Elastase and metalloproteinase activities regulate soluble complement receptor 1 release

Sadallah, Salima; Hess, Christoph; Miot, Sylvie; Spertini, Olivier; Lutz, Hans; Ja, Schifferli

doi:10.1002/(sici)1521-4141(199911)29:11<3754::aid-immu3754>3.0.co;2-5

Cited by 47 publications

(23 citation statements)

References 21 publications

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“…Under these conditions, as a low-affinity IgG receptor, soluble CD16 could play a role in binding immune complexes (10). Elevated levels of soluble CD35 have also been observed in synovial fluid obtained from individuals with arthritis, suggesting that this complement receptor might be shed from neutrophils to control complement activation and downregulate local inflammation (22). The increase in plasma Mb concentration and CK activity after exercise in our study is indirect evidence that some muscle damage may have occurred during exercise.…”

Section: Discussionsupporting

confidence: 50%

“…One possibility is that the downregulation of CD11b and CD35 expression was the result of the cleavage of receptors from the neutrophil cell membrane by proteolytic enzymes. Incubation of neutrophils in vitro with serine or metalloproteinase enzymes similar to those enzymes released during neutrophil degranulation causes the proteolytic degradation of the plasma membrane portion of the CD11b, CD16, and CD35 receptors (3,7,22). The proteolytic cleavage of neutrophil surface receptors could possibly be part of a regulatory control loop to prevent excessive neutrophil infiltration and activation within tissues.…”

Section: Discussionmentioning

confidence: 99%

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Changes in neutrophil surface receptor expression, degranulation, and respiratory burst activity after moderate- and high-intensity exercise

Peake¹,

Wilson²,

Hordern³

et al. 2004

Journal of Applied Physiology

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Intense exercise stimulates the systemic release of a variety of factors that alter neutrophil surface receptor expression and functional activity. These alterations may influence resistance to infection after intense exercise. The aim of this study was to examine the influence of exercise intensity on neutrophil receptor expression, degranulation (measured by plasma and intracellular myeloperoxidase concentrations), and respiratory burst activity. Ten well-trained male runners ran on a treadmill for 60 min at 60% [moderate-intensity exercise (MI)] and 85% maximal oxygen consumption [high-intensity exercise (HI)]. Blood was drawn immediately before and after exercise and at 1 h postexercise. Immediately after HI, the expression of the neutrophil receptor CD16 was significantly below preexercise values (P < 0.01), whereas MI significantly reduced CD35 expression below preexercise values (P < 0.05). One hour after exercise at both intensities, there was a significant decline in CD11b expression (P < 0.05) and a further decrease in CD16 expression compared with preexercise values (P < 0.01). CD16 expression was lower 1 h after HI than 1 h after MI (P < 0.01). Immediately after HI, intracellular myeloperoxidase concentration was less than preexercise values (P < 0.01), whereas plasma myeloperoxidase concentration was greater (P < 0.01), indicating that HI stimulated neutrophil degranulation. Plasma myeloperoxidase concentration was higher immediately after HI than after MI (P < 0.01). Neutrophil respiratory burst activity increased after HI (P < 0.01). In summary, both MI and HI reduced neutrophil surface receptor expression. Although CD16 expression was reduced to a greater extent after HI, this reduction did not impair neutrophil degranulation and respiratory burst activity.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Changes in neutrophil surface receptor expression, degranulation, and respiratory burst activity after moderate- and high-intensity exercise

Peake¹,

Wilson²,

Hordern³

et al. 2004

Journal of Applied Physiology

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“…Recent studies have shown that NE cleaves vitamin D-binding protein, a molecule that binds to the surface of neutrophils and amplifies the complement C5a chemotactic activity (13). At the same time, it was shown elsewhere that NE is able to release complement receptor 1, which acts as an inhibitor of complement (14). The substrate repertoire of NE also comprises ␣ 1 -antiprotease inhibitor and proteins of the extracellular matrix (ECM) such as collagen and laminin.…”

