ArticleInfection and immunity2012
The alveolar epithelial cell chemokine response to pneumocystis requires adaptor molecule MyD88 and interleukin-1 receptor but not toll-like receptor 2 or 4.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Strain-Dependent Protective Innate Immunity AgainstJournal of fungi (Basel, Switzerland) · 2026Article
- Modulation of host lung immunity in Pneumocystis pneumonia: a review of current concepts and future prospects for novel adjunctive immune-based therapies.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Epithelial responses to fungal pathogens.Current opinion in microbiology · 2024Review
- A review of pulmonary neutrophilia and insights into the key role of neutrophils in particle-induced pathogenesis in the lung from animal studies of lunar dusts and other poorly soluble dust particles.Critical reviews in toxicology · 2023Review
- Immunity to fungi in the lung.Seminars in immunology · 2023Review
- They shall not grow mold: Soldiers of innate and adaptive immunity to fungi.Seminars in immunology · 2023Review
- Targeting β-glucans, vital components of theFrontiers in immunology · 2023Review
- Cellular and functional heterogeneity of the airway epithelium.Mucosal immunology · 2021Review
- Effects of the Cytoplasm and Mitochondrial Specific Hydroxyl Radical Scavengers TA293 and mitoTA293 in Bleomycin-Induced Pulmonary Fibrosis Model Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Flagellin/TLR5 Stimulate Myeloid Progenitors to Enter Lung Tissue and to Locally Differentiate Into Macrophages.Frontiers in immunology · 2021Article
- Residual endotoxin induces primary graft dysfunction through ischemia/reperfusion-primed alveolar macrophages.The Journal of clinical investigation · 2020Article
- Combination Immunotherapy with Passive Antibody and Sulfasalazine Accelerates Fungal Clearance and Promotes the Resolution ofInfection and immunity · 2020Article
- How Adhesion Molecule Patterns Change While Neutrophils Traffic through the Lung during Inflammation.Mediators of inflammation · 2019Article
- Helper T-cell responses and pulmonary fungal infections.Immunology · 2018Review
- Lung Epithelial Cells Coordinate Innate Lymphocytes and Immunity against Pulmonary Fungal Infection.Cell host & microbe · 2018Article
- Cerium oxide and barium sulfate nanoparticle inhalation affects gene expression in alveolar epithelial cells type II.Journal of nanobiotechnology · 2018Article
- Lung epithelium: barrier immunity to inhaled fungi and driver of fungal-associated allergic asthma.Current opinion in microbiology · 2017Review
- Genetic variants of innate immune receptors and infections after liver transplantation.World journal of gastroenterology · 2014Review
- Clearance of Pneumocystis murina infection is not dependent on MyD88.Microbes and infection · 2014Article
- Interleukin-1 receptor but not Toll-like receptor 2 is essential for MyD88-dependent Th17 immunity to Coccidioides infection.Infection and immunity · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Pneumocystis is an opportunistic fungal pathogen that causes pneumonia in a variety of clinical settings. An early step in Pneumocystis infection involves the attachment of organisms to alveolar epithelial cells (AECs). AECs produce chemokines in response to Pneumocystis stimulation, but the upstream host-pathogen interactions that activate AEC signaling cascades are not well-defined. MyD88 is an adaptor molecule required for activation of proinflammatory signaling cascades following Toll-like receptor (TLR)-dependent recognition of conserved molecular patterns on pathogens. To determine whether the TLR/MyD88 pathway is required for the AEC chemokine response to Pneumocystis, wild-type (WT) and MyD88-deficient AECs were incubated with Pneumocystis. As expected, WT AECs produced CCL2 and CXCL2 following Pneumocystis stimulation. In contrast, MyD88-deficient AECs were severely impaired in their ability to respond to Pneumocystis. MyD88-deficient AECs did not display Pneumocystis-induced Jun N-terminal protein kinase activation and produced much less chemokine than Pneumocystis-stimulated WT AECs. Using a panel of TLR agonists, primary murine AECs were found to respond vigorously to TLR2 and TLR4 agonists. However, the AEC chemokine response to Pneumocystis did not require TLR2 or TLR4. Surprisingly, the interleukin-1 receptor (IL-1R) was required for an AEC chemokine response to Pneumocystis. The role of MyD88 in early responses during Pneumocystis infection was supported by in vivo studies demonstrating that MyD88-deficient mice showed impaired Pneumocystis-stimulated chemokine production and impaired inflammatory cell recruitment. These data indicate an important role for MyD88 in the AEC inflammatory response to Pneumocystis.
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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.