ArticleInfection and immunity2008
Enhanced innate immune responsiveness to pulmonary Cryptococcus neoformans infection is associated with resistance to progressive infection.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 68 citations in OpenAlex.
- Blood neutrophil counts in HIV-infected patients with cryptococcal meningitis: Association with mortality.PloS one · 2018Trial
- Global proteomic analysis ofmSystems · 2025Article
- The power of GM-CSF: immune regulation in the defense againstFrontiers in immunology · 2025Article
- Card9 Broadly Regulates Host Immunity against Experimental PulmonaryJournal of fungi (Basel, Switzerland) · 2024Article
- Immune evasion byFrontiers in immunology · 2024Article
- Kicking sleepers out of bed: Macrophages promote reactivation of dormant Cryptococcus neoformans by extracellular vesicle release and non-lytic exocytosis.PLoS pathogens · 2023Article
- CD146 deficiency promotes inflammatory type 2 responses in pulmonary cryptococcosis.Medical microbiology and immunology · 2023Article
- Adjuvant Curdlan Contributes to Immunization againstVaccines · 2022Article
- Anti-inflammatory actions of aspirin-triggered resolvin D1 (AT-RvD1) in bronchial epithelial cells infected with Cryptococcus neoformans.Inflammopharmacology · 2021Article
- Use of Clinical Isolates to Establish Criteria for a Mouse Model of LatentFrontiers in cellular and infection microbiology · 2021Article
- Functional heterogeneity of alveolar macrophage population based on expression of CXCL2.Science immunology · 2020Article
- Contribution of Laccase Expression to Immune Response against Cryptococcus gattii Infection.Infection and immunity · 2020Article
- Animal Models ofFrontiers in immunology · 2020Review
- Mechanism of pulmonary immunosuppression: extrapulmonary burn injury suppresses bacterial endotoxin-induced pulmonary neutrophil recruitment and neutrophil extracellular trap (NET) formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Article
- Mechanisms of Pulmonary Escape and Dissemination by Cryptococcus neoformans.Journal of fungi (Basel, Switzerland) · 2018Review
- Article
- CD4mBio · 2017Article
- Trojan Horse Transit Contributes to Blood-Brain Barrier Crossing of a Eukaryotic Pathogen.mBio · 2017Article
- The role of macrophages in the susceptibility of Fc gamma receptor IIb deficient mice to Cryptococcus neoformans.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetically regulated mechanisms of host defense against Cryptococcus neoformans infection are not well understood. In this study, pulmonary infection with the moderately virulent C. neoformans strain 24067 was used to compare the host resistance phenotype of C57BL/6J with that of inbred mouse strain SJL/J. At 7 days or later after infection, C57BL/6J mice exhibited a significantly greater fungal burden in the lungs than SJL/J mice. Characterization of the pulmonary innate immune response at 3 h after cryptococcal infection revealed that resistant SJL/J mice exhibited significantly higher neutrophilia, with elevated levels of inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) and keratinocyte-derived chemokine (KC)/CXCL1 in the airways, as well as increased whole-lung mRNA expression of chemokines KC/CXCL1, MIP-1alpha/CCL3, MIP-1beta/CCL4, MIP-2/CXCL2, and MCP-1/CCL2 and cytokines interleukin 1beta (IL-1beta) and IL-1Ra. At 7 and 14 days after infection, SJL/J mice maintained significantly higher levels of TNF-alpha and KC/CXCL1 in the airways and exhibited a Th1 response characterized by elevated levels of lung gamma interferon (IFN-gamma) and IL-12/IL-23p40, while C57BL/6J mice exhibited Th2 immunity as defined by eosinophilia and IL-4 production. Alveolar and resident peritoneal macrophages from SJL/J mice also secreted significantly greater amounts of TNF-alpha and KC/CXCL1 following in vitro stimulation with C. neoformans. Intracellular signaling analysis demonstrated that TNF-alpha and KC/CXCL1 production was regulated by NF-kappaB and phosphatidylinositol 3 kinase in both strains; however, SJL/J macrophages exhibited heightened and prolonged activation in response to C. neoformans infection compared to that of C57BL/6J. Taken together, these data demonstrate that an enhanced innate immune response against pulmonary C. neoformans infection in SJL/J mice is associated with natural resistance to progressive infection.
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