ArticleInfection and immunity2005
Differential involvement of toll-like receptors 2 and 4 in the host response to acute respiratory infections with wild-type and mutant Haemophilus influenzae strains.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
15 citing papers in PubMed, 35 citations in OpenAlex.
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- Antimicrobial and Anti-Inflammatory Activity of Apple Polyphenol Phloretin on Respiratory Pathogens Associated With Chronic Obstructive Pulmonary Disease.Frontiers in cellular and infection microbiology · 2021Article
- Neuronal Damage and Neuroinflammation, a Bridge Between Bacterial Meningitis and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- Immunomodulatory role for membrane vesicles released by THP-1 macrophages and respiratory pathogens during macrophage infection.BMC microbiology · 2017Article
- Toll-like receptor 6 plays an important role in host innate resistance to Brucella abortus infection in mice.Infection and immunity · 2013Article
- The Role of TLR2 in Infection and Immunity.Frontiers in immunology · 2012Article
- Genome-scale approaches to identify genes essential for Haemophilus influenzae pathogenesis.Frontiers in cellular and infection microbiology · 2012Review
- TLR4-mediated induction of TLR2 signaling is critical in the pathogenesis and resolution of otitis media.Innate immunity · 2009Article
- Early bacterial colonization induces toll-like receptor-dependent transforming growth factor beta signaling in the epithelium.Infection and immunity · 2009Article
- Klebsiella pneumoniae increases the levels of Toll-like receptors 2 and 4 in human airway epithelial cells.Infection and immunity · 2009Article
- Differential expression of cytokine genes and iNOS induced by nonviable nontypeable Haemophilus influenzae or its LOS mutants during acute otitis media in the rat.International journal of pediatric otorhinolaryngology · 2008Article
- Toll-like receptor 2-dependent NF-kappaB activation is involved in nontypeable Haemophilus influenzae-induced monocyte chemotactic protein 1 up-regulation in the spiral ligament fibrocytes of the inner ear.Infection and immunity · 2007Article
- Signal transduction pathways of tumor necrosis factor--mediated lung injury induced by ozone in mice.American journal of respiratory and critical care medicine · 2007Article
- Toll-like receptor 2 mediates alveolar macrophage response to Pneumocystis murina.Infection and immunity · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We used a mouse model of acute respiratory infections to investigate the role of Toll-like receptor 2 (TLR2) and TLR4 in the host response to Haemophilus influenzae. Acute aerosol exposures to wild-type strains of H. influenzae showed that TLR4 function was essential for TNF-alpha induction, neutrophil influx, and bacterial clearance. To determine how lipooligosaccharide (LOS) modifications would affect the role of TLR4 in inducing the host response, we used acute infections with an H. influenzae strain expressing a mutation in the htrB gene. This mutant strain expresses an LOS subunit with decreased acylation. In response to H. influenzae htrB infection, tumor necrosis factor alpha (TNF-alpha) secretion remained TLR4 dependent. But the decrease in LOS acylation made the neutrophil influx and the bacterial clearance also dependent on TLR2, as shown by the decreased host response elicited in TLR2 knockout mice compared to C57BL/6 mice. A subsequent analysis of TLR2 and TLR4 gene expression by quantitative PCR indicated that TLR4 function induces TLR2 expression and vice versa. These results indicate that some changes in the LOS subunit of H. influenzae can favor signaling through non-TLR4 receptors, such as TLR2. The results also indicate a close interaction between TLR4 and TLR2 that tightly regulates the expression of both receptors.
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