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Updated: Feb 18, 2026

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Immune Function in Critically Ill Dogs.

D Hoffman¹, J Amorim¹, A DeClue¹

¹The Comparative Internal Medicine Laboratory, University of Missouri College of Veterinary Medicine, Columbia, MO.

Journal of Veterinary Internal Medicine

|November 14, 2017

Summary

This summary is machine-generated.

Critical illness in dogs impairs immune function, leading to decreased respiratory burst capacity and cytokine production. However, Toll-like receptor 4 (TLR-4) expression is increased in these dogs.

Keywords:

Cytokines Phagocytosis Respiratory burst Sepsis

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Last Updated: Feb 18, 2026

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Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation

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Published on: May 16, 2016

Area of Science:

Veterinary immunology
Critical care medicine
Canine health

Background:

Critical illness (CI) in humans is often associated with immune dysfunction.
Limited data exists on immune dysfunction in dogs with critical illness.

Purpose of the Study:

To investigate and compare the immune response in critically ill dogs versus healthy controls.
To identify specific alterations in immune cell function and cytokine production in canine critical illness.

Main Methods:

A cohort study compared immunologic variables in 14 critically ill dogs (APPLE_fast score >20) with 15 healthy controls.
Evaluated lipopolysaccharide (LPS)-stimulated cytokine production (TNF-α, IL-6, IL-10), phagocytosis, respiratory burst capacity, lymphocyte phenotype, and monocyte expressions of HLA-DR and TLR-4.

Main Results:

Critically ill dogs showed significantly reduced production of TNF-α, IL-6, and IL-10 after LPS stimulation compared to controls.
Respiratory burst capacity was significantly decreased in critically ill dogs following E. coli or PMA stimulation.
Monocytes from critically ill dogs exhibited increased expression of Toll-like receptor 4 (TLR-4).

Conclusions:

Dogs with critical illness exhibit significant immune system alterations.
These alterations include diminished respiratory burst function and reduced cytokine production.
Despite functional deficits, there is an upregulation of TLR-4 expression on monocytes in critically ill dogs.