ArticleLaboratory animal research2015
Tumor necrosis factor-alpha deficiency impairs host defense against Streptococcus pneumoniae.
Article in Laboratory animal research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 21 citations in OpenAlex.
- Orally Administered Porcine Intestinal Lactobacilli Improve the Respiratory Innate Immune Response AgainstAnimals : an open access journal from MDPI · 2026Article
- Occupationally Relevant Zinc- and Copper-Containing Metal Fumes Inhibit Human THP-1 Macrophage TNF and IL-6 Responses to Bacterial Stimuli.Global challenges (Hoboken, NJ) · 2025Article
- Cannabidiol and nano-selenium mediate intestinal barrier function by affecting mucosal microstructures, and gut-associated immunological and oxidative stress response in the gut of chickens infected withFrontiers in immunology · 2025Article
- Article
- Use of immunomodulatory therapy as part of comprehensive treatment of non-severe community-acquired pneumonia and its long-term results.Drugs in context · 2023Article
- Neutrophil Recruitment in Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022Review
- Contribution of Puma to Inflammatory Resolution During Early Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022Article
- Infectious Complications of Biological and Small Molecule Targeted Immunomodulatory Therapies.Clinical microbiology reviews · 2020Review
- Comparison of the virulence ofLaboratory animal research · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus pneumoniae is a major human pathogen that is involved in community-acquired pneumonia. Tumor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine that activates immune responses against infection, invasion, injury, or inflammation. To study the role of TNF-α during S. pneumoniae infection, a murine pneumococcal pneumonia model was used. We intranasally infected C57BL/6J wild-type (WT) and TNF-α knockout (KO) mice with S. pneumoniae D39 serotype 2. In TNF-α KO mice, continuous and distinct loss of body weight, and low survival rates were observed. Bacterial counts in the lungs and blood of TNF-α KO mice were significantly higher than those in WT mice. Histopathological lesions in the spleen of TNF-α KO mice were more severe than those in WT mice. In TNF-α KO mice, severe depletion of white pulp was observed and the number of apoptotic cells was significantly increased. Interferon-gamma (IFN-γ), IL-12p70 and IL-10 levels in serum were significantly increased in TNF-α KO mice. TNF-α is clearly involved in the regulation of S. pneumoniae infections. Early death and low survival rates of TNF-α KO mice were likely caused by a combination of impaired bacterial clearance and damage to the spleen. Our findings suggest that TNF-α plays a critical role in protecting the host from systemic S. pneumoniae infection.
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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.