ArticleBMC immunology2016
Cytosolic phospholipase A2 contributes to innate immune defense against Candida albicans lung infection.
Article in BMC immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Phospholipase A2 Isoforms in Lung Immunity and Respiratory Infections: Potential Targets for Next-Generation Therapy.International journal of molecular sciences · 2026Review
- Bronchoalveolar lavage fluid in immune checkpoint inhibitor-related pneumonitis: from pathophysiological window to a precision diagnostic tool.Frontiers in immunology · 2026Review
- Characterization of Pathogens in Respiratory Tract Infection Using Targeted Next-Generation Sequencing: A Population-Based Study in Foshan City from 2022 to 2024.Current medicinal chemistry · 2026Article
- Bioactive lipid-based therapeutic approach to COVID-19 and other similar infections.Archives of medical science : AMS · 2023Article
- Review
- Candida albicans-induced leukotriene biosynthesis in neutrophils is restricted to the hyphal morphology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Candida Albicans Lung Abscess in an Illicit Drugs User With Hepatitis C Virus Chronic Infection.Cureus · 2021Article
- A Genome-Wide Functional Genomics Approach Identifies Susceptibility Pathways to Fungal Bloodstream Infection in Humans.The Journal of infectious diseases · 2019Article
- Comparative Metabolomics Analysis of Cervicitis in Human Patients and a Phenol Mucilage-Induced Rat Model Using Liquid Chromatography Tandem Mass Spectrometry.Frontiers in pharmacology · 2018Article
- Host-Derived Leukotriene BFrontiers in immunology · 2017Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe lung is exposed to airborne fungal spores, and fungi that colonize the oral cavity such as Candida albicans, but does not develop disease to opportunistic fungal pathogens unless the immune system is compromised. The Group IVA cytosolic phospholipase A2 (cPLA2α) is activated in response to Candida albicans infection resulting in the release of arachidonic acid for eicosanoid production. Although eicosanoids such as prostaglandins and leukotrienes modulate inflammation and immune responses, the role of cPLA2α and eicosanoids in regulating C. albicans lung infection is not understood.
methodsThe responses of cPLA2α(+/+) and cPLA2α(-/-) Balb/c mice to intratracheal instillation of C. albicans were compared. After challenge, we evaluated weight loss, organ fungal burden, and the recruitment of cells and the levels of cytokines and eicosanoids in bronchoalveolar lavage fluid. The ability of macrophages and neutrophils from cPLA2α(+/+) and cPLA2α(-/-) mice to recognize and kill C. albicans was also compared.
resultsAfter C. albicans instillation, cPLA2α(+/+) mice recovered a modest weight loss by 48 h and completely cleared fungi from the lung by 12 h with no dissemination to the kidneys. In cPLA2α(-/-) mice, weight loss continued for 72 h, C. albicans was not completely cleared from the lung and disseminated to the kidneys. cPLA2α(-/-) mice exhibited greater signs of inflammation including higher neutrophil influx, and elevated levels of albumin and pro-inflammatory cytokines/chemokines (IL1α, IL1β, TNFα, IL6, CSF2, CXCL1, CCL20) in bronchoalveolar lavage fluid. The amounts of cysteinyl leukotrienes, thromboxane B2 and prostaglandin E2 were significantly lower in bronchoalveolar lavage fluid from C. albicans-infected cPLA2α(-/-) mice compared to cPLA2α(+/+) mice. Alveolar macrophages and neutrophils from uninfected cPLA2α(-/-) mice exhibited less killing of C. albicans in vitro than cells from cPLA2α(+/+) mice. In addition alveolar macrophages from cPLA2α(-/-) mice isolated 6 h after instillation of GFP-C. albicans contained fewer internalized fungi than cPLA2α(+/+) macrophages.
conclusionsThe results demonstrate that cPLA2α contributes to immune surveillance and host defense in the lung to prevent infection by the commensal fungus C. albicans and to dampen inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.