Expression of Human Neutrophil L-Selectin During the Systemic Inflammatory Response Syndrome Is Partly Mediated by Tumor Necrosis Factor α

Ahmed, Najma; Yee, John; Giannias, Betty; Kapadia, Bomi; Christou, Nicolas V.

doi:10.1001/archsurg.1996.01430130033006

Cited by 21 publications

(7 citation statements)

References 26 publications

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“…In this investigation by (16). In septic shock and in critically ill patients with SIRS, the level of expression of circulating PMN L-selectin was decreased (17,18). The results of the present investigation are able to explain the increased expression of L-selectin on PMN observed after trauma.…”

Section: Discussionsupporting

confidence: 48%

Functional and phenotypic changes in polymorphonuclear neutrophils induced by catecholamines

Trabold

Gruber

Fröhlich

2007

Scandinavian Cardiovascular Journal

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Section: Discussionsupporting

confidence: 48%

Functional and phenotypic changes in polymorphonuclear neutrophils induced by catecholamines

Trabold

Gruber

Fröhlich

2007

Scandinavian Cardiovascular Journal

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“…For both hypotonicity (Fig. 1) and hypertonicity (15), the decrease was much slower than in the case of cytokines, where a near-maximum effect is usually seen within 30 min (1).…”

Section: Effect Of Hypotonicity On L-selectin Sheddingmentioning

confidence: 77%

Hypotonicity induces L-selectin shedding in human neutrophils

Kaba

Knauf

2001

American Journal of Physiology-Cell Physiology

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Expression levels of adhesion molecules on neutrophils are affected under various conditions, including ischemia, possibly because of associated increases in cell volume. We examined the effects of cell swelling in hypotonic media on the level of L-selectin (CD62L) and beta(2)-integrin (CD18) on human neutrophils. In hypotonic media, neutrophils shed L-selectin. The shedding was greatly reduced by 30 microM RO31-9790, the metalloprotease (sheddase) inhibitor. Hypotonicity-induced L-selectin shedding was also time and tonicity dependent. Decreasing tonicity caused increased shedding. In 0.6x medium (0.6x the normal tonicity of 300 mosmol/kgH(2)O), shedding increased over a 2-h period, after which >70% of the neutrophils had lost L-selectin. In contrast to L-selectin, the level of beta(2)-integrin on the neutrophil surface was not significantly affected. Thus L-selectin shedding, which occurs on neutrophil activation and is usually accompanied by beta(2)-integrin upregulation, was selectively induced by hypotonicity without a corresponding effect on beta(2)-integrin.

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“…L-Selectin (CD62L) is a constitutively expressed adhesion molecule present on neutrophils that participates in the initiation of this cell's migration into the extravascular space (8,9,23,48). L-Selectin has been linked to the pathogenesis of several neutrophil-mediated inflammatory disorders, including sepsis, acute lung injury, ischemia-reperfusion injury, and renal allograft rejection (1,2,13,26,28,29,45,46). Both HRL-3 and other L-selectin-directed monoclonal antibodies have been demonstrated previously to strongly influence neutrophil trafficking in the lung and other organs (24,26,28,44).…”

mentioning

confidence: 99%

Neutrophil inhibition with L-selectin-directed MAb improves or worsens survival dependent on the route but not severity of infection in a rat sepsis model

Haley¹,

Parent

Cui

et al. 2005

Journal of Applied Physiology

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Both route and severity of infection may influence immunomodulator agents in sepsis. We studied the effect of each variable on HRL-3, an L-selectin-directed MAb that inhibits neutrophil function, in a rat sepsis model. Animals (n = 800) were randomized to be treated with either HRL-3 or placebo and to receive Escherichia coli either intravenously (IV) or intrabronchially (IB) in doses producing low or high mortality rates. Animals received antibiotics and were observed for 168 h. Route but not dose of E. coli altered the effects HRL-3 on mortality rate (mean hazards ratio +/- SE). With IV E. coli, compared with control, HRL-3 was beneficial and reduced the hazards ratio both early (0 to 6 h; -0.75 +/- 0.23) and late (6 to 168 h; -0.72 +/- 0.36) (P = 0.001 and 0.04, respectively, over all E. coli doses). In contrast, with IB E. coli HRL-3 reduced the hazards ratio early (-1.1 +/- 0.36) but worsened it late (0.87 +/- 0.23) (P = 0.002 for both effects over all E. coli doses) in patterns significantly different from IV E. coli (P < 0.0001). Compared with control, although HRL-3 did not alter lung neutrophil numbers or injury score at 6 or 168 h with IV E. coli (P = ns for all), it reduced both early and increased them late with IB E. coli (P

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Expression of Human Neutrophil L-Selectin During the Systemic Inflammatory Response Syndrome Is Partly Mediated by Tumor Necrosis Factor α

Abstract: Tumor necrosis factor alpha may act as a paracrine modulator of site-specific neutrophil rolling, adhesion, and exudation via mechanisms that involve the down-regulation of L-selectin.

Cited by 21 publications

References 26 publications

Functional and phenotypic changes in polymorphonuclear neutrophils induced by catecholamines

Functional and phenotypic changes in polymorphonuclear neutrophils induced by catecholamines

Hypotonicity induces L-selectin shedding in human neutrophils

Neutrophil inhibition with L-selectin-directed MAb improves or worsens survival dependent on the route but not severity of infection in a rat sepsis model

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