ArticleExpert review of anti-infective therapy2015
Lethal influenza infection: Is a macrophage to blame?
Article in Expert review of anti-infective therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 17 citations in OpenAlex.
- PROS1/AXL signaling protects mice from lethal influenza infection by inducing M2 macrophage polarization.Acta biochimica et biophysica Sinica · 2025Article
- Surfactant protein A alters endosomal trafficking of influenza A virus in macrophages.Frontiers in immunology · 2023Article
- Pathogenesis of Respiratory Viral and Fungal Coinfections.Clinical microbiology reviews · 2022Review
- Resident macrophages of the lung and liver: The guardians of our tissues.Frontiers in immunology · 2022Review
- Genomic and epigenomic adaptation in SP-R210 (Myo18A) isoform-deficient macrophages.Immunobiology · 2021Article
- Innate immune responses at the asymptomatic stage of influenza A viral infections of Streptococcus pneumoniae colonized and non-colonized mice.Scientific reports · 2021Article
- Article
- The annexin A1/FPR2 signaling axis expands alveolar macrophages, limits viral replication, and attenuates pathogenesis in the murine influenza A virus infection model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Obtaining insights from high-dimensional data: sparse principal covariates regression.BMC bioinformatics · 2018Article
- GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization.Respiratory research · 2018Article
- SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection.Scientific reports · 2017Article
- Antiviral activity of chlorogenic acid against influenza A (H1N1/H3N2) virus and its inhibition of neuraminidase.Scientific reports · 2017Article
- Human lung ex vivo infection models.Cell and tissue research · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar macrophages (AMs) are critical for immunity against influenza A virus (IAV) infection. Depletion, hyporeactivity, and disruption of AM development and differentiation are all associated with lethal IAV infection. AMs drive the innate immune response that limits IAV infection. AMs are crucial for steady-state homeostasis of pulmonary surfactant, and in turn surfactant proteins regulate AMs and participate in host defense against IAV. Known factors that are necessary for AM function and differentiation in vivo include surfactant proteins, the growth factor GM-CSF, the hormone receptor PPARγ, and the transcription factors PU.1 and Bach2. Although PU.1 and PPARγ are downstream effectors of GM-CSF, Bach2 works independently. GM-CSF and Bach2-deficient AMs have phenotypes with immature or alternatively activated states of differentiation, respectively, and both extremes are unsuitable for surfactant homeostasis. The activation state of AMs and the local microenvironment may determine the development of symptomatic versus asymptomatic IAV infection in different individuals.
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.