ArticleInfection and immunity2003
Up-regulation of interleukin-8 by novel small cytoplasmic molecules of nontypeable Haemophilus influenzae via p38 and extracellular signal-regulated kinase pathways.
Article in Infection and immunity, 2003. 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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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Apical periodontitis microbiome association with salivary and serum inflammatory burden.International endodontic journal · 2025Article
- A Comparative Inflammation-on-a-Chip with a Complete 3D Interface: Pharmacological Applications in COPD-Induced Neutrophil Migration.Advanced healthcare materials · 2023Article
- Effective-Component Compatibility of Bufei Yishen Formula III Combined with Electroacupuncture Suppresses Inflammatory Response in Rats with Chronic Obstructive Pulmonary Disease via Regulating SIRT1/NF-BioMed research international · 2022Article
- Progress in the mechanism and targeted drug therapy for COPD.Signal transduction and targeted therapy · 2020Review
- Animal models of emphysema.Chinese medical journal · 2019Review
- CD30 Is Highly Expressed in Chronic Obstructive Pulmonary Disease and Induces the Pulmonary Vascular Remodeling.BioMed research international · 2018Article
- Peroxiredoxin 1 interacts with and blocks the redox factor APE1 from activating interleukin-8 expression.Scientific reports · 2016Article
- Haemophilus haemolyticus Interaction with Host Cells Is Different to Nontypeable Haemophilus influenzae and Prevents NTHi Association with Epithelial Cells.Frontiers in cellular and infection microbiology · 2016Article
- Haemophilus influenzae induces steroid-resistant inflammatory responses in COPD.BMC pulmonary medicine · 2015Article
- Article
- CYLD negatively regulates nontypeable Haemophilus influenzae-induced IL-8 expression via phosphatase MKP-1-dependent inhibition of ERK.PloS one · 2014Article
- CCN1 secretion induced by cigarette smoking extracts augments IL-8 release from bronchial epithelial cells.PloS one · 2013Article
- ERK2-dependent activation of c-Jun is required for nontypeable Haemophilus influenzae-induced CXCL2 upregulation in inner ear fibrocytes.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Antiinflammatory role of MUC1 mucin during infection with nontypeable Haemophilus influenzae.American journal of respiratory cell and molecular biology · 2012Article
- Sap transporter mediated import and subsequent degradation of antimicrobial peptides in Haemophilus.PLoS pathogens · 2011Article
- Activation of epidermal growth factor receptor is required for NTHi-induced NF-κB-dependent inflammation.PloS one · 2011Article
- Regulation of bacteria-induced intercellular adhesion molecule-1 by CCAAT/enhancer binding proteins.American journal of respiratory cell and molecular biology · 2009Article
- Synergistic effect of interleukin 1 alpha on nontypeable Haemophilus influenzae-induced up-regulation of human beta-defensin 2 in middle ear epithelial cells.BMC infectious diseases · 2006Article
- New aspects of p38 mitogen activated protein kinase (MAPK) biology in lung inflammation.Drug discovery today. Disease mechanisms · 2006Review
- The role of innate immune responses in the outcome of interspecies competition for colonization of mucosal surfaces.PLoS pathogens · 2005Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Nontypeable Haemophilus influenzae (NTHI) is an important etiological agent of otitis media (OM) and of exacerbated chronic obstructive pulmonary diseases (COPD). Inflammation is a hallmark of both diseases. Interleukin-8 (IL-8), one of the important inflammatory mediators, is induced by NTHI and may play a significant role in the pathogenesis of these diseases. Our studies demonstrated that a soluble cytoplasmic fraction (SCF) from NTHI induced much greater IL-8 expression by human epithelial cells than did NTHI lipooligosaccharides and envelope proteins. The IL-8-inducing activity was associated with molecules of < or =3 kDa from SCF and was peptidase and lipase sensitive, suggesting that small lipopeptides are responsible for the strong IL-8 induction. Moreover, multiple intracellular signaling pathways were activated in response to cytoplasmic molecules. The results indicated that the p38 mitogen-activated protein kinase (MAPK) and Src-dependent Raf-1-Mek1/2-extracellular signal-regulated kinase mitogen-activated protein kinase (ERK MAPK) pathways are required for NTHI-induced IL-8 production. In contrast, the phosphatidylinositol 3-kinase (PI3K)-Akt pathway did not affect IL-8 expression, although this pathway was concomitantly activated upon exposure to NTHI SCF. The PI3K-Akt pathway was also directly activated by IL-8 and significantly inhibited by an antagonist of IL-8 receptors during NTHI stimulation. These results indicated that the PI3K-Akt pathway is activated in response to IL-8 that is induced by NTHI and may lead to other important epithelial cell responses. This work provides insight into essential molecular and cellular events that may impact on the pathogenesis of OM and COPD and identifies rational targets for anti-inflammatory intervention.
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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.