Macrophages Acquire Neutrophil Granules for Antimicrobial Activity against Intracellular Pathogens
Open accessAbstract
A key target of many intracellular pathogens is the macrophage. Although macrophages can generate antimicrobial activity, neutrophils have been shown to have a key role in host defense, presumably by their preformed granules containing antimicrobial agents. Yet the mechanism by which neutrophils can mediate antimicrobial activity against intracellular pathogens such as Mycobacterium tuberculosis has been a long-standing enigma. We demonstrate that apoptotic neutrophils and purified granules inhibit the growth of extracellular mycobacteria. Phagocytosis of apoptotic neutrophils by macrophages results in decreased viability of intracellular M. tuberculosis. Concomitant with uptake of apoptotic neutrophils, granule contents traffic to early endosomes, and colocalize with mycobacteria. Uptake of purified granules alone decreased growth of intracellular mycobacteria. Therefore, the transfer of antimicrobial peptides from neutrophils to macrophages provides a cooperative defense strategy between innate immune cells against intracellular pathogens and may complement other pathways that involve delivery of antimicrobial peptides to macrophages.
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Co-uptake of apoptotic PMN granules or HNP-1 enhanced killing of M. tuberculosis by macrophages.
“In another study, co-uptake of apoptotic PMN granules or HNP-1 enhanced killing of M. tuberculosis by MΦs (156).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [156]
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References 43 · Cited by 267
- Authors
- Tan, B. H., Meinken, C., Bastian, M., Bruns, H., Legaspi, A., Ochoa, M. T., Krutzik, S. R., Bloom, B. R., Ganz, T., Modlin, R. L., & Stenger, S.
- Affiliations
- University of California, Los Angeles (US)
- Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
- Division of Dermatology, University of California , Los Angeles, CA 90095
- Harvard University (US)
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-08-01
- Volume
- 177
- Issue
- 3
- Pages
- 1864-1871
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2119724532
- Cited by
- 267
- References
- 43
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 9 · 2023: 9 · 2022: 11 · 2021: 10 · 2020: 14 · 2019: 18 · 2018: 6 · 2017: 12 · 2016: 8 · 2015: 18 · 2014: 15 · 2013: 12 · 2012: 17
- FWCI
- 10.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Commission
- Deutsche Forschungsgemeinschaft (SFB643)
- National Institutes of Health (AI28697, CA16042, AI22553)
- University of California, Los Angeles
- Center for AIDS Research, University of Washington
- National Cancer Institute (CA-16 042, P30CA016042)
- National Institute of Allergy and Infectious Diseases (T32AI007126, R01AI047866, AI-07126, AI47866, AI-28 697, AI-22553, P30AI028697)
- Jonsson Comprehensive Cancer Center
- David Geffen School of Medicine, University of California, Los Angeles
- UCLA AIDS Institute
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- neutrophil granules, macrophages, Mycobacterium tuberculosis, intracellular pathogens, antimicrobial peptides, apoptotic neutrophils, phagocytosis, early endosomes, host defense
- MeSH terms
- Blood Bactericidal Activity, Cytoplasmic Granules, Extracellular Space, Growth Inhibitors, Humans, Intracellular Fluid, Mycobacterium tuberculosis, Neutrophils, Phagocytosis, Phagosomes, Endosomes, Biomarkers, Macrophages, Alveolar, Apoptosis, alpha-Defensins
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