Recognizing the mobilization of neutrophils with banded nuclei early after trauma

Hellebrekers, Pien; Hesselink, Lilian; Huisman, Albert; Berg, Maarten ten; Koenderman, Leo; Leenen, Luke P. H.; Hietbrink, Falco

doi:10.1111/ijlh.13272

Cited by 6 publications

(9 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The ADMTS13 downmodulation could be explained by the inhibitory effect of pro-inflammatory molecules such as IL-1β and C reactive protein, as shown by Chen and colleagues in patients with lymphoblastic leukemia [ 64 ]. Indeed, several studies have shown that plasma of COVID-19 patients with microangiopathy contains low ADAMTS13 activity and increased vWF and factor VII levels [ 65 , 66 ]. However, in a recent study conducted by Escher and colleagues, no role of ADAMTS13 in the pathogenesis of COVID-19 coagulopathy was observed [ 67 ].…”

Section: Pathophysology Of Covid-19mentioning

confidence: 99%

Phosphatidylserine inside out: a possible underlying mechanism in the inflammation and coagulation abnormalities of COVID-19

Palmeira

Argañaraz

2020

Cell Commun Signal

View full text Add to dashboard Cite

The rapid ability of SARS-CoV-2 to spread among humans, along with the clinical complications of coronavirus disease 2019—COVID-19, have represented a significant challenge to the health management systems worldwide. The acute inflammation and coagulation abnormalities appear as the main causes for thousands of deaths worldwide. The intense inflammatory response could be involved with the formation of thrombi. For instance, the presence of uncleaved large multimers of von Willebrand (vWF), due to low ADAMTS13 activity in plasma could be explained by the inhibitory action of pro-inflammatory molecules such as IL-1β and C reactive protein. In addition, the damage to endothelial cells after viral infection and/or activation of endothelium by pro-inflammatory cytokines, such as IL-1β, IL-6, IFN-γ, IL-8, and TNF-α induces platelets and monocyte aggregation in the vascular wall and expression of tissue factor (TF). The TF expression may culminate in the formation of thrombi, and activation of cascade by the extrinsic pathway by association with factor VII. In this scenario, the phosphatidylserine—PtdSer exposure on the outer leaflet of the cell membrane as consequence of viral infection emerges as another possible underlying mechanism to acute immune inflammatory response and activation of coagulation cascade. The PtdSer exposure may be an important mechanism related to ADAM17—mediated ACE2, TNF-α, EGFR and IL-6R shedding, and the activation of TF on the surface of infected endothelial cells. In this review, we address the underlying mechanisms involved in the pathophysiology of inflammation and coagulation abnormalities. Moreover, we introduce key biochemical and pathophysiological concepts that support the possible participation of PtdSer exposure on the outer side of the SARS-CoV-2 infected cells membrane, in the pathophysiology of COVID-19.

show abstract

Section: Pathophysology Of Covid-19mentioning

confidence: 99%

Phosphatidylserine inside out: a possible underlying mechanism in the inflammation and coagulation abnormalities of COVID-19

Palmeira

Argañaraz

2020

Cell Commun Signal

View full text Add to dashboard Cite

show abstract

“…Yet the increase in neutrophil size for trauma patients was less, compared to sepsis patients. At the same time, trauma bands were not larger compared to segmented neutrophils in trauma as all cells increased size in this population [8], which might explain the inability of flagging trauma bands.…”

Section: Discussionmentioning

confidence: 76%

“…Automated hematology analyzers are able to flag samples based on the presence of band neutrophils yet are not able to directly measure these cells. This complicates defining the characteristics of these cells in automated hematology analysis, as there are heterogeneous characteristics, e.g., size differences of band neutrophils in different patient populations [8].…”

Section: Discussionmentioning

confidence: 99%

“…We selected hematology data as measured by the Abbott Cell-Dyn Sapphire hematology analyzer (Abbott Diagnostics, Santa Clara, CA, USA). Data from 20 well-phenotyped sepsis and trauma samples from previous collaborations were kindly provided by the traumatology department and consisted of surgical infection patients ('sepsis') and multitrauma patients ('trauma') as described before [8]. Patients were measured during their stay in the Intensive Care Unit (ICU), where band neutrophils were observed during microscopic examination of a routine blood smear.…”

