The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Shock and Tissue Injury Induced by Recombinant Human Cachectin
Abstract
Cachectin (tumor necrosis factor), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. Recombinant human cachectin was infused into rats in an effort to determine whether cachectin, by itself, can elicit the derangements of host physiology caused by administration of endotoxin. When administered in quantities similar to those produced endogenously in response to endotoxin, cachectin causes hypotension, metabolic acidosis, hemoconcentration, and death within minutes to hours, as a result of respiratory arrest. Hyperglycemia and hyperkalemia were also observed after infusion. At necropsy, diffuse pulmonary inflammation and hemorrhage were apparent on gross and histopathologic examination, along with ischemic and hemorrhagic lesions of the gastrointestinal tract, and acute renal tubular necrosis. Thus, it appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.
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In the citing paper
“Consider as one example the case of TNF, a cytokine implicated as a necessary and sufficient mediator of lethal septic shock caused by infection with Gram-negative bacteria.”
From Physiology and immunology of the cholinergic antiinflammatory pathway (2007) · cites this paper as [4]
In the citing paper
“Administration of TNF to healthy mammals (including humans) reproduces the hemodynamic, metabolic, immunological, and pathological manifestations of the disease (4)”
From Physiology and immunology of the cholinergic antiinflammatory pathway (2007) · cites this paper as [4]
In the citing paper
“Other pathophysiological activities ascribed to TNF were the capacity to cause fever and localized inflammation (4, 6).”
From Physiology and immunology of the cholinergic antiinflammatory pathway (2007) · cites this paper as [4]
Citations
Cites
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Self-citationCachectin and tumour necrosis factor as two sides of the same biological coin
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Self-citationTumor necrosis factor (cachectin) is an endogenous pyrogen and induces production of interleukin 1.
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Sepsis and Acute Kidney Injury
Bilgili, B., Haliloglu, M., & Cinel, I. (2014) · Turkish Journal of Anesthesia and Reanimation · doi:10.5152/tjar.2014.83436 · Cited by 42
Wang, Z., Feng, J., Yu, J., & Chen, G. (2019) · Journal of Cell Science · doi:10.1242/jcs.227777 · Cited by 35
Modares, N. F., Hendrikse, L. D., Smith, L. K., Paul, M. S., Haight, J., Luo, P., Liu, S., Fortin, J., Tