Stimulated expression of TNF-α and IL-8, but not of lingual antimicrobial peptide reflects the concentration of pathogens contacting bovine mammary epithelial cells

Juliane Günther, Shuzhen Liu, Kathrin Esch, Hans Joachim Schuberth, Hans Martin Seyfert

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

We examined if and how mammary epithelial cells (MECs) calibrate and confine the intensity of an inflammatory response elicited by different concentrations of mastitis pathogens. Therefore we quantified in primary bovine MEC the effect of different E. coli pathogen concentrations upon the abundance of mRNA molecules encoding factors of immune defence. Induced synthesis of the mRNAs encoding tumor necrosis factor alpha and interleukin 8 both clearly correlated with the E. coli dose 1. h after stimulation. Also the decay rate of those mRNAs reflected the pathogen load. The higher the concentration of E. coli, the faster and stronger was the up regulation and also the subsequent degradation of those particular mRNA species. Modulation of the mRNA concentration of tristetraprolin, a factor crucially involved in the mRNA degradation, followed the same pattern. In contrast, extent and kinetics of increasing the mRNA concentrations of serum amyloid A3 and lingual antimicrobial peptide were almost independent of the pathogen dose. We show that MEC perceive the information about the different pathogen concentrations and convert this signal into a calibrated synthesis of pro-inflammatory cytokines. We suggest that selective degradation of the mRNA molecules encoding those inflammatory cytokines contributes significantly to prevent an overshooting immune response in the udder.

Original languageEnglish (US)
Pages (from-to)152-157
Number of pages6
JournalVeterinary Immunology and Immunopathology
Volume135
Issue number1-2
DOIs
StatePublished - May 1 2010
Externally publishedYes

Fingerprint

antimicrobial peptides
interleukin-8
tongue
Interleukin-8
breasts
Breast
epithelial cells
Epithelial Cells
Messenger RNA
pathogens
cattle
Escherichia coli
RNA Stability
degradation
cytokines
Tristetraprolin
synthesis
Cytokines
amyloid
Animal Mammary Glands

Keywords

  • E. coli
  • Mammary epithelial cell
  • Mastitis
  • Pathogen dose
  • Pro-inflammatory cytokines

ASJC Scopus subject areas

  • Immunology
  • veterinary(all)

Cite this

Stimulated expression of TNF-α and IL-8, but not of lingual antimicrobial peptide reflects the concentration of pathogens contacting bovine mammary epithelial cells. / Günther, Juliane; Liu, Shuzhen; Esch, Kathrin; Schuberth, Hans Joachim; Seyfert, Hans Martin.

In: Veterinary Immunology and Immunopathology, Vol. 135, No. 1-2, 01.05.2010, p. 152-157.

Research output: Contribution to journalArticle

@article{2f62c23a85164ff68210a4987a396bc6,
title = "Stimulated expression of TNF-α and IL-8, but not of lingual antimicrobial peptide reflects the concentration of pathogens contacting bovine mammary epithelial cells",
abstract = "We examined if and how mammary epithelial cells (MECs) calibrate and confine the intensity of an inflammatory response elicited by different concentrations of mastitis pathogens. Therefore we quantified in primary bovine MEC the effect of different E. coli pathogen concentrations upon the abundance of mRNA molecules encoding factors of immune defence. Induced synthesis of the mRNAs encoding tumor necrosis factor alpha and interleukin 8 both clearly correlated with the E. coli dose 1. h after stimulation. Also the decay rate of those mRNAs reflected the pathogen load. The higher the concentration of E. coli, the faster and stronger was the up regulation and also the subsequent degradation of those particular mRNA species. Modulation of the mRNA concentration of tristetraprolin, a factor crucially involved in the mRNA degradation, followed the same pattern. In contrast, extent and kinetics of increasing the mRNA concentrations of serum amyloid A3 and lingual antimicrobial peptide were almost independent of the pathogen dose. We show that MEC perceive the information about the different pathogen concentrations and convert this signal into a calibrated synthesis of pro-inflammatory cytokines. We suggest that selective degradation of the mRNA molecules encoding those inflammatory cytokines contributes significantly to prevent an overshooting immune response in the udder.",
keywords = "E. coli, Mammary epithelial cell, Mastitis, Pathogen dose, Pro-inflammatory cytokines",
author = "Juliane G{\"u}nther and Shuzhen Liu and Kathrin Esch and Schuberth, {Hans Joachim} and Seyfert, {Hans Martin}",
year = "2010",
month = "5",
day = "1",
doi = "10.1016/j.vetimm.2009.11.004",
language = "English (US)",
volume = "135",
pages = "152--157",
journal = "Veterinary Immunology and Immunopathology",
issn = "0165-2427",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Stimulated expression of TNF-α and IL-8, but not of lingual antimicrobial peptide reflects the concentration of pathogens contacting bovine mammary epithelial cells

