ArticleInfection and immunity2014
Impact of surfactant protein D, interleukin-5, and eosinophilia on Cryptococcosis.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Comparative miRNA transcriptomics of macaques and mice revealsEmerging microbes & infections · 2022Article
- Pulmonary Fibrosis and Hypereosinophilia in TLR9Pathogens (Basel, Switzerland) · 2022Article
- Detection of Cytokines and Collectins in Bronchoalveolar Fluid Samples of Patients Infected withJournal of fungi (Basel, Switzerland) · 2021Article
- Surfactant Protein D Recognizes Multiple Fungal Ligands: A Key Step to Initiate and Intensify the Anti-fungal Host Defense.Frontiers in cellular and infection microbiology · 2020Review
- Animal Models ofFrontiers in immunology · 2020Review
- Basic principles of the virulence ofVirulence · 2019Review
- Unveil the transcriptional landscape at the Cryptococcus-host axis in mice and nonhuman primates.PLoS neglected tropical diseases · 2019Article
- Inflammatory monocytes are detrimental to the host immune response during acute infection with Cryptococcus neoformans.PLoS pathogens · 2019Article
- Surfactant Protein D in Respiratory and Non-Respiratory Diseases.Frontiers in medicine · 2018Review
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- Frequency-dependent airway hyperresponsiveness in a mouse model of emphysema and allergic inflammation.Physiological reports · 2018Article
- Immunology of Cryptococcal Infections: Developing a Rational Approach to Patient Therapy.Frontiers in immunology · 2018Review
- Innate Immune Responses toJournal of fungi (Basel, Switzerland) · 2017Article
- RIPK3/Fas-Associated Death Domain Axis Regulates Pulmonary Immunopathology to Cryptococcal Infection Independent of Necroptosis.Frontiers in immunology · 2017Article
- C-type lectin receptors in tuberculosis: what we know.Medical microbiology and immunology · 2016Review
- DAP12 Inhibits Pulmonary Immune Responses to Cryptococcus neoformans.Infection and immunity · 2016Article
- Surfactant proteins, SP-A and SP-D, in respiratory fungal infections: their role in the inflammatory response.Respiratory research · 2016Review
- Innate host defenses against Cryptococcus neoformans.Journal of microbiology (Seoul, Korea) · 2016Review
- Type I IFN Induction via Poly-ICLC Protects Mice against Cryptococcosis.PLoS pathogens · 2015Article
- Immunity to Cryptococcus neoformans and C. gattii during cryptococcosis.Fungal genetics and biology : FG & B · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Cryptococcus neoformans is an opportunistic fungal pathogen that initiates infection following inhalation. As a result, the pulmonary immune response provides a first line of defense against C. neoformans. Surfactant protein D (SP-D) is an important regulator of pulmonary immune responses and is typically host protective against bacterial and viral respiratory infections. However, SP-D is not protective against C. neoformans. This is evidenced by previous work from our laboratory demonstrating that SP-D-deficient mice infected with C. neoformans have a lower fungal burden and live longer than wild-type (WT) control animals. We hypothesized that SP-D alters susceptibility to C. neoformans by dysregulating the innate pulmonary immune response following infection. Thus, inflammatory cells and cytokines were compared in the bronchoalveolar lavage fluid from WT and SP-D(-/-) mice after C. neoformans infection. Postinfection, mice lacking SP-D have reduced eosinophil infiltration and interleukin-5 (IL-5) in lung lavage fluid. To further explore the interplay of SP-D, eosinophils, and IL-5, mice expressing altered levels of eosinophils and/or IL-5 were infected with C. neoformans to assess the role of these innate immune mediators. IL-5-overexpressing mice have increased pulmonary eosinophilia and are more susceptible to C. neoformans infection than WT mice. Furthermore, susceptibility of SP-D(-/-) mice to C. neoformans infection could be restored to the level of WT mice by increasing IL-5 and eosinophils by crossing the IL-5-overexpressing mice with SP-D(-/-) mice. Together, these studies support the conclusion that SP-D increases susceptibility to C. neoformans infection by promoting C. neoformans-driven pulmonary IL-5 and eosinophil infiltration.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.