ArticleInfection and immunity2001
Macrophage inflammatory protein 1alpha/CCL3 is required for clearance of an acute Klebsiella pneumoniae pulmonary infection.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 77 citations in OpenAlex.
- Article
- Malvidin-3-O-Rhamnoside Alleviates Klebsiella pneumoniae -Induced Acute Lung Injury by Regulating Macrophage-Mediated Inflammatory and Oxidative Pathways.Phytotherapy research : PTR · 2026Article
- Bioprinted Ventilated 3D Alveoliform Epithelial Sacculoids.Research square · 2025Article
- Evaluation of biomarkers and immune microenvironment of gestational diabetes mellitus evidence from omics data and machine learning.Scientific reports · 2025Article
- Follicular CD8+ T cells in Trypanosoma cruzi infection: helpers or killers depending on the target B cell population.PLoS pathogens · 2025Article
- Spatial transcriptomic analysis of HIV and tuberculosis coinfection in a humanized mouse model reveals unique transcription patterns, immune responses and early morphological alterations.bioRxiv : the preprint server for biology · 2025Article
- CCR5 promotes the migration of pathological CD8+ T cells to the leishmanial lesions.PLoS pathogens · 2024Article
- Spotlight on pro-inflammatory chemokines: regulators of cellular communication in cognitive impairment.Frontiers in immunology · 2024Review
- Integrated mRNA-miRNA transcriptome profiling of blood immune responses potentially related to pulmonary fibrosis in forest musk deer.Frontiers in immunology · 2024Article
- Autophagy, cell death, and cytokines inEmerging microbes & infections · 2023Review
- CCR5 promotes the migration of CD8bioRxiv : the preprint server for biology · 2023Article
- Role of chemokines in the crosstalk between tumor and tumor-associated macrophages.Clinical and experimental medicine · 2023Review
- A2BAR Antagonism Decreases the Glomerular Expression and Secretion of Chemoattractants for Monocytes and the Pro-Fibrotic M2 Macrophages Polarization during Diabetic Nephropathy.International journal of molecular sciences · 2023Article
- Characterization of Chemotaxis-Associated Gene Dysregulation in Myeloid Cell Populations in the Lungs during Lipopolysaccharide-Mediated Acute Lung Injury.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Exploring causal relationships between inflammatory cytokines and allergic rhinitis, chronic rhinosinusitis, and nasal polyps: a Mendelian randomization study.Frontiers in immunology · 2023Article
- Roles of CCL2 and CCL3 in intraocular inflammation during Bacillus endophthalmitis.Experimental eye research · 2022Article
- Implication of the IL-10-Expression Signature in the Pathogenicity ofMicrobiology spectrum · 2022Article
- Synergism and Antagonism of Bacterial-Viral Coinfection in the Upper Respiratory Tract.mSphere · 2022Article
- Host Immune Response to Clinical HypervirulentJournal of immunology research · 2022Article
- 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 1 institution in 1 country.
Funding
Abstract
The objective of these studies was to determine the role of macrophage inflammatory protein 1alpha/CCL3 in pulmonary host defense during Klebsiella pneumoniae infection. Following intratracheal inoculation, 7-day survival of CCL3(-/-) mice was less than 10%, compared to 60% for CCL3(+/+) mice. Survival of CCR5(-/-) mice was equivalent to that of controls, indicating that the enhanced susceptibility of CCL3(-/-) mice to K. pneumoniae is mediated via another CCL3 receptor, presumably CCR1. At day 3, CFU burden in the lungs of CCL3(-/-) mice was 800-fold higher than in CCL3(+/+) mice, demonstrating that CCL3 is critical for control of bacterial growth in the lung. Surprisingly, CCL3(-/-) mice had no differences in the recruitment of monocytes/macrophages and even showed enhanced neutrophil recruitment at days 1, 2, and 3 postinfection, compared to CCL3(+/+) mice. Therefore, the defect in clearance was not due to insufficient recruitment of leukocytes. No significant differences in cytokine levels of monocyte chemoattractant protein 1 (MCP-1), interleukin 12, gamma interferon, or tumor necrosis factor alpha in lung lavages were found between CCL3(+/+) and CCL3(-/-) mice. CCL3(-/-) alveolar macrophages were found to have significantly lower phagocytic activity toward K. pneumoniae than CCL3(+/+) alveolar macrophages. These findings demonstrate that CCL3 production is critical for activation of alveolar macrophages to control the pulmonary growth of the gram-negative bacterium K. pneumoniae.
Indexed as
Identifiers
What OpenQuestion holds
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.