Lipocalin 2 mediates an innate immune response to bacterial infection by sequestrating iron

By T. Flo, Kelly D. Smith, Shintaro Sato, David J. Rodriguez, M. Holmes, R. Strong, Shizuo Akira, Alan Aderem. Nature, 2004

1,812 citations recorded by the source corpus.

Subfields: Endocrinology, Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f64686717a4da116c201bb6eb085ea671505c455

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology

1. G. Núñez
2. M. Zeng
3. N. Inohara

In Hematology

1. G. Núñez
2. M. Zeng
3. N. Inohara
4. Mohamed A. Marahiel
5. N. Borregaard
6. M. Miethke
7. Eric P. Skaar

In Molecular Biology

1. G. Núñez
2. M. Zeng
3. B. Barres
4. N. Inohara
5. N. Borregaard
6. Mohamed A. Marahiel
7. Eric P. Skaar
8. M. Sofroniew

Citations in the corpus

• Neutrophil granules: a library of innate immunity proteins. (2007, background): “These mice succomb rapidly after intraperitoneal injection of enterochalin-producing E. coli, whereas their wild-type littermates survive [ 40 ].”
• Genomic Analysis of Reactive Astrogliosis (2012, background): “Lcn2, a secreted lipophilic protein that is induced after infection and that limits bacterial growth by sequestering bacterial iron sidephores (Goetz et al., 2002; Flo et al., 2004), and which was recently implicated in astrocyte reactive gliosis (Lee et 4”
• Iron in Infection and Immunity (2013, background): “Accordingly, siderocalin-deficient mice display an enhanced susceptibility to E. coli septicemia (Flo et al., 2004).”
• Siderophore-Based Iron Acquisition and Pathogen Control (2007, background): “This, in contrast, is ensured by the ligand binding protein siderocalin (also known as uterocalin, lipocalin 2 [Lcn2], NGAL, or 24p3), which is a member of the lipocalin superfamily and is found as an acute-phase protein in mammals (99, 193).”
• Mechanisms of inflammation-driven bacterial dysbiosis in the gut (2016, positive): “Lipocalin-2, for instance, is produced by both mucosal epithelial cells and infiltrating neutrophils in response to inflammation, as a strategy to prevent bacterial iron acquisition by binding and sequestering the siderophore enterobactin.(83,84) A recent study showed that enterobactin, a catecholat”
• The Battle for Iron between Bacterial Pathogens and Their Vertebrate Hosts (2010, background): “Mice lacking siderocalin exhibit increased sensitivity to enterobactin-expressing bacteria, demonstrating the pathophysiological relevance of this anti-siderophore defense system [19].”
• The biological functions of T helper 17 cell effector cytokines in inflammation. (2008, neutral): “Lipocalin-2 is required for lung-epithelial killing of K. pneumoniae in vitro (Aujla et al., 2008) and killing of E. coli in vivo (Flo et al., 2004) On the other hand, Reg-family antimicrobial peptides, such as RegIIIg and RegIIIb, are among the key downstream anti-infectious agents that are…”