Inhibition of Cytochalasin-Primed Neutrophils By Hyperosmolarity

GIAMBELLUCA MIRIAM S.; GENDE OSCAR A.

SHOCK

Lippincott Williams and Wilkins

Lugar: Augusta; Año: 2008 vol. 30 p. 473 - 480

1073-2322

Experimental and clinical investigations using hyperosmotic solutions for resuscitation of hemorrhagic shock demonstrated modulation of the inflammatory response. Decreased postinjury hyperinflammation has been attributed to a reduction in neutrophil-mediated tissue damage. This study shows that cytoskeletal disruption with cytochalasinB did not reverse or prevent the inhibitory effect of an osmolarity increase on the neutrophil cytotoxic response to a formyl peptide. In cytochalasin-primed neutrophils, the hyperosmolarity-dependent inhibition promptly reversed after returning to iso-osmotic levels. Paradoxically, an increase in osmolarity after stimulation produced an increase in the release of reactive oxygen species to the extracellular medium. The inhibitory effect of hyperosmotic NaCl can be reproduced by solutions of similar osmolarity containing N-methyl glucamine or sucrose, but solutions containing mannitol allowed an almost complete response to N-formyl methionyl leucyl phenylalanine. The effects on the release of reactive oxygen species to the extracellular media found with the OxyBURSTYbovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. extracellular media found with the OxyBURSTYbovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. response to N-formyl methionyl leucyl phenylalanine. The effects on the release of reactive oxygen species to the extracellular media found with the OxyBURSTYbovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. extracellular media found with the OxyBURSTYbovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. N-methyl glucamine or sucrose, but solutions containing mannitol allowed an almost complete response to N-formyl methionyl leucyl phenylalanine. The effects on the release of reactive oxygen species to the extracellular media found with the OxyBURSTYbovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. extracellular media found with the OxyBURSTYbovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. N-formyl methionyl leucyl phenylalanine. The effects on the release of reactive oxygen species to the extracellular media found with the OxyBURSTYbovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level. Ybovine serum albumin assay correlated with the changes of the intracellular calcium signal, indicating that the inhibition by hyperosmolarity occurs near the receptor level.