Infection Induces the Resistance of the Interferon-γ Response in Mouse Spleen Cells at Late Stages of Infection

Overview

Journal Inflamm Regen

Publisher Biomed Central

Date 2017 Dec 21

PMID 29259694

Authors

Atsuko Masumi

Keiko Mochida

Kazuya Takizawa

Takuo Mizukami

Madoka Kuramitsu

Momoka Tsuruhara

Shigetarou Mori

Keigo Shibayama

Kazunari Yamaguchi

Isao Hamaguchi

Affiliations

Soon will be listed here.

Abstract

Background: Bacterial infections cause an increase in the population of hematopoietic stem cells (HSCs). To investigate the downstream factors associated with hematopoietic stem cells, mice are infected with ().

Results: () infection induces the enlargement of the spleen and changes in histopathology, including changes to the lineage populations. A dramatic expansion of Linc-kitSca-1 (KSL) cells in mouse bone marrow cells and spleen cells was detected 4 weeks after infection with ; however, there was no difference in the engraft activity between infected and un-infected mouse bone marrow cells. We tested the cytokine and cytokine-related gene expression after infection and found that IFN-γ expression increased and peaked at 4 weeks in both bone marrow and spleen cells. The expression of Sca-1 gene peaked at 4 weeks in the bone marrow but peaked at 2 weeks in spleen cells, although the Sca-1 surface marker peaked at 4 weeks after infection in both bone marrow and spleen cells. Interferon regulatory factor-2 (IRF-2) expression did not change in the bone marrow cells, whereas it decreased in spleen cells at 4 weeks and IRF-1 expression was up-regulated in both bone marrow and spleen cells after infection. However, the up-regulation of IRF-1 was not correlated with IFN-γ expression in the -infected mouse spleen cells.

Conclusions: This finding suggests that the IFN-γ production mediated by infection alters the population of KSL cells during host defense, and the down-regulation of the IFN-γ response in spleen cells occurs at the late stage after infection.

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