infection induces the resistance of the interferon-γ response in mouse spleen cells at late stages of infection.

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.