The temporo-spatial localization of polymorphonuclear cells related to the neurovascular unit after transient focal cerebral ischemia

Brain Res. 2014 Oct 24:1586:184-92. doi: 10.1016/j.brainres.2014.08.037. Epub 2014 Aug 22.

Abstract

Inflammatory responses after cerebral ischemia are important for the development of final infarct size but the role of polymorphonuclear cells (PMN) is still a matter of debate, since previously used antibodies were recently declared as non-specific. In the present study, we investigated the temporo-spatial localization of PMN related to the neurovascular unit using specific antibodies, 7/4 and Ly6G, and application of G-CSF to induce proliferation and mobilization of PMN precursors after transient focal cerebral ischemia in mice. Infarct volumes, sensorimotor function, neurological outcome and immunohistochemical analysis of PMN were performed after G-CSF administration or placebo treatment. G-CSF-treated mice showed reduced infarct size (51.15±15.68 mm(2) vs. 39.31±16.13 mm(2) at day 1; 50.11±16.68 mm(2) vs. 33.16±4.86 mm(2) at day 4; p<0.05). They showed improved motor-function recovery and had a significantly better outcome compared to placebo-treated animals. Comparison of the two PMN detecting antibodies showed no difference in saturation plots or cell quantification. Studying the basement membrane-associated localization revealed ca. 60% extravascular PMN, independent of G-CSF administration. Extravascular PMNs were without any connection to laminin, but all near to the vessels. We conclude that 7/4 is a suitable marker to investigate PMN compared to Ly6G, which confirms results from former studies using the 7/4-antibody. Furthermore we report the observation that PMN were detected outside the laminin barrier but almost exclusively in close vicinity to the neurovascular unit.

Keywords: Experimental stroke; Granulocyte colony stimulating factor; Neurovascular unit; Polymorphonuclear cell.

MeSH terms

  • Analysis of Variance
  • Animals
  • Antigens, Ly / metabolism
  • Brain Edema / etiology
  • Brain Infarction / drug therapy
  • Brain Infarction / etiology
  • Disease Models, Animal
  • Functional Laterality
  • Granulocyte Colony-Stimulating Factor / pharmacology
  • Granulocyte Colony-Stimulating Factor / therapeutic use
  • Ischemic Attack, Transient / complications
  • Ischemic Attack, Transient / drug therapy
  • Ischemic Attack, Transient / pathology*
  • Lymphocytes / drug effects
  • Lymphocytes / metabolism
  • Lymphocytes / pathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Motor Activity / drug effects
  • Neurologic Examination
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use
  • Neutrophils / drug effects
  • Neutrophils / metabolism
  • Neutrophils / pathology*
  • Phycoerythrin / metabolism
  • Time Factors

Substances

  • Antigens, Ly
  • Ly6G antigen, mouse
  • Neuroprotective Agents
  • Phycoerythrin
  • Granulocyte Colony-Stimulating Factor