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confidence: 99%

Deficiency in Neutrophil Elastase Does Not Impair Neutrophil Recruitment to Inflamed Sites

Hirche

Atkinson

Bahr

et al. 2004

Am J Respir Cell Mol Biol

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To reach the sites of inflammation, neutrophils traverse the endothelium, its underlying basement membrane, and other barriers depending on the localization of the insulting agent. Whether neutrophil elastase (NE) plays a role in neutrophil recruitment to inflamed sites is still debatable. By exploiting mice deficient in NE (NE(-/-)), we sought to address this dilemma. We recruited neutrophils to the lungs or the peritoneum of wild-type (WT) or NE(-/-) mice by intranasal or intraperitoneal challenge with Pseudomonas aeruginosa or its lipopolysaccharide. At designated times post-inoculation (0, 4, 24, and 48 h), groups of mice were killed to assess changes in leukocyte counts and inflammatory responses. NE(-/-) and WT mice had normal circulating leukocyte numbers including neutrophils and changes in the hemograms in the setting of acute inflammation were indistinguishable. Analyses of lung tissues or fluids from the lungs and peritoneum found that regardless of the inflammatory model, the leukocyte counts including neutrophils and the inflammatory response were similar in NE(-/-) and WT mice at all time points. In vitro, neutrophils isolated from the lungs or the peritoneum of NE(-/-) and WT mice had comparable chemotactic and respiratory-burst functions and migrated normally through Matrigel in response to various stimuli. Interestingly, preincubation of human peripheral blood neutrophils with NE physiologic inhibitors did not alter the migration of the cells through Matrigel. In sum, our findings present the first in vivo description that the absence of NE does not impair neutrophil recruitment to inflamed sites and that NE is not required for basement membrane transmigration of neutrophils.

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“…In our case, the decrease in neutrophil response is most likely due to both the high concentration of microorganisms and, therefore, a high share of the internalization of CR3-receptors and the possible splitting of neutrophil CR1-receptors in the presence of high levels of serine proteases [22, 23]. …”

Section: Discussionmentioning

confidence: 99%

The Level of Oxidative Neutrophil Response When Determining Endotoxin Activity Assay: A New Biomarker for Defining the Indications and Effectiveness of Intensive Care in Patients with Sepsis

Yaroustovsky

Rogalskaya

Plyushch

et al. 2017

International Journal of Inflammation

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Background. To analyse the clinical informativity of the neutrophil oxidative response level (“Response”) during an Endotoxin Activity Assay (EAA) as a new biomarker defining the indications and effectiveness of intensive care in cardiac surgical patients with septic complications. Methods. Blood samples were taken from 198 adult patients who were admitted to the ICU after cardiac surgery (SIRS: 34, MODS: 36, and sepsis: 128). The composite of laboratory studies included CRP, PCT, EAA with “Response” level, and presepsin. Results. 83% of patients had a “normal” neutrophil response, 12% of patients had a low neutrophil response, and 5% of patients had a critically low neutrophil response. Patients with critically low responses had the lowest values of the EAA and the highest concentrations of PSP and D-dimer (p < 0.05). Conclusions. EAA results should be interpreted with the level of neutrophil response. “Response” > 0.5 has a negative predictive value; the EAA < 0.6 at “Response” < 0.5 may indicate a high level of endotoxaemia.

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Elastase and metalloproteinase activities regulate soluble complement receptor 1 release

Cited by 47 publications

References 21 publications

Changes in neutrophil surface receptor expression, degranulation, and respiratory burst activity after moderate- and high-intensity exercise

Changes in neutrophil surface receptor expression, degranulation, and respiratory burst activity after moderate- and high-intensity exercise

Deficiency in Neutrophil Elastase Does Not Impair Neutrophil Recruitment to Inflamed Sites

The Level of Oxidative Neutrophil Response When Determining Endotoxin Activity Assay: A New Biomarker for Defining the Indications and Effectiveness of Intensive Care in Patients with Sepsis

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