Inverse association between endogenous glucocorticoid secretion and L-selectin (CD62L) expression in trauma patients

Faßbender, Klaus; Kaptur, S.; Becker, Peter L.; Gröschel, Joachim; Schmidt, Roland; Hennerici, Michael G.

doi:10.1016/s0024-3205(99)00513-5

Cited by 16 publications

(13 citation statements)

References 24 publications

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“…Increased expression of CD11b and decreased expression of CD62L markers 4 and 6 h after HC administration is consistent with the changes in adhesive molecule expression observed during conditions of increased endogenous cortisol secretion such as surgical trauma [21]. A similar pattern of CD11b and CD62L changes was also observed in myocardial infarction; however, no cortisol data are available in that study [22].…”

Section: Discussionsupporting

confidence: 75%

Pharmacological Hyperprolactinemia Attenuates Hydrocortisone-Induced Expression of CD11b on Human CD8+ Cells in vivo

Imrich

Tibenská²,

Koška³

et al. 2004

Neuroimmunomodulation

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Objective: To study the short-term influences of pharmacologic hyperprolactinemia on hydrocortisone (HC)-induced effects on selected immune parameters. Methods: A single dose of HC (40 mg per os) was administered to eleven healthy female volunteers 1 h after domperidone (10 mg per os) or placebo administration. Immune cell subsets and expression of adhesion molecules was assessed by flow cytometry at baseline and 4 and 6 h after HC administration. Intracellular staining of interleukin-4 (IL-4) and interferon-gamma (IFN-γ) production in CD4+ lymphocytes after phorbol myristate acetate and ionomycin stimulation was performed at the same time points. Results: HC administration was followed by a significant increase in cortisol levels, numbers of leukocytes and granulocytes and the percentage of CD16+, CD19+, CD11a+, CD11a+CD8+, CD11b+ and CD11b+CD8+ cells. The number of lymphocytes and monocytes and the percentage of CD3+, CD4+, CD4+/CD8+ ratio, CD62L+, CD54+ and CD54+CD16+ cells decreased, while the percentage of CD8+ cells was unaffected. Domperidone administration resulted in a significant increase in prolactin (PRL) concentrations. During hyperprolactinemia, the HC-induced increase in CD11b+CD8+ cells was significantly (p < 0.05) attenuated at 4 h. HC-induced changes in other immune parameters remained unaffected. No significant changes in the intracellular production of IL-4 and IFN-γ in CD4+ lymphocytes were observed after a single dose of HC alone or during hyperprolactinemia. Conclusions: This study shows an attenuated HC-induced increase in CD11b+CD8+ cells in the peripheral blood of healthy females during hyperprolactinemia. Our in vivo observations suggest that short-term interactions occur between PRL and glucocorticoids, affecting selected immune functions. Further studies are needed for confirmation of these results.

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Section: Discussionsupporting

confidence: 75%

Pharmacological Hyperprolactinemia Attenuates Hydrocortisone-Induced Expression of CD11b on Human CD8+ Cells in vivo

Imrich

Tibenská²,

Koška³

et al. 2004

Neuroimmunomodulation

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“…When interpreting the data it is important to recognize that high CD11b expression is not specific for infection-triggered inflammation and may, at least in adults, be induced by a variety of noninfectious conditions, such as trauma and autoimmune diseases (15)(16)(17)(21)(22)(23)(24)(25). In the present study, specificity and sensitivity of the CD11b test for sepsis were reasonably high in monocytes, but the specificity was quite poor in neutrophils.…”

Section: Discussionmentioning

confidence: 51%

Increased CD11b-Density on Circulating Phagocytes as an Early Sign of Late-Onset Sepsis in Extremely Low-Birth-Weight Infants

Turunen¹,

Andersson²,

Nupponen³

et al. 2005

Pediatr Res

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“…Although intriguing, this hypothesis cannot account for effects of glucocorticoids observed at earlier time points. For example, Fassbender et al reported dexamethasone-induced shedding of L-selectin 1 h after systemic treatment (19). In addition, our previous studies indicate that L-selectin is shed from circulating neutrophils within 30 min of exposure to elevated systemic levels of glucocorticoids (16).…”

Section: Discussionmentioning

confidence: 87%

“…Conflicting results exist as to whether in vivo glucocorticoid treatment affects Mac-1 expression on neutrophils. Some studies show decreased CD18 expression (11), whereas others show increased expression (19) or no change (17). To determine whether ANX1 activates neutrophils, we investigated the effect of ANX1 treatment on Mac-1 expression.…”

Section: Effect Of Anx1 On Neutrophil Activationmentioning

confidence: 99%

“…In addition, our previous work has shown that inhibition of L-selectin-dependent plasma extravasation is blocked by both adrenalectomy and a glucocorticoid synthesis inhibitor (15,16). However, when neutrophils are treated in vitro with doses of glucocorticoids that produce L-selectin shedding in vivo, shedding is not observed (17)(18)(19). This discrepancy between in vivo and in vitro results suggests that glucocorticoids do not directly affect neutrophil L-selectin expression but instead act indirectly via a heretofore unknown mediator.…”

mentioning

confidence: 93%

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A Potential Role for Annexin 1 as a Physiologic Mediator of Glucocorticoid-Induced L-Selectin Shedding from Myeloid Cells

Strausbaugh

Rosen

2001

The Journal of Immunology

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Glucocorticoids can dampen inflammatory responses by inhibiting neutrophil recruitment to tissue sites. The detailed mechanism by which glucocorticoids exert this affect on neutrophils is unknown. L-selectin is a leukocyte cell surface receptor that is implicated in several steps of neutrophil recruitment. Recently, several studies have shown that systemic treatment of animals and humans with glucocorticoids induces decreased L-selectin expression on neutrophils, suggesting one mechanism by which inflammation may be negatively regulated. However, when neutrophils are treated in vitro with glucocorticoids, no effect on L-selectin expression is observed. Thus, the existence of an additional mediator is plausible. In this study, we investigate whether annexin 1 (ANX1), a recognized second messenger of glucocorticoids, could be such a mediator. We show that ANX1 induces a dose- and time-dependent decrease in L-selectin expression on both peripheral blood neutrophils and monocytes but has no effect on lymphocytes. The loss of L-selectin from neutrophils is due to shedding that is mediated by a cell surface metalloprotease (“sheddase”). Using cell shape and a β2 integrin activation epitope, we show that the ANX1-induced shedding of L-selectin appears to occur without overt cell activation. These data may provide the basis for further understanding of mechanisms involved in the down-regulation of inflammatory responses.

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Inverse association between endogenous glucocorticoid secretion and L-selectin (CD62L) expression in trauma patients

Cited by 16 publications

References 24 publications

Pharmacological Hyperprolactinemia Attenuates Hydrocortisone-Induced Expression of CD11b on Human CD8+ Cells in vivo

Pharmacological Hyperprolactinemia Attenuates Hydrocortisone-Induced Expression of CD11b on Human CD8+ Cells in vivo

Increased CD11b-Density on Circulating Phagocytes as an Early Sign of Late-Onset Sepsis in Extremely Low-Birth-Weight Infants

A Potential Role for Annexin 1 as a Physiologic Mediator of Glucocorticoid-Induced L-Selectin Shedding from Myeloid Cells

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