Hypoxia inducible factor (HIF) function in innate immunity and infection
Open accessAbstract
The hypoxia-inducible transcription factor (HIF-1alpha) is a major regulator of energy homeostasis and cellular adaptation to low oxygen stress. Recently, HIF-1alpha has been discovered to function as a global regulator of macrophage and neutrophil inflammatory and innate immune functions, as befits these specialized phagocytic cells who must operate effectively in the hypoxic microenvironments of infected tissues. This review summarizes current knowledge of the role of HIF-1alpha in mammalian innate immunity, emphasizing insight gained from conditional gene targeting of the transcription factor in the myeloid cell lineage. Dynamic changes in HIF-1alpha expression in the course of bacterial, viral, or parasitic infections are outlined and inferences drawn regarding the consequences for pathogen and host. A better understanding of HIF-1alpha function may provide novel and rational approaches for boosting innate immune function in the therapy of certain complicated infectious disease conditions.
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Tissue hypoxia that may result from anemia of chronic disease is sensed by HIF in various cell types including macrophages and dendritic cells.
“The tissue hypoxia that may results from ACD is sensed by HIF in various cell types including macrophages and dendritic cells (Jantsch and Schodel, 2015;Zinkernagel et al., 2007).”
From Iron in infection and immunity (2020) · cites this paper as Zinkernagel et al., 2007
The Introduction explains that hypoxia stabilizes HIF-1α, and the paper discusses HIF function in macrophages in hypoxic inflammatory tissue. The HIF-1α and sepsis section mentions anemia accompanying chronic infection, but does not say that anemia causes tissue hypoxia; the passages found also do not address dendritic cells. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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Research works printed but not linked: 1
- Zinkernagel AS, Peyssonnaux C, Johnson RS, Nizet V (2007) Pharmacologic augmentation of HIF-1a with mimosine boosts the bactericidal capacity of phagocytes. J Infect Dis (in press)
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Self-citation
- Authors
- Zinkernagel, A. S., Johnson, R. S., & Nizet, V.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Nizet, Victor
- Venue
- Journal of Molecular Medicine
- Published
- 2007-11-21
- Volume
- 85
- Issue
- 12
- Pages
- 1339-1346
- ISSN
- 0946-2716 (ISSN-L)
- 1432-1440
- OpenAlex
- W2108435172
- Cited by
- 265
- References
- 61
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 9 · 2023: 13 · 2022: 8 · 2021: 21 · 2020: 11 · 2019: 5 · 2018: 16 · 2017: 11 · 2016: 20 · 2015: 16 · 2014: 12 · 2013: 18 · 2012: 21
- FWCI
- 1.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (AI060840, R01AI060840)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- hypoxia-inducible factor-1α, HIF-1α, innate immunity, macrophages, neutrophils, myeloid cells, hypoxia, infection, bacterial infection, viral infection, parasitic infection, energy homeostasis, conditional gene targeting
- MeSH terms
- Animals, Bacterial Infections, Humans, Immunity, Innate, Immunologic Factors, Parasitic Diseases, Virus Diseases, Signal Transduction, Sepsis, Myeloid Cells, Hypoxia-Inducible Factor 1, alpha Subunit
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