ArticleInfection and immunity2009
Klebsiella pneumoniae increases the levels of Toll-like receptors 2 and 4 in human airway epithelial cells.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 86 citations in OpenAlex.
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- Transcriptomic Analysis Reveals Key Regulatory Genes and Pathways Involved in Macrophage Inflammation Induced by Hypervirulent Klebsiella pneumoniae Infection.Current microbiology · 2025Article
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- Selenium elicited an enhanced anti-inflammatory effect in primary bovine endometrial stromal cells with high cortisol background.BMC veterinary research · 2024Article
- Immunometabolic control byImmunometabolism (Cobham, Surrey) · 2023Review
- A subunit vaccine against pneumonia: targeting SNetwork modeling and analysis in health informatics and bioinformatics · 2023Article
- In vivo single-cell transcriptomics reveal Klebsiella pneumoniae skews lung macrophages to promote infection.EMBO molecular medicine · 2022Article
- Combing Immunoinformatics with Pangenome Analysis To Design a Multiepitope Subunit Vaccine against Klebsiella pneumoniae K1, K2, K47, and K64.Microbiology spectrum · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway epithelial cells act as the first barrier against pathogens. These cells recognize conserved structural motifs expressed by microbial pathogens via Toll-like receptors (TLRs) expressed on the surface. In contrast to the level of expression in lymphoid cells, the level of expression of TLR2 and TLR4 in airway epithelial cells is low under physiological conditions. Here we explored whether Klebsiella pneumoniae upregulates the expression of TLRs in human airway epithelial cells. We found that the expression of TLR2 and TLR4 by A549 cells and human primary airway cells was upregulated upon infection with K. pneumoniae. The increased expression of TLRs resulted in enhancement of the cellular response upon stimulation with Pam3CSK4 and lipopolysaccharide, which are TLR2 and TLR4 agonists, respectively. Klebsiella-dependent upregulation of TLR expression occurred via a positive IkappaBalpha-dependent NF-kappaBeta pathway and via negative p38 and p44/42 mitogen-activated protein kinase-dependent pathways. We showed that Klebsiella-induced TLR2 and TLR4 upregulation was dependent on TLR activation. An isogenic capsule polysaccharide (CPS) mutant did not increase TLR2 and TLR4 expression. Purified CPS upregulated TLR2 and TLR4 expression, and polymyxin B did not abrogate CPS-induced TLR upregulation. Although no proteins were detected in the CPS preparation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and colloidal gold staining, we could not rule out the possibility that traces of protein in our CPS preparation could have been responsible, at least in part, for the TLR upregulation.
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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.