ArticleInfection and immunity2012
Interleukin-1β regulates CXCL8 release and influences disease outcome in response to Streptococcus pneumoniae, defining intercellular cooperation between pulmonary epithelial cells and macrophages.
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 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
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- Hypoxia-inducible factor-1α exacerbates immune injury induced by influenza A virus and Streptococcus pneumoniae coinfection.BMC infectious diseases · 2025Article
- Systemic Inflammation Indices, Chemokines, and Metabolic Markers in Perimenopausal Women.Nutrients · 2025Article
- Cross-sectional analysis of wound-associated soluble factors in early, established, and chronic wounds of recessive dystrophic epidermolysis bullosa patients.Archives of dermatological research · 2025Article
- Influence of macrophages and neutrophilic granulocyte-like cells on crystalline silica-induced toxicity in human lung epithelial cells.Toxicology research · 2025Article
- Cytokine secretion by in vitro cultures of lung epithelial cells, differentiated macrophages and differentiated dendritic cells incubated with pneumococci and pneumococcal extracellular vesicles.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2024Article
- Deciphering the similarities and disparities of molecular mechanisms behind respiratory epithelium response to HCoV-229E and SARS-CoV-2 and drug repurposing, a systems biology approach.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024Article
- Vitamin D promotes epithelial tissue repair and host defense responses against influenza H1N1 virus and Staphylococcus aureus infections.Respiratory research · 2023Article
- Temporal and Spatial Patterns of Inflammation and Tissue Injury in Patients with Postoperative Respiratory Failure after Lung Resection Surgery: A Nested Case-Control Study.International journal of molecular sciences · 2023Article
- The Serum Level of CXCL9, CXCL10, and CXCL11 and the Expression of CXCR3 of Peripheral Blood Mononuclear Cells in Brucellosis Patients.Current microbiology · 2023Article
- Local and Systemic Effects ofMicroorganisms · 2023Review
- Role of the cGAS/STING pathway in the control ofFrontiers in immunology · 2023Article
- Pneumolysin suppresses the initial macrophage pro-inflammatory response to Streptococcus pneumoniae.Immunology · 2022Article
- Identification of Cell Markers and Their Expression Patterns in Skin Based on Single-Cell RNA-Sequencing Profiles.Life (Basel, Switzerland) · 2022Article
- A novel Streptococcus pneumoniae human challenge model demonstrates Treg lymphocyte recruitment to the infection site.Scientific reports · 2022Article
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- Ceramide kinase regulates TNF-α-induced immune responses in human monocytic cells.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The success of Streptococcus pneumoniae (the pneumococcus) as a pulmonary pathogen is related to its restriction of innate immune responses by respiratory epithelial cells. The mechanisms used to overcome this restriction are incompletely elucidated. Pulmonary chemokine expression involves complex cellular and molecular networks, involving the pulmonary epithelium, but the specific cellular interactions and the cytokines that control them are incompletely defined. We show that serotype 2 or 4 pneumococci induce only modest levels of CXCL8 expression from epithelial cell lines, even in the absence of a polysaccharide capsule. In contrast, coculture of A549 cells with the macrophage-like THP-1 cell line, differentiated with vitamin D, or monocyte-derived macrophages enhanced CXCL8 release. Supernatants from the THP-1 cell line prime A549 cells to release CXCL8 at levels similar to cocultures. Interleukin-1Ra (IL-1Ra) inhibits CXCL8 release from cocultures and reduces the activity of macrophage-conditioned media, but inhibition of tumor necrosis factor alpha (TNF-α) had only a minimal effect on CXCL8 release. Release of IL-1β but not TNF-α was upregulated in cocultures. IL-1 type 1 receptor knockout C57BL/6 and BALB/c mice confirmed the importance of IL-1 signaling in CXC chemokine expression and neutrophil recruitment in vivo. In fulminant disease, increased IL-1 signaling resulted in increased neutrophils in the airway and more invasive disease. These results demonstrate that IL-1 is an important component of the cellular network involving macrophages and epithelial cells, which facilitates CXC chemokine expression and aids neutrophil recruitment during pneumococcal pneumonia. They also highlight a potential clinical role for anti-IL-1 treatment to limit excessive neutrophilic inflammation in the lung.
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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.