Temporal and Anatomical Host Resistance to Chronic Salmonella Infection Is Quantitatively Dictated by Nramp1 and Influenced by Host Genetic Background

The course is considered of a second type of Salmonella infection naturally appearing in a guinea pig population during the endemic stage of an earlier outbreak. After a quiescent period of 5 months the percentage mortality increased abruptly; fluctuated, with a second rise during the 9th month; and then declined. With the exception of a high rate during the 2nd month the percentage mortality from the initial infection tended to remain on a low level. The spread of infection in the cages of the breeding stock is recorded from the time of the first fatal case. There was a slow but general dissemination of the second organism through the group. Fatal cases were confirmed solely to the sows. It is suggested that a lowered individual resistance occuring during pregnancy might be associated with the regular cage spread and with the apparent difference in susceptibility of the sexes. Natural host resistance, virulence of the organisms and acquired host resistance are discussed from the standpoint of their bearing on the unequal distribution of deaths from the two infections.

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Role of strain differences on host resistance and the transcriptional response of macrophages to infection withYersinia enterocolitica

Physiological Genomics ◽

10.1152/physiolgenomics.00188.2005 ◽

2006 ◽

Vol 25 (1) ◽

pp. 75-84 ◽

Cited By ~ 20

Author(s):

Katrin van Erp ◽

Kristina Dach ◽

Isabel Koch ◽

Jürgen Heesemann ◽

Reinhard Hoffmann

Keyword(s):

Transcription Factors ◽

Host Resistance ◽

Genetic Background ◽

Antibacterial Properties ◽

Differentially Expressed ◽

Transcriptional Responses ◽

Yersinia Infection ◽

Ifn Γ ◽

The Impact

The outcome of a host-pathogen encounter is determined by virulence factors of the pathogen and defense factors of the host. We characterized the impact of host factors [resistant (C57BL/6) or susceptible (BALB/c) genetic background and exposure to interferon (IFN)-γ] on transcriptional responses of bone marrow-derived macrophages (BMDM) to infection with Yersinia enterocolitica. IFN-γ treatment more profoundly altered the transcriptome of BMDM than did bacterial infection or genetic background. In BALB/c BMDM, 1,161 genes were differentially expressed in response to Yersinia infection with or without IFN-γ prestimulation. Fourteen genes (1.2%) could only be induced by BALB/c BMDM in response to Yersinia infection after IFN-γ pretreatment. These genes inhibit apoptosis, activate NF-κB and Erk signaling, are chemotactic to neutrophils, and are involved in cytoskeletal reorganization, hence possibly in phagocytosis. Ten of these genes possess a common module of binding sites for Hox, Pou, and Creb transcription factors in 2 kb of upstream genomic sequence, suggesting a possible novel role of these transcription factors in regulation of immune responses. Fifty-two of one thousand fifty differentially expressed genes (4.9%) were induced more strongly by C57BL/6 BMDM in response to Yersinia infection than BALB/c BMDM. These genes activate NK cells, have antibacterial properties, or are involved in sensing chemokines and lipopolysaccharide (LPS). These data show that host resistance factors modulate a surprisingly small, but identifiable and functionally significant, portion of the macrophage transcriptome in response to Yersinia infection.

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