Development of platelets during steady state and inflammation

Müller‐Newen, Gerhard; Stope, Matthias B.; Kraus, Thomas; Ziegler, Patrick

doi:10.1189/jlb.1ru0916-391rr

Cited by 23 publications

(22 citation statements)

References 143 publications

(130 reference statements)

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“…Similar to increased serum levels of CRP, the evidence indicates that platelet parameters are markers that reflect a systemic inflammatory response [17,18]. Chronic inflammation is typically associated with reactive thrombocytosis, induced by the overproduction of pro-inflammatory cytokines, leading to megakaryocytic proliferation [19]. Platelets play an important role in various inflammatory diseases by interacting with almost all known immune cells.…”

Section: Discussionmentioning

confidence: 93%

Relationship between CRP, systemic immune-inflammation index and routine hemogram related inflammatory markers in low grade inflammation

Üstündağ¹

2018

Int J Med Biochem

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Research ArticleR ecent advances in technology led to the quantitation of new parameters with automated hematology analyzers. Some of these parameters have been accepted as additional markers in diagnosing various clinical conditions [1][2][3][4][5]. They are cost effective and easier to perform in a routine setting than tests for some other markers. C-reactive protein (CRP) is a commonly used inflammation marker in both acute and chronic inflammation. Most healthy individuals have a CRP concentration of 3 mg/L or less; a CRP level higher than 10 mg/L indicates a clinically significant inflammatory disease [6]. Low-grade inflammation typically refers to conditions in which Objectives: The term low-grade inflammation is usually used to indicate chronic conditions in which the findings of classic, clinical inflammation are lacking, but there is an elevated C-reactive protein (CRP) level of 3 to 10 mg/L. Recently, the systemic immune-inflammation index (SII) was developed based on lymphocyte, neutrophil, and platelet counts, which can project the inflammatory and immune imbalances. The aim of this study was to examine the SII and new parameters derived from hemograms to determine if they have the potential to detect patients with subclinical lowgrade inflammation in an unselected, elderly, outpatient population. Methods: The CRP level was analyzed with a BN II System nepholometer (Siemens Healthineers, Erlangen, Germany). Participants were stratified according to CRP level: Group 1 had a serum CRP result <3.0 mg/L and Group 2 had a serum CRP result 3.0-9.0 mg/L. Blood samples that had been analyzed with an automated hematology analyzer (Mindray BC-5800; Mindray Biomedical Electronics Co., Ltd., Shenzhen, China) were selected for evaluation of the results. The SII (neutrophil x platelet / lymphocyte), platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte ratio (NLR) were calculated. PLR (r=0.773; p<0.001), and the platelet count (r=0.653; p<0.001) was found. However, there was no correlation between the CRP, SII (r=-0.312; p=0.210), and PLR (r=-0.165; p=0.117). Conclusion: A high PLR and SII appears to be associated with subclinical low-grade inflammation. These data do not support hematological screening parameters as a substitute for CRP. These findings are limited to the cohort studied here, and may not be entirely applicable to other ethnic origins. Keywords: C-reactive protein, lymphocyte, neutrophil, platelet Relationship between C-reactive protein, systemic immuneinflammation index, and routine hemogram-related inflammatory markers in low-grade inflammation

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Section: Discussionmentioning

confidence: 93%

Relationship between CRP, systemic immune-inflammation index and routine hemogram related inflammatory markers in low grade inflammation

Üstündağ¹

2018

Int J Med Biochem

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“…More recently, alternative pathways originating from MK-biased or MK-primed HSCs that bypass intermediate commitment stages have emerged ( 49 ). These direct pathways to megakaryopoiesis are gaining consideration for their relevance to platelet production in nonhomeostatic stress situations ( 50 ). For example, stem-like megakaryocyte-committed progenitors (SL-MKPs) have been identified as an emergency machinery to produce platelets under inflammatory stress ( 51 ).…”

Section: Discussionmentioning

confidence: 99%

Tyrosyl-tRNA synthetase stimulates thrombopoietin-independent hematopoiesis accelerating recovery from thrombocytopenia

Kanaji

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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SignificanceAminoacyl-tRNA synthetases (aaRSs) catalyze aminoacylation of tRNAs in the first step of protein synthesis in the cytoplasm. However, in higher eukaryotes, they acquired additional functions beyond translation. In the present study, we show that an activated form of tyrosyl-tRNA synthetase (YRSACT) functions to enhance megakaryopoiesis and platelet production in vitro and in vivo. These findings were confirmed with human megakaryocytes differentiated from peripheral blood CD34+ hematopoietic stem cells and with human induced pluripotent stem (iPS) cells. The activity of YRSACT is independent of thrombopoietin (TPO), as evidenced by expansion of the megakaryocytes from iPS cell-derived hematopoietic stem cells from a patient deficient in TPO signaling. These findings demonstrate a previously unrecognized function of an aaRS which may have implications for therapeutic interventions.

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“…16 Platelets are, of course, important in this microthrombi formation, and having the platelet production factory to churn out a large amount of these cells locally in the lungs may indeed be beneficial. 17 An intriguing observation in this regard was made by Sharma and Talbot, who postulated pulmonary megakaryocytes as the "missing link" between cardiovascular and respiratory disease. 18 They suggested that the number of pulmonary megakaryocytes increased in association with atherosclerotic disease because of enhanced thrombopoiesis following increased platelet adherence to atheromatous plaques.…”

Section: Lung Megakaryocytes and Pulmonary Thrombimentioning

confidence: 99%

Pulmonary Megakaryocytes in Coronavirus Disease 2019 (COVID-19): Roles in Thrombi and Fibrosis

Thachil

Lisman

2020

Semin Thromb Hemost

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Coronavirus disease 2019 (COVID-19) has already claimed many lives and continues to do so in different parts of the world. Autopsy reports of patients who succumbed to this viral infection have been published despite concerns about health care professional safety. One of the unusual findings in COVID-19 lung autopsy reports is the increase in pulmonary megakaryocytes. 1,2 Although the presence of megakaryocytes in the lungs is a well-established concept in the medical literature, it is still not widely accepted in the clinical fraternity. In this article, we discuss the role of lung megakaryocytes in relation to the clinicopathological findings in COVID-19 and discuss how this may impact on our understanding of acute respiratory distress syndrome (ARDS), pulmonary thrombi, and lung fibrosis, in general.

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Development of platelets during steady state and inflammation

Cited by 23 publications

References 143 publications

Relationship between CRP, systemic immune-inflammation index and routine hemogram related inflammatory markers in low grade inflammation

Relationship between CRP, systemic immune-inflammation index and routine hemogram related inflammatory markers in low grade inflammation

Tyrosyl-tRNA synthetase stimulates thrombopoietin-independent hematopoiesis accelerating recovery from thrombocytopenia

Pulmonary Megakaryocytes in Coronavirus Disease 2019 (COVID-19): Roles in Thrombi and Fibrosis

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