Section: Population and Datamentioning

confidence: 99%

“…After (severe) trauma, patients are known to be at increased risk for complications because of the activation of neutrophils after tissue damage through damage-associated molecular patterns (DAMPs) and microbe-associated molecular patterns (MAMPs) [4,5]. The activation and increase of neutrophils accompanied by a left-shift [6,7] and release of band neutrophils [8] after trauma-from here on referred to as "trauma bands" vs. "sepsis-bands"-has been linked to increased risk for infection and, eventually, organ failure [4][5][6]9,10]. Although microscopically indistinguishable from the band neutrophils released during sepsis, their counterparts in trauma patients are not detected as such by the current cell identification algorithms used in automated hematology analyzers [8].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Describing Characteristics and Differences of Neutrophils in Sepsis, Trauma, and Control Patients in Routinely Measured Hematology Data

et al. 2022

Self Cite

View full text Add to dashboard Cite

Neutrophils have an important role in the immune response. These cells can be subjected to an impaired function and a shift in population depending on disease states. In sepsis, this shift is recognized and flagged by automated hematology analyzers, including the presence of band neutrophils, while these cells, although present, appear not to be detected in trauma patients. To better understand this suspected error in flagging, we set out to distinguish neutrophil populations of these two patient groups and compared these with controls. Different data-driven methods were used compared to standard algorithms used by the software of the analyzers. Using K-means clustering, we extracted neutrophils from raw hematology analyzer datafiles, and compared characteristics of these clusters between the patient groups. We observed an increased neutrophil size for both sepsis and trauma patients, but trauma patients had a smaller increase. Trauma patients also had a high proportion of cells with relatively high nuclear segmentation, which is contradictory with the presence of band neutrophils. This, in combination with the smaller size increase, might explain the inability to flag band neutrophils in trauma.

show abstract

The coagulopathy, endotheliopathy, and vasculitis of COVID-19

2020

View full text Add to dashboard Cite

Background COVID-19-associated coagulopathy (CAC) characterized by the elevated D-dimer without remarkable changes of other global coagulation markers is associated with various thrombotic complications and disease severity. The purpose of this review is to elucidate the pathophysiology of this unique coagulopathy. Methods The authors performed online search of published medical literature through PubMed using the MeSH (Medical Subject Headings) term "COVID-19," "SARS-CoV-2," "coronavirus," "coagulopathy," and "thrombus." Then, selected 51 articles that closely relevant to coagulopathy in COVID-19. Results The primary targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the pneumocytes, immune cells, and vascular endothelial cells. The alveolar damage and the pulmonary microvascular thrombosis are the major causes of acute lung injury in COVID-19. The endotheliopathy that occurs is due to direct SARS-CoV-2 infection and activation of other pathways that include the immune system and thromboinflammatory responses leading to what is termed CAC. As a result, both microvascular and macrovascular thrombotic events occur in arterial, capillary, venule, and large vein vascular beds to produce multiorgan dysfunction and thrombotic complications. In addition to the endothelial damage, SARS-CoV-2 also can cause vasculitis and presents as a systemic inflammatory vascular disease. Clinical management of COVID-19 includes anticoagulation but novel therapies for endotheliopathy, hypercoagulability, and vasculitis are needed. Conclusion The endotheliopathy due to direct endothelial infection with SARS-COV-2 and the indirect damage caused by inflammation play the predominant role in the development of CAC. The intensive control of thromboinflammation is necessary to improve the outcome of this highly detrimental contagious disease.

show abstract

Recognizing the mobilization of neutrophils with banded nuclei early after trauma

Cited by 6 publications

References 9 publications

Phosphatidylserine inside out: a possible underlying mechanism in the inflammation and coagulation abnormalities of COVID-19

Phosphatidylserine inside out: a possible underlying mechanism in the inflammation and coagulation abnormalities of COVID-19

Describing Characteristics and Differences of Neutrophils in Sepsis, Trauma, and Control Patients in Routinely Measured Hematology Data

The coagulopathy, endotheliopathy, and vasculitis of COVID-19

Contact Info

Product

Resources

About