to cause myocardial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids Preserve Calpastatin and Troponin I during Cardiopulmonary Bypass in Immature Pigs

et al. 2003

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Degradation of troponin I (TnI) by calpain occurs with myocardial stunning in ischemia-reperfusion injury. Glucocorticoids attenuate myocardial ischemia-reperfusion injury, but their effect on TnI degradation is unknown. A piglet model was used to test the hypotheses that cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) are associated with TnI degradation and that TnI alterations could be prevented by glucocorticoid treatment. Piglets were cooled to 18°C, subjected to 2 h of circulatory arrest, rewarmed to 37°C, and allowed to recover for 2 h. Methylprednisolone was administered 6 h before surgery (3 0 mg/kg) and at initiation of CPB (30 mg/kg). The untreated group received saline. Left ventricular tissue was collected after recovery and analyzed by Western blot for TnI, calpain, and calpastatin (the natural inhibitor of calpain). CPB/ DHCA animals had 27.4 Ϯ 0.2% of total detected TnI present in degraded form. Glucocorticoid treatment significantly decreased the percentage of degraded TnI (12.0 Ϯ 0.1%, p Ͻ 0.05). Calpain I and calpain II increased after CPB/DHCA compared with non-CPB/DHCA controls (p Ͻ 0.05), with or without glucocorticoid treatment. Calpastatin significantly decreased in untreated CPB/DHCA animals compared with non-CPB/DHCA controls (p Ͻ 0.05), but levels were preserved by glucocorticoids. Glucocorticoids were associated with preservation of maximum rate of increase of left ventricular pressure at 95 Ϯ 10% of baseline, whereas maximum rate of increase of left ventricular pressure decreased to 62 Ϯ 12% of baseline without steroids. TnI degradation occurs after CPB/DHCA in neonatal pigs. Reduction in reperfusion injury by glucocorticoids may depend partly on preservation of calpastatin activity and intact TnI. Surgery for congenital heart disease often requires CPB and periods of myocardial ischemia. A period of total circulatory arrest may also be required, particularly for complex neonatal repairs. In the first 8 to 12 h after CPB there is a transient decrease in myocardial function consistent with reperfusion injury (1). Although the exact mechanisms of CPB-related myocardial injury remain unknown, there is substantial evidence that CPB can produce a systemic inflammatory response or free radical injury (2-4). The cysteine protease calpain exists in the myocardium in two isoforms, calpain I and calpain II. Recently, it has been suggested that activation of calpain during reperfusion of ischemic myocardium may be a key event in the process of myocardial stunning (5, 6). Calcium influx that occurs when ischemic myocardium is reperfused promotes dissociation of calpain from its inhibitor, calpastatin. Activated calpain then degrades the contractile regulatory protein TnI by cleavage at the C-terminus to form the fragment . Additional systematic degradation of the amino terminus can lead to subsequent smaller degradation products. Degradation products and covalent complexes of TnI have been observed in humans with ischemic heart disease (7,8).The use of glucocorticoids ...

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Corticosteroids increase blood interleukin-10 levels during cardiopulmonary bypass in men

Cited by 161 publications

References 17 publications

Effects of Prednisolone Treatment on Cytokine Expression in Patients with Leprosy Type 1 Reactions

Effects of Prednisolone Treatment on Cytokine Expression in Patients with Leprosy Type 1 Reactions

Dexamethasone, a Drug for Attenuation ofSchistosoma mansoniInfection Morbidity

Glucocorticoids Preserve Calpastatin and Troponin I during Cardiopulmonary Bypass in Immature Pigs

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