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Updated: Jul 3, 2026

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

Published on: February 22, 2019

IL-10 helps control pathogen load during high-level bacteremia.

Diana Londoño¹, Adriana Marques, Ronald L Hornung

¹Department of Neurology and Neuroscience and Center for Emerging Pathogens, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.

Journal of Immunology (Baltimore, Md. : 1950)

|July 22, 2008

Summary

Interleukin-10 (IL-10) protects innate immune cells from apoptosis during Borrelia turicatae infection. This protection, mediated by inhibiting tumor necrosis factor (TNF), improves pathogen control and prevents early mortality in relapsing fever borreliosis.

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Area of Science:

Immunology
Infectious Diseases
Microbiology

Background:

Relapsing fever borreliosis involves high pathogen loads during peak bacteremia.
B cells and specific IgM antibodies are crucial for spirochetal clearance.
Previous studies indicated IL-10 reduces bacteremia in B cell-deficient mice, suggesting a B cell-independent mechanism.

Purpose of the Study:

To investigate the role of IL-10 in B cell-independent control of Borrelia turicatae infection.
To elucidate the mechanisms by which IL-10 influences innate immunity during high pathogen loads.

Main Methods:

Comparison of Borrelia turicatae infection in RAG2/IL-10(-/-) and RAG2(-/-) mice.
Analysis of bacteremia, cytokine levels (TNF), immune cell apoptosis, and survival.
Investigation of the effects of TNF neutralization on immune responses and disease outcome.

Main Results:

IL-10 deficiency led to significantly higher bacteremia, elevated TNF levels, and increased early mortality.
Infected RAG2/IL-10(-/-) mice exhibited increased apoptosis of immune cells in spleen and peripheral blood.
TNF neutralization reduced immune cell apoptosis, enhanced NK cell IFN-gamma production, increased splenic phagocytosis, decreased spirochetemia, and improved survival.

Conclusions:

IL-10 protects innate immune cells from apoptosis by inhibiting TNF during high pathogen loads in relapsing fever borreliosis.
This IL-10-mediated protection of innate immunity is critical for controlling Borrelia infection and preventing early mortality.