AU - Günther, Juliane

AU - Liu, Shuzhen

AU - Esch, Kathrin

AU - Schuberth, Hans Joachim

AU - Seyfert, Hans Martin

PY - 2010/5/1

Y1 - 2010/5/1

N2 - We examined if and how mammary epithelial cells (MECs) calibrate and confine the intensity of an inflammatory response elicited by different concentrations of mastitis pathogens. Therefore we quantified in primary bovine MEC the effect of different E. coli pathogen concentrations upon the abundance of mRNA molecules encoding factors of immune defence. Induced synthesis of the mRNAs encoding tumor necrosis factor alpha and interleukin 8 both clearly correlated with the E. coli dose 1. h after stimulation. Also the decay rate of those mRNAs reflected the pathogen load. The higher the concentration of E. coli, the faster and stronger was the up regulation and also the subsequent degradation of those particular mRNA species. Modulation of the mRNA concentration of tristetraprolin, a factor crucially involved in the mRNA degradation, followed the same pattern. In contrast, extent and kinetics of increasing the mRNA concentrations of serum amyloid A3 and lingual antimicrobial peptide were almost independent of the pathogen dose. We show that MEC perceive the information about the different pathogen concentrations and convert this signal into a calibrated synthesis of pro-inflammatory cytokines. We suggest that selective degradation of the mRNA molecules encoding those inflammatory cytokines contributes significantly to prevent an overshooting immune response in the udder.

AB - We examined if and how mammary epithelial cells (MECs) calibrate and confine the intensity of an inflammatory response elicited by different concentrations of mastitis pathogens. Therefore we quantified in primary bovine MEC the effect of different E. coli pathogen concentrations upon the abundance of mRNA molecules encoding factors of immune defence. Induced synthesis of the mRNAs encoding tumor necrosis factor alpha and interleukin 8 both clearly correlated with the E. coli dose 1. h after stimulation. Also the decay rate of those mRNAs reflected the pathogen load. The higher the concentration of E. coli, the faster and stronger was the up regulation and also the subsequent degradation of those particular mRNA species. Modulation of the mRNA concentration of tristetraprolin, a factor crucially involved in the mRNA degradation, followed the same pattern. In contrast, extent and kinetics of increasing the mRNA concentrations of serum amyloid A3 and lingual antimicrobial peptide were almost independent of the pathogen dose. We show that MEC perceive the information about the different pathogen concentrations and convert this signal into a calibrated synthesis of pro-inflammatory cytokines. We suggest that selective degradation of the mRNA molecules encoding those inflammatory cytokines contributes significantly to prevent an overshooting immune response in the udder.

KW - E. coli

KW - Mammary epithelial cell

KW - Mastitis

KW - Pathogen dose

KW - Pro-inflammatory cytokines

UR - http://www.scopus.com/inward/record.url?scp=77951205621&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77951205621&partnerID=8YFLogxK

U2 - 10.1016/j.vetimm.2009.11.004

DO - 10.1016/j.vetimm.2009.11.004

M3 - Article

C2 - 19963279

AN - SCOPUS:77951205621

VL - 135

SP - 152

EP - 157

JO - Veterinary Immunology and Immunopathology

JF - Veterinary Immunology and Immunopathology

SN - 0165-2427

IS - 1-2

ER -