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Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production. / Kerstholt, Mariska; van de Schoor, Freek R; Oosting, Marije et al.

In: Clinical and experimental immunology, Vol. 210, No. 1, 01.10.2022, p. 53-67.

Research output: Contribution to journal › Article › Academic › peer-review

Harvard

Kerstholt, M, van de Schoor, FR, Oosting, M, Moorlag, SJCFM, Li, Y, Jaeger, M, van der Heijden, WA, Tunjungputri, RN, Dos Santos, JC, Kischkel, B, Vrijmoeth, HD, Baarsma, ME, Kullberg, B-J, Lupse, M, Hovius, JW, van den Wijngaard, CC, Netea, MG, de Mast, Q & Joosten, LAB 2022, 'Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production', Clinical and experimental immunology, vol. 210, no. 1, pp. 53-67. https://doi.org/10.1093/cei/uxac073

APA

Kerstholt, M., van de Schoor, F. R., Oosting, M., Moorlag, S. J. C. F. M., Li, Y., Jaeger, M., van der Heijden, W. A., Tunjungputri, R. N., Dos Santos, J. C., Kischkel, B., Vrijmoeth, H. D., Baarsma, M. E., Kullberg, B-J., Lupse, M., Hovius, J. W., van den Wijngaard, C. C., Netea, M. G., de Mast, Q., & Joosten, L. A. B. (2022). Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production. Clinical and experimental immunology, 210(1), 53-67. https://doi.org/10.1093/cei/uxac073

Vancouver

Kerstholt M, van de Schoor FR, Oosting M, Moorlag SJCFM, Li Y, Jaeger M et al. Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production. Clinical and experimental immunology. 2022 Oct 1;210(1):53-67. doi: 10.1093/cei/uxac073

Author

Kerstholt, Mariska ; van de Schoor, Freek R ; Oosting, Marije et al. / Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production. In: Clinical and experimental immunology. 2022 ; Vol. 210, No. 1. pp. 53-67.

BibTeX

@article{caae6ece01324ed5b22b2ac856d0a284,
title = "Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production",
abstract = "Previous studies have shown that monocytes can be 'trained' or tolerized by certain stimuli to respond stronger or weaker to a secondary stimulation. Rewiring of glucose metabolism was found to be important in inducing this phenotype. As we previously found that Borrelia burgdorferi (B. burgdorferi), the causative agent of Lyme borreliosis (LB), alters glucose metabolism in monocytes, we hypothesized that this may also induce long-term changes in innate immune responses. We found that exposure to B. burgdorferi decreased cytokine production in response to the TLR4-ligand lipopolysaccharide (LPS). In addition, B. burgdorferi exposure decreased baseline levels of glycolysis, as assessed by lactate production. Using GWAS analysis, we identified a gene, microfibril-associated protein 3-like (MFAP3L) as a factor influencing lactate production after B. burgdorferi exposure. Validation experiments proved that MFAP3L affects lactate- and cytokine production following B. burgdorferi stimulation. This is mediated by functions of MFAP3L, which includes activating ERK2 and through activation of platelet degranulation. Moreover, we showed that platelets and platelet-derived factors play important roles in B. burgdorferi-induced cytokine production. Certain platelet-derived factors, such chemokine C-X-C motif ligand 7 (CXCL7) and (C-C motif) ligand 5 (CCL5), were elevated in the circulation of LB patients in comparison to healthy individuals.",
keywords = "Humans, Lipopolysaccharides, Ligands, Toll-Like Receptor 4, Lyme Disease, Chemokines/metabolism, Glucose, Lactates",
author = "Mariska Kerstholt and {van de Schoor}, {Freek R} and Marije Oosting and Moorlag, {Simone J C F M} and Yang Li and Martin Jaeger and {van der Heijden}, {Wouter A} and Tunjungputri, {Rahajeng N} and {Dos Santos}, {J{\'e}ssica C} and Brenda Kischkel and Vrijmoeth, {Hedwig D} and Baarsma, {M E} and Bart-Jan Kullberg and Mihaela Lupse and Hovius, {Joppe W} and {van den Wijngaard}, {Cees C} and Netea, {Mihai G} and {de Mast}, Quirijn and Joosten, {Leo A B}",
note = "{\textcopyright} The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Immunology.",
year = "2022",
month = oct,
day = "1",
doi = "10.1093/cei/uxac073",
language = "English",
volume = "210",
pages = "53--67",
journal = "Clinical and experimental immunology",
issn = "0009-9104",
publisher = "Wiley-Blackwell",
number = "1",

}

RIS

TY - JOUR

T1 - Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production

AU - Kerstholt, Mariska

AU - van de Schoor, Freek R

AU - Oosting, Marije

AU - Moorlag, Simone J C F M

AU - Li, Yang

AU - Jaeger, Martin

AU - van der Heijden, Wouter A

AU - Tunjungputri, Rahajeng N

AU - Dos Santos, Jéssica C

AU - Kischkel, Brenda

AU - Vrijmoeth, Hedwig D

AU - Baarsma, M E

AU - Kullberg, Bart-Jan

AU - Lupse, Mihaela

AU - Hovius, Joppe W

AU - van den Wijngaard, Cees C

AU - Netea, Mihai G

AU - de Mast, Quirijn

AU - Joosten, Leo A B

N1 - © The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Immunology.

PY - 2022/10/1

Y1 - 2022/10/1

N2 - Previous studies have shown that monocytes can be 'trained' or tolerized by certain stimuli to respond stronger or weaker to a secondary stimulation. Rewiring of glucose metabolism was found to be important in inducing this phenotype. As we previously found that Borrelia burgdorferi (B. burgdorferi), the causative agent of Lyme borreliosis (LB), alters glucose metabolism in monocytes, we hypothesized that this may also induce long-term changes in innate immune responses. We found that exposure to B. burgdorferi decreased cytokine production in response to the TLR4-ligand lipopolysaccharide (LPS). In addition, B. burgdorferi exposure decreased baseline levels of glycolysis, as assessed by lactate production. Using GWAS analysis, we identified a gene, microfibril-associated protein 3-like (MFAP3L) as a factor influencing lactate production after B. burgdorferi exposure. Validation experiments proved that MFAP3L affects lactate- and cytokine production following B. burgdorferi stimulation. This is mediated by functions of MFAP3L, which includes activating ERK2 and through activation of platelet degranulation. Moreover, we showed that platelets and platelet-derived factors play important roles in B. burgdorferi-induced cytokine production. Certain platelet-derived factors, such chemokine C-X-C motif ligand 7 (CXCL7) and (C-C motif) ligand 5 (CCL5), were elevated in the circulation of LB patients in comparison to healthy individuals.

AB - Previous studies have shown that monocytes can be 'trained' or tolerized by certain stimuli to respond stronger or weaker to a secondary stimulation. Rewiring of glucose metabolism was found to be important in inducing this phenotype. As we previously found that Borrelia burgdorferi (B. burgdorferi), the causative agent of Lyme borreliosis (LB), alters glucose metabolism in monocytes, we hypothesized that this may also induce long-term changes in innate immune responses. We found that exposure to B. burgdorferi decreased cytokine production in response to the TLR4-ligand lipopolysaccharide (LPS). In addition, B. burgdorferi exposure decreased baseline levels of glycolysis, as assessed by lactate production. Using GWAS analysis, we identified a gene, microfibril-associated protein 3-like (MFAP3L) as a factor influencing lactate production after B. burgdorferi exposure. Validation experiments proved that MFAP3L affects lactate- and cytokine production following B. burgdorferi stimulation. This is mediated by functions of MFAP3L, which includes activating ERK2 and through activation of platelet degranulation. Moreover, we showed that platelets and platelet-derived factors play important roles in B. burgdorferi-induced cytokine production. Certain platelet-derived factors, such chemokine C-X-C motif ligand 7 (CXCL7) and (C-C motif) ligand 5 (CCL5), were elevated in the circulation of LB patients in comparison to healthy individuals.

KW - Humans

KW - Lipopolysaccharides

KW - Ligands

KW - Toll-Like Receptor 4

KW - Lyme Disease

KW - Chemokines/metabolism

KW - Glucose

KW - Lactates

UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85153526577&origin=inward

UR - https://www.ncbi.nlm.nih.gov/pubmed/36001729

U2 - 10.1093/cei/uxac073

DO - 10.1093/cei/uxac073

M3 - Article

C2 - 36001729

VL - 210

SP - 53

EP - 67

JO - Clinical and experimental immunology

JF - Clinical and experimental immunology

SN - 0009-9104

IS - 1

ER -

ID: 31244077