ArticleThe Journal of clinical investigation2005
Dynamic changes in Mcl-1 expression regulate macrophage viability or commitment to apoptosis during bacterial clearance.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 88 citations in OpenAlex.
- Kinetic control of macrophage death by PTM-turnover crosstalk in infection and inflammation.Cell chemical biology · 2026Review
- Modulation of host cell pathways bymLife · 2025Review
- Dynamic changes in RNA mCellular and molecular life sciences : CMLS · 2024Article
- Macrophage Function Modulated by tPA Signaling in Mouse Experimental Kidney Disease Models.International journal of molecular sciences · 2023Review
- TREM2 inhibition triggers antitumor cell activity of myeloid cells in glioblastoma.Science advances · 2023Article
- Differential responses of COPD macrophages to respiratory bacterial pathogens.ERJ open research · 2022Article
- A disintegrin and metalloproteinase domain-15 deficiency leads to exaggerated cigarette smoke-induced chronic obstructive pulmonary disease (COPD)-like disease in mice.Mucosal immunology · 2021Article
- Aging and Lung Disease.Annual review of physiology · 2020Review
- Importance of Mcl-1 for Alveolar Macrophage Apoptosis-associated Bacterial Killing.American journal of respiratory and critical care medicine · 2019Article
- Alveolar Macrophage Apoptosis-associated Bacterial Killing Helps Prevent Murine Pneumonia.American journal of respiratory and critical care medicine · 2019Article
- Integrative Physiology of Pneumonia.Physiological reviews · 2018Review
- HIV gp120 in the Lungs of Antiretroviral Therapy-treated Individuals Impairs Alveolar Macrophage Responses to Pneumococci.American journal of respiratory and critical care medicine · 2018Article
- Genetic neutrophil deficiency ameliorates cerebral ischemia-reperfusion injury.Experimental neurology · 2017Article
- Impaired Mitochondrial Microbicidal Responses in Chronic Obstructive Pulmonary Disease Macrophages.American journal of respiratory and critical care medicine · 2017Article
- Fortilin binds IRE1α and prevents ER stress from signaling apoptotic cell death.Nature communications · 2017Article
- The cellular autophagy/apoptosis checkpoint during inflammation.Cellular and molecular life sciences : CMLS · 2017Review
- Delay in Human Neutrophil Constitutive Apoptosis after Infection withFrontiers in cellular and infection microbiology · 2017Article
- A small hairpin RNA targeting myeloid cell leukemia-1 enhances apoptosis in host macrophages infected with Mycobacterium tuberculosis.Journal of microbiology (Seoul, Korea) · 2016Article
- Fortilin potentiates the peroxidase activity of Peroxiredoxin-1 and protects against alcohol-induced liver damage in mice.Scientific reports · 2016Article
- Inability to sustain intraphagolysosomal killing of Staphylococcus aureus predisposes to bacterial persistence in macrophages.Cellular microbiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 4 countries.
Funding
Abstract
Macrophages are critical effectors of bacterial clearance and must retain viability, despite exposure to toxic bacterial products, until key antimicrobial functions are performed. Subsequently, host-mediated macrophage apoptosis aids resolution of infection. The ability of macrophages to make this transition from resistance to susceptibility to apoptosis is important for effective host innate immune responses. We investigated the role of Mcl-1, an essential regulator of macrophage lifespan, in this switch from viability to apoptosis, using the model of pneumococcal-associated macrophage apoptosis. Upon exposure to pneumococci, macrophages initially upregulate Mcl-1 protein and maintain viability for up to 14 hours. Subsequently, macrophages reduce expression of full-length Mcl-1 and upregulate a 34-kDa isoform of Mcl-1 corresponding to a novel BH3-only splice variant, Mcl-1(Exon-1). Change in expression of Mcl-1 protein is associated with mitochondrial membrane permeabilization, which is characterized by loss of mitochondrial inner transmembrane potential and translocation of cytochrome c and apoptosis-inducing factor. Following pneumococcal infection, macrophages expressing full-length human Mcl-1 as a transgene exhibit a delay in apoptosis and in bacterial killing. Mcl-1 transgenic mice clear pneumococci from the lung less efficiently than nontransgenic mice. Dynamic changes in Mcl-1 expression determine macrophage viability as well as antibacterial host defense.
Indexed as
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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.