Concomitant lipopolysaccharide-induced transfer of blood-derived components including immunoglobulins into milk

M Lehmann1, O Wellnitz, R M Bruckmaier

  • 1Veterinary Physiology, Vetsuisse Faculty University of Bern, Bremgartenstrasse 109a, CH-3001 Bern, Switzerland.

Journal of Dairy Science
|December 11, 2012
PubMed

Insights

Lipopolysaccharide (LPS) infusion during mastitis increases blood components in milk, indicating a leaky blood-milk barrier. These changes, while blood-derived, may not benefit the mammary immune system.

Area of Science:

  • Veterinary Immunology
  • Dairy Science
  • Animal Physiology

Background:

  • Mammary immune responses compromise blood-milk barrier integrity, leading to increased permeability.
  • Lipopolysaccharide (LPS) is a key component of bacterial cell walls, often implicated in mastitis.

Purpose of the Study:

  • To determine the blood origin of milk constituents during early-stage LPS-induced mastitis.
  • To investigate changes in immunoglobulin and other component concentrations in blood and milk post-LPS challenge.

Main Methods:

  • Lactating dairy cows were infused with LPS in one udder quarter and monitored for 8 hours.
  • Blood and milk samples were collected hourly to analyze somatic cell count, lactate, BHBA, LDH, and immunoglobulins (IgG1, IgG2).
  • An in vitro experiment assessed the impact of milk cell disruption on lactate and LDH levels.

Main Results:

  • LPS challenge significantly increased somatic cell count, lactate, BHBA, LDH, IgG1, and IgG2 in challenged quarters.
  • Elevated blood lactate concentrations post-LPS indicated a systemic response.
  • Increased nonspecific antibodies in milk suggested enhanced transfer from blood due to barrier dysfunction.

Conclusions:

  • Intramammary LPS infusion triggers a systemic response and elevates blood components in milk.
  • The observed increases in milk constituents are blood-derived, confirming compromised blood-milk barrier integrity.
  • Increased blood component transfer into milk is likely a consequence of barrier leakage, not a direct immune benefit.

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