Platelets: at the nexus of antimicrobial defence

Yeaman, Michael R.

doi:10.1038/nrmicro3269

Cited by 288 publications

(285 citation statements)

References 146 publications

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“…The increase observed in MPV occurs before the increase in the platelet count (2). Since platelets have a significant role during inflammation, the platelet count is increased in many inflammatory diseases (10). In our study, the platelet count was found to be statistically significantly higher in the patients who had acute bronchiolits compared to the healthy children ( Table 2, p<0,05).…”

Section: Discussionsupporting

confidence: 56%

Reduction in mean platelet volume in children with acute bronchiolitis

et al. 2016

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Aim: Platelets which are known to play a role in inflamation change their shapes when they are activated and this change is reflected in mean platelet volume and platelet distribution width values. Therefore, the mean platelet volume and platelet distribution width values are considered to be beneficial parameters for the diagnosis and treatment of many inflammatory diseases. The aim of the study was to evaluate platelet volume indices in children with acute bronchiolitis. Material and Methods:A total of 514 infants who were below the age of 2 years old were evaluated in this study. Three hundred thirteen of these infants were diagnosed with acute bronchiolitis patients and 201 were healthy children. The patients were separated into four groups as mild, moderate, severe bronchiolitis and the control patient group. The groups were evaluated in terms of significant differences in the values of mean platelet volume and platelet distribution width. A p value of <0.05 was considered statistically significant for all results. Results:The mean platelet volume was found to be 6.8±0.6 fL in the patients with mild bronchiolitis attack, 6.7±0.6 fL in the patients with moderate bronchiolitis attack, 6.5±0.5 fL in the patients with severe bronchiolitis attack and 7.3±1.1 fL in the control group. The mean platalet volume was statistically significantly lower in the mild, moderate and severe bronchiolitis attack groups compared to the control group (p=0.000). The platelet distribution width was found to be 17.2%±0.83 in the mild bronchiolitis attack group, 17.1%±0.96 in the moderate bronchiolitis attack group, 17.3%±0.87 in the severe bronchiolitis attack group and 16.9±1.6% in the control patient group. This difference was not statistically significant (p=0.159). The platelet count was statistically significantly higher in the mild, moderate and severe bronchiolitis attack groups compared to the control group (p=0.000).

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Section: Discussionsupporting

confidence: 56%

Reduction in mean platelet volume in children with acute bronchiolitis

et al. 2016

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“…Aside from their well‐established role in thrombosis, platelets are increasingly recognised as participants in vascular inflammation1 and contribute to inflammation, at least in part, via their TLRs. Platelets are known to express various TLRs,5 and TLR stimulation can mediate a number of thrombotic7, 8, 21 and inflammatory processes 9, 10.…”

Section: Discussionmentioning

confidence: 99%

“…In infection‐related vascular injury, platelets are important effectors of antimicrobial host defence1 and platelets also enhance leucocyte effector functions in a number of inflammatory pathologies which are characterised by sterile vascular injury 2, 3, 4. Platelets express a range of Toll‐like receptors (TLRs),5, 6 which are responsible for mediating early immune responses to both infection and sterile injury.…”

Section: Introductionmentioning

confidence: 99%

Platelets regulate leucocyte responses to Toll‐like receptor stimulation

et al. 2018

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ObjectivesPlatelets are important regulators of vascular thrombosis and inflammation and are known to express Toll‐like receptors (TLRs). Through TLRs, platelets mediate a number of responses by interacting with leucocytes. Here, we report the extent to which platelets modulate in vitro peripheral blood mononuclear cells (PBMCs) and granulocyte responses to TLR4, TLR2/1 and TLR2/6 stimulation in healthy subjects.MethodsPeripheral blood mononuclear cells and granulocytes from 10 healthy volunteers were cultured alone or cocultured with platelets. Cultures were left unstimulated or stimulated with 1 or 100 ng mL−1 of either LPS (TLR4 agonist), Pam3CSK4 (TLR2/1 agonist) or fibroblast‐stimulating lipopeptide (FSL)‐1 (TLR2/6 agonist). Neutrophil activation (CD66b expression), monocyte activation (HLA‐DR), granulocyte elastase production and PBMC cytokine and chemokine production were examined.ResultsPlatelet coculture decreased neutrophil CD66b expression in response to LPS, Pam3CSK4 and FSL‐1, and modestly decreased monocyte HLA‐DR expression in response to low‐dose LPS. Platelets reduced granulocyte elastase secretion in response to low doses of all TLR agonists tested. In response to LPS, platelet coculture reduced IL‐6, tumor necrosis factor (TNF)‐α and MIP‐1β production, and increased IL‐10 production by PBMCs. In response to FSL‐1, platelets increased IL‐6, IL‐10 and MIP‐1β production, but reduced TNF‐α production. Platelet coculture did not alter PBMC cytokine/chemokine production in response to Pam3CSK4.ConclusionThis study challenges the notion that platelets act solely in a pro‐inflammatory manner. Rather, platelets are complex immunomodulators that regulate leucocyte responses to TLR stimulation in a TLR agonist‐specific manner. Platelets may modulate leucocyte responses to dampen inflammation, and this platelet effect may play an important role in reducing inflammation‐mediated host damage.

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“…[20][21][22] Their immunoregulatory effects are in part related to platelet interactions with innate immune cells such as neutrophils and monocytes. In line with this, activated platelets are substantially involved in the formation of NET by neutrophils.…”

Section: Extracellular Nucleosomes Enhance Blood Coagulation and Platmentioning

confidence: 99%