The appearance of L‐selectin^low polymorphonuclear leukocytes in the circulating pool of peripheral blood during myocardial infarction correlates with neutrophilia and with the size of the infarct

Abstract

SummaryBackground: It is assumed that not only leukocytosis, but also the activation of white blood cells (WBC) may play a role in the pathogenesis and prognosis of patients with myocardial infarction (MI). Activation of WBC includes upregulation of CDI lb\CD18 and downregulation of CD62L (Lselectin) antigens.Hypothesis: The activation of WBC is associated with the appearance of a larger MI.Methods: CDl1 b\CD I8 and CD62L were measured on the surface of WBC on Day 1 and Day 3 from the onset of MI. The size of the infarct was estimated by calculating the area under the curve of the creatine kinase enzyme, which was measured every 6 h.Results: A negative correlation was noted between the absolute polymorphonuclear count and the availability of the CD62L on these cells during Day 1 (r = -0.46, p = 0.003) and Day 3 (r = -0.3.5, p = 0.05). There was a positive correlation between the size of MI and the WBC count (r = 0.46, p = 0.004) and a negative correlation with CD62L on polymorphonuclears (r = -0.35, p = 0.03). During Day 3, the CD1 lb\ CD 1 8 on the polymorphonuclears increased despite a decre-

Impaired mobilization of hematopoietic stem/progenitor cells in C5-deficient mice supports the pivotal involvement of innate immunity in this process and reveals novel promobilization effects of granulocytes

“…With CC activation also observed during inflammation16,48 and tissue/organ injury,49,50 this phenomenon has broader implications. While HSPCs mobilized from BM during infection may patrol peripheral tissues and thus perform an important role in host defense,1,2 other types of BM-derived stem cells may be released to act in regeneration of damaged tissues 3,4,43. To support this concept in all these processes, both CC activation and granulocytosis is involved.…”

“… 1 This route of “circulation/tissue patrolling” is enforced during infection 2 , wherein mobilized HSPCs could be recruited to the affected peripheral tissues and give rise to tissue-resident myeloid and dendritic cells. In addition to infection, HSPCs are mobilized from BM into PB during tissue injury 3 , 4 and after administration of some pharmacological agents [e.g., granulocyte colony stimulating factor (G-CSF)]. 5 - 8 …”

Novel insight into stem cell mobilization-Plasma sphingosine-1-phosphate is a major chemoattractant that directs the egress of hematopoietic stem progenitor cells from the bone marrow and its level in peripheral blood increases during mobilization due to activation of complement cascade/membrane attack complex

“…Therefore, PB could be envisioned as a highway by which HSPCs relocate in the body between hematopoietic BM endosteal and endothelial niches. HSPCs are mobilized from BM into PB during infection, 1 , 2 and tissue injury, 3 , 4 and after administration of some pharmacological agents [e.g., granulocyte colony stimulating factor (G-CSF) 5 or some polysaccharides (e.g., Zymosan) 6 ]. However, the molecular mechanisms controlling mobilization of HSPCs are still not well understood.…”

Whole body and hematopoietic ADAM8 deficiency does not influence advanced atherosclerotic lesion development, despite its association with human plaque progression

“…Interestingly, ligation of PSGL-1 on hematopoietic progenitor cells to P-selectin results in suppression of hematopoiesis 37 . Additionally, L-selectin may function as a retention cue for granulocytes to remain in the bone marrow 38 , 39 . Although ADAM8 might indirectly affect both processes, via these two substrates, the fact that whole-body ADAM8 deficient mice failed to display leukopenia does not plead for this notion.…”