ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
CD4+ lymphocytes control gut epithelial apoptosis and mediate survival in sepsis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
- The role of gut microbiota in the onset and development of sepsis and its therapeutic potential: mechanisms and research progress.Frontiers in microbiology · 2025Review
- Overexpression of BCL-2 in the Intestinal Epithelium Prevents Sepsis-Induced Gut Barrier Dysfunction via Altering Tight Junction Protein Expression.Shock (Augusta, Ga.) · 2020Article
- Mechanisms of Organ Dysfunction in Sepsis.Critical care clinics · 2018Review
- Lymphocyte integrin expression differences between SIRS and sepsis patients.Irish journal of medical science · 2017Article
- The Gut as the Motor of Multiple Organ Dysfunction in Critical Illness.Critical care clinics · 2016Review
- Adenosine promotes Foxp3 expression in Treg cells in sepsis model by activating JNK/AP-1 pathway.American journal of translational research · 2016Article
- Receptor-interacting protein kinase 3 deficiency inhibits immune cell infiltration and attenuates organ injury in sepsis.Critical care (London, England) · 2014Article
- Redefining the gut as the motor of critical illness.Trends in molecular medicine · 2014Review
- Article
- Intestine-specific deletion of microsomal triglyceride transfer protein increases mortality in aged mice.PloS one · 2014Article
- Inhibition of IKKβ in enterocytes exacerbates sepsis-induced intestinal injury and worsens mortality.Critical care medicine · 2013Article
- Inhibition of intestinal epithelial apoptosis improves survival in a murine model of radiation combined injury.PloS one · 2013Article
- Article
- The endogenous bacteria alter gut epithelial apoptosis and decrease mortality following Pseudomonas aeruginosa pneumonia.Shock (Augusta, Ga.) · 2012Article
- Mechanisms of methicillin-resistant Staphylococcus aureus pneumonia-induced intestinal epithelial apoptosis.Shock (Augusta, Ga.) · 2012Article
- Article
- Cecal ligation and puncture followed by methicillin-resistant Staphylococcus aureus pneumonia increases mortality in mice and blunts production of local and systemic cytokines.Shock (Augusta, Ga.) · 2012Article
- The outcome of polymicrobial sepsis is independent of T and B cells.Shock (Augusta, Ga.) · 2011Article
- Prevention of lymphocyte apoptosis in septic mice with cancer increases mortality.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Lymphocytes help determine whether gut epithelial cells proliferate or differentiate but are not known to affect whether they live or die. Here, we report that lymphocytes play a controlling role in mediating gut epithelial apoptosis in sepsis but not under basal conditions. Gut epithelial apoptosis is similar in unmanipulated Rag-1(-/-) and wild-type (WT) mice. However, Rag-1(-/-) animals have a 5-fold augmentation in gut epithelial apoptosis following cecal ligation and puncture (CLP) compared to septic WT mice. Reconstitution of lymphocytes in Rag-1(-/-) mice via adoptive transfer decreases intestinal apoptosis to levels seen in WT animals. Subset analysis indicates that CD4(+) but not CD8(+), gammadelta, or B cells are responsible for the antiapoptotic effect of lymphocytes on the gut epithelium. Gut-specific overexpression of Bcl-2 in transgenic mice decreases mortality following CLP. This survival benefit is lymphocyte dependent since gut-specific overexpression of Bcl-2 fails to alter survival when the transgene is overexpressed in Rag-1(-/-) mice. Further, adoptively transferring lymphocytes to Rag-1(-/-) mice that simultaneously overexpress gut-specific Bcl-2 results in improved mortality following sepsis. Thus, sepsis unmasks CD4(+) lymphocyte control of gut apoptosis that is not present under homeostatic conditions, which acts as a key determinant of both cellular survival and host mortality.
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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.