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Apoptosis of bovine neutrophils during mastitis experimentally induced with Escherichia coli or endotoxin.

K Van Oostveldt, GM Tomita, Max Paape UGent, Anthony Capuco UGent and Christian Burvenich UGent (2002) AMERICAN JOURNAL OF VETERINARY RESEARCH. 63(3). p.448-453
abstract
Objective-To determine whether apoptosis of neutrophils was accelerated during mastits experimentally induced by use of Escherichia coli or E coli endotoxin and whether differences were apparent in the response to E coli or endotoxin. Animals-11 healthy lactating Holstein cows. Procedure-Blood samples were collected from cows at various intervals after intramammary inoculation with E coli or endotoxin. Percentage of apoptotic neutrophils detected after in vitro incubation for 3 hours was determined. Fluorescein isothiocyanate-labeled annexin-V in combination with propidium iodide was used to distinguish apoptosis and necrosis of neutrophils. Total and differential circulating leukocyte counts and rectal temperature were determined at the time of collection of blood samples. Milk yield and milk somatic cell counts were determined at the time of milking. Results-Inoculation of endotoxin did not accelerate in vitro induction of neutrophil apoptosis. However, inoculation of E coli increased the percentage of apoptotic neutrophils. At 18 hours after inoculation, 20% of the neutrophils were apoptotic, compared with 5% before inoculation. Milk somatic cell count and rectal temperature increased, milk production and total leukocyte count decreased, and percentage of immature neutrophils increased after inoculation with E coli or endotoxin. However, kinetics of the responses were more rapid, more severe, and of shorter duration during, endotoxin-induced mastitis. Conclusions and Clinical Relevance-In vitro induction of apoptosis of neutrophils was accelerated only during E col induced mastitis and not during endotoxin-induced mastitis. Endotoxin inoculation as a model for studying coliform mastitis in dairy cows should be viewed with caution.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
RESPIRATORY BURST ACTIVITY, CLEARANCE, NECROSIS-FACTOR-ALPHA, AGING NEUTROPHILS, MAMMARY-GLAND, LEUKOCYTES, COWS, RECEPTOR, ADHESION
journal title
AMERICAN JOURNAL OF VETERINARY RESEARCH
Am. J. Vet. Res.
volume
63
issue
3
pages
448-453 pages
Web of Science type
Article
Web of Science id
000174134200024
JCR category
VETERINARY SCIENCES
JCR impact factor
1.148 (2002)
JCR rank
26/129 (2002)
JCR quartile
1 (2002)
ISSN
0002-9645
language
English
UGent publication?
yes
classification
A1
additional info
No full text available
id
149269
handle
http://hdl.handle.net/1854/LU-149269
date created
2004-01-14 13:38:00
date last changed
2016-12-19 15:37:50
@article{149269,
  abstract     = {Objective-To determine whether apoptosis of neutrophils was accelerated during mastits experimentally induced by use of Escherichia coli or E coli endotoxin and whether differences were apparent in the response to E coli or endotoxin. Animals-11 healthy lactating Holstein cows. Procedure-Blood samples were collected from cows at various intervals after intramammary inoculation with E coli or endotoxin. Percentage of apoptotic neutrophils detected after in vitro incubation for 3 hours was determined. Fluorescein isothiocyanate-labeled annexin-V in combination with propidium iodide was used to distinguish apoptosis and necrosis of neutrophils. Total and differential circulating leukocyte counts and rectal temperature were determined at the time of collection of blood samples. Milk yield and milk somatic cell counts were determined at the time of milking. Results-Inoculation of endotoxin did not accelerate in vitro induction of neutrophil apoptosis. However, inoculation of E coli increased the percentage of apoptotic neutrophils. At 18 hours after inoculation, 20\% of the neutrophils were apoptotic, compared with 5\% before inoculation. Milk somatic cell count and rectal temperature increased, milk production and total leukocyte count decreased, and percentage of immature neutrophils increased after inoculation with E coli or endotoxin. However, kinetics of the responses were more rapid, more severe, and of shorter duration during, endotoxin-induced mastitis. Conclusions and Clinical Relevance-In vitro induction of apoptosis of neutrophils was accelerated only during E col induced mastitis and not during endotoxin-induced mastitis. Endotoxin inoculation as a model for studying coliform mastitis in dairy cows should be viewed with caution.},
  author       = {Van Oostveldt, K and Tomita, GM and Paape, Max and Capuco, Anthony and Burvenich, Christian},
  issn         = {0002-9645},
  journal      = {AMERICAN JOURNAL OF VETERINARY RESEARCH},
  keyword      = {RESPIRATORY BURST ACTIVITY,CLEARANCE,NECROSIS-FACTOR-ALPHA,AGING NEUTROPHILS,MAMMARY-GLAND,LEUKOCYTES,COWS,RECEPTOR,ADHESION},
  language     = {eng},
  number       = {3},
  pages        = {448--453},
  title        = {Apoptosis of bovine neutrophils during mastitis experimentally induced with Escherichia coli or endotoxin.},
  volume       = {63},
  year         = {2002},
}

Chicago
Van Oostveldt, K, GM Tomita, Max Paape, Anthony Capuco, and Christian Burvenich. 2002. “Apoptosis of Bovine Neutrophils During Mastitis Experimentally Induced with Escherichia Coli or Endotoxin.” American Journal of Veterinary Research 63 (3): 448–453.
APA
Van Oostveldt, K, Tomita, G., Paape, M., Capuco, A., & Burvenich, C. (2002). Apoptosis of bovine neutrophils during mastitis experimentally induced with Escherichia coli or endotoxin. AMERICAN JOURNAL OF VETERINARY RESEARCH, 63(3), 448–453.
Vancouver
1.
Van Oostveldt K, Tomita G, Paape M, Capuco A, Burvenich C. Apoptosis of bovine neutrophils during mastitis experimentally induced with Escherichia coli or endotoxin. AMERICAN JOURNAL OF VETERINARY RESEARCH. 2002;63(3):448–53.
MLA
Van Oostveldt, K, GM Tomita, Max Paape, et al. “Apoptosis of Bovine Neutrophils During Mastitis Experimentally Induced with Escherichia Coli or Endotoxin.” AMERICAN JOURNAL OF VETERINARY RESEARCH 63.3 (2002): 448–453. Print.