PIR-B-deficient mice are susceptible to Salmonella infection

Ikuko Torii, Satoshi Oka, Muneki Hotomi, William H. Benjamin, Toshiyuki Takai, John F. Kearney, David E. Briles, Hiromi Kubagawa

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)

Abstract

Paired Ig-like receptors of activating (PIR-A) and inhibitory (PIR-B) isoforms are expressed by many hematopoietic cells, including B lymphocytes and myeloid cells. To determine the functional roles of PIR-A and PIR-B in primary bacterial infection, PIR-B-deficient (PIR-B-/-) and wild-type (WT) control mice were injected i.v. with an attenuated strain of Salmonella enterica Typhimurium (WB335). PIR-B-/- mice were found to be more susceptible to Salmonella infection than WT mice, as evidenced by high mortality rate, high bacterial loads in the liver and spleen, and a failure to clear bacteria from the circulation. Although blood levels of major cytokines and Salmonella-specific Abs were mostly comparable in the two groups of mice, distinct patterns of inflammatory lesions were found in their livers at 7-14 days postinfection: diffuse spreading along the sinusoids in PIR-B-/- mice vs nodular restricted localization in WT mice. PIR-B-/- mice have more inflammatory cells in the liver but fewer B cells and CD8+ T cells in the spleen than WT mice at 14 days postinfection. PIR-B-/- bone marrow-derived macrophages (BMMφ) failed to control intracellular replication of Salmonella in vitro, in part due to inefficient phagosomal oxidant production, when compared with WT BMMφ. PIR-B-/- BMMφ also produced more nitrite and TNF-α upon exposure to Salmonella than WT BMMφ did. These findings suggest that the disruption of PIR-A and PIR-B balance affects their regulatory roles in host defense to bacterial infection.

Original languageEnglish
Pages (from-to)4229-4239
Number of pages11
JournalJournal of Immunology
Volume181
Issue number6
DOIs
Publication statusPublished - 2008 Sep 15

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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