Cited by 92Immune responses and vaccinationsImmune Response and InflammationCalcium signaling and nucleotide metabolism

CD38 Controls the Innate Immune Response against Listeria monocytogenes

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Lischke, Timo, Heesch, Kira, Schumacher, Valéa, Schneider, Michael, Haag, Friedrich, Koch-Nolte, Friedrich, Mittrücker, Hans-Willi·2013·Infection and Immunity

Abstract

CD38, adenosine-5′-diphosphate-ribosyl cyclase 1, is a multifunctional enzyme, expressed on a wide variety of cell types. CD38 has been assigned diverse functions, including generation of calcium-mobilizing metabolites, cell activation, and chemotaxis. Using a murine Listeria monocytogenes infection model, we found that CD38 knockout (KO) mice were highly susceptible to infection. Enhanced susceptibility was already evident within 3 days of infection, suggesting a function of CD38 in the innate immune response. CD38 was expressed on neutrophils and inflammatory monocytes, and especially inflammatory monocytes further upregulated CD38 during infection. Absence of CD38 caused alterations of the migration pattern of both cell types to sites of infection. We observed impaired accumulation of cells in the spleen but surprisingly similar or even higher accumulation of cells in the liver. CD38 KO and wild-type mice showed similar changes in the composition of neutrophils and inflammatory monocytes in blood and bone marrow, indicating that mobilization of these cells from the bone marrow was CD38 independent. In vitro , macrophages of CD38 KO mice were less efficient in uptake of listeria but still able to kill the bacteria. Dendritic cells also displayed enhanced CD38 expression following infection. However, absence of CD38 did not impair the capacity of mice to prime CD8 + T cells against L. monocytogenes , and CD38 KO mice could efficiently control secondary listeria infection. In conclusion, our results demonstrate an essential role for CD38 in the innate immune response against L. monocytogenes .

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  1. [23]Gellin BG, Broome CV. 1989. Listeriosis. JAMA 261:1313–1320 [PubMed] [Google Scholar]

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Authors
Lischke, T., Heesch, K., Schumacher, V., Schneider, M., Haag, F., Koch-Nolte, F., & Mittrücker, H.-W.
Affiliations
  • University Medical Center Hamburg-Eppendorf (DE)
  • Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Venue
Infection and Immunity
Published
2013-11
Volume
81
Issue
11
Pages
4091-4099
ISSN
  • 0019-9567 (ISSN-L)
  • 1098-5522
OpenAlex
W2117373786
Cited by
92
References
40
Citations by year
2026: 3 · 2025: 7 · 2024: 8 · 2023: 10 · 2022: 7 · 2021: 11 · 2020: 15 · 2019: 8 · 2018: 9 · 2017: 3 · 2016: 3 · 2015: 7 · 2014: 1
FWCI
2.03
Type
journal article
Language
en
Open access
Locations
  • Infection and Immunity (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Deutsche Forschungsgemeinschaft
  • Universitat de Barcelona
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Keywords
CD38, Listeria monocytogenes, innate immunity, neutrophils, inflammatory monocytes, dendritic cells, macrophages, cell migration, bacterial phagocytosis, CD8+ T cell priming, secondary infection, CD38 knockout mice
MeSH terms
Animals, Cell Movement, Dendritic Cells, Disease Models, Animal, Disease Susceptibility, Immunity, Innate, Listeriosis, Listeria monocytogenes, Liver, Macrophages, Membrane Glycoproteins, Monocytes, Neutrophils, Phagocytosis, Spleen, Gene Deletion, Mice, Knockout, Mice, ADP-ribosyl Cyclase 1, Host-Pathogen Interactions

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