Innate immune activation during Salmonella infection initiates extramedullary erythropoiesis and splenomegaly

Amy Jackson, Minelva R. Nanton, Hope O'Donnell, Adovi D. Akue, Stephen J Mcsorley

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Systemic Salmonella infection commonly induces prolonged splenomegaly in murine or human hosts. Although this increase in splenic cellularity is often assumed to be due to the recruitment and expansion of leukocytes, the actual cause of splenomegaly remains unclear. We monitored spleen cell populations during Salmonella infection and found that the most prominent increase is found in the erythroid compartment. At the peak of infection, the majority of spleen cells are immature CD71-Ter119+ reticulocytes, indicating that massive erythropoiesis occurs in response to Salmonella infection. Indeed, this increase in RBC precursors corresponded with marked elevation of serum erythropoietin (EPO). Furthermore, the increase in RBC precursors and EPO production required innate immune signaling mediated by Myd88/TRIF. Neutralization of EPO substantially reduced the immature RBC population in the spleen and allowed a modest increase in host control of infection. These data indicate that early innate immunity to Salmonella initiates marked splenic erythropoiesis and may hinder bacterial clearance.

Original languageEnglish (US)
Pages (from-to)6198-6204
Number of pages7
JournalJournal of Immunology
Volume185
Issue number10
DOIs
StatePublished - Nov 15 2010
Externally publishedYes

Fingerprint

Salmonella Infections
Erythropoiesis
Splenomegaly
Erythropoietin
Spleen
Reticulocytes
Infection Control
Innate Immunity
Salmonella
Population
Leukocytes
Infection
Serum

ASJC Scopus subject areas

  • Immunology

Cite this

Innate immune activation during Salmonella infection initiates extramedullary erythropoiesis and splenomegaly. / Jackson, Amy; Nanton, Minelva R.; O'Donnell, Hope; Akue, Adovi D.; Mcsorley, Stephen J.

In: Journal of Immunology, Vol. 185, No. 10, 15.11.2010, p. 6198-6204.

Research output: Contribution to journalArticle

Jackson, Amy ; Nanton, Minelva R. ; O'Donnell, Hope ; Akue, Adovi D. ; Mcsorley, Stephen J. / Innate immune activation during Salmonella infection initiates extramedullary erythropoiesis and splenomegaly. In: Journal of Immunology. 2010 ; Vol. 185, No. 10. pp. 6198-6204.
@article{a4b9e6e85c254300a77138f025537eb1,
title = "Innate immune activation during Salmonella infection initiates extramedullary erythropoiesis and splenomegaly",
abstract = "Systemic Salmonella infection commonly induces prolonged splenomegaly in murine or human hosts. Although this increase in splenic cellularity is often assumed to be due to the recruitment and expansion of leukocytes, the actual cause of splenomegaly remains unclear. We monitored spleen cell populations during Salmonella infection and found that the most prominent increase is found in the erythroid compartment. At the peak of infection, the majority of spleen cells are immature CD71-Ter119+ reticulocytes, indicating that massive erythropoiesis occurs in response to Salmonella infection. Indeed, this increase in RBC precursors corresponded with marked elevation of serum erythropoietin (EPO). Furthermore, the increase in RBC precursors and EPO production required innate immune signaling mediated by Myd88/TRIF. Neutralization of EPO substantially reduced the immature RBC population in the spleen and allowed a modest increase in host control of infection. These data indicate that early innate immunity to Salmonella initiates marked splenic erythropoiesis and may hinder bacterial clearance.",
author = "Amy Jackson and Nanton, {Minelva R.} and Hope O'Donnell and Akue, {Adovi D.} and Mcsorley, {Stephen J}",
year = "2010",
month = "11",
day = "15",
doi = "10.4049/jimmunol.1001198",
language = "English (US)",
volume = "185",
pages = "6198--6204",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "10",

}

TY - JOUR

T1 - Innate immune activation during Salmonella infection initiates extramedullary erythropoiesis and splenomegaly

AU - Jackson, Amy

AU - Nanton, Minelva R.

AU - O'Donnell, Hope

AU - Akue, Adovi D.

AU - Mcsorley, Stephen J

PY - 2010/11/15

Y1 - 2010/11/15

N2 - Systemic Salmonella infection commonly induces prolonged splenomegaly in murine or human hosts. Although this increase in splenic cellularity is often assumed to be due to the recruitment and expansion of leukocytes, the actual cause of splenomegaly remains unclear. We monitored spleen cell populations during Salmonella infection and found that the most prominent increase is found in the erythroid compartment. At the peak of infection, the majority of spleen cells are immature CD71-Ter119+ reticulocytes, indicating that massive erythropoiesis occurs in response to Salmonella infection. Indeed, this increase in RBC precursors corresponded with marked elevation of serum erythropoietin (EPO). Furthermore, the increase in RBC precursors and EPO production required innate immune signaling mediated by Myd88/TRIF. Neutralization of EPO substantially reduced the immature RBC population in the spleen and allowed a modest increase in host control of infection. These data indicate that early innate immunity to Salmonella initiates marked splenic erythropoiesis and may hinder bacterial clearance.

AB - Systemic Salmonella infection commonly induces prolonged splenomegaly in murine or human hosts. Although this increase in splenic cellularity is often assumed to be due to the recruitment and expansion of leukocytes, the actual cause of splenomegaly remains unclear. We monitored spleen cell populations during Salmonella infection and found that the most prominent increase is found in the erythroid compartment. At the peak of infection, the majority of spleen cells are immature CD71-Ter119+ reticulocytes, indicating that massive erythropoiesis occurs in response to Salmonella infection. Indeed, this increase in RBC precursors corresponded with marked elevation of serum erythropoietin (EPO). Furthermore, the increase in RBC precursors and EPO production required innate immune signaling mediated by Myd88/TRIF. Neutralization of EPO substantially reduced the immature RBC population in the spleen and allowed a modest increase in host control of infection. These data indicate that early innate immunity to Salmonella initiates marked splenic erythropoiesis and may hinder bacterial clearance.

UR - http://www.scopus.com/inward/record.url?scp=78650660175&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78650660175&partnerID=8YFLogxK

U2 - 10.4049/jimmunol.1001198

DO - 10.4049/jimmunol.1001198

M3 - Article

C2 - 20952675

AN - SCOPUS:78650660175

VL - 185

SP - 6198

EP - 6204

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 10

ER -