Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Cutting edge: myeloid differentiation factor 88 is essential for pulmonary host defense against Pseudomonas aeruginosa but not Staphylococcus aureus.

Journal of immunology (Baltimore, Md. : 1950) - 15 Mar 2004

Skerrett Shawn J, Liggitt H Denny, Hajjar Adeline M, Wilson Christopher B

Abstract excerpt

Myeloid differentiation factor 88 (MyD88) is an adapter molecule required for signal transduction via Toll-like receptors (TLRs) and receptors of the IL-1 family. Consequently, MyD88-deficient mice are highly susceptible to bacterial infections, including systemic infection with Staphylococcus aureus. To determine the role of MyD88 in innate immunity to bacterial pneumonia, we exposed MyD88-deficient and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antigens, Differentiation
Share to Inflammation Mediators

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Myeloid Differentiation Factor 88

Share to Necrosis

Share to Neutrophil Infiltration

Share to Pneumonia, Bacterial

Share to Pseudomonas Infections

Share to Respiratory Mucosa

Source

Identifiers

PMID: 15004134
DOI: 10.4049/jimmunol.172.6.3377

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cutting edge: myeloid differentiation factor 88 is essential for pulmonary host defense against Pseudomonas aeruginosa but not Staphylococcus aureus.PMID 15004134Read ↗

The development of early host response to Pseudomonas aeruginosa lung infection is critically dependent on myeloid differentiation factor 88 in mice.Semantic proximity Read ↗

Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection.Semantic proximity Read ↗

Myeloid Differentiation Primary Response Gene (88)– and Toll‐Like Receptor 2–Deficient Mice Are Susceptible to Infection with Aerosolized<i>Legionella pneumophila</i>Semantic proximity Read ↗

MyD88-dependent signaling influences fibrosis and alternative macrophage activation during Staphylococcus aureus biofilm infection.Semantic proximity Read ↗

Cutting edge: protective cell-mediated immunity to Listeria monocytogenes in the absence of myeloid differentiation factor 88.Semantic proximity Read ↗

The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88.Semantic proximity Read ↗

Functional analysis of a zebrafish myd88 mutant identifies key transcriptional components of the innate immune system.Semantic proximity Read ↗

Host-to-Host Group A Streptococcus Transmission Causes Infection of the Lamina Propria but Not Epithelium of the Upper Respiratory Tract in MyD88-Deficient Mice.Semantic proximity Read ↗

MyD88 as a therapeutic target for inflammatory lung diseasesSemantic proximity Read ↗

Aberrant inflammatory response to Streptococcus pyogenes in mice lacking myeloid differentiation factor 88.Semantic proximity Read ↗

Toll-like receptors are temporally involved in host defense.Semantic proximity Read ↗

Clinical features and outcome of patients with IRAK-4 and MyD88 deficiency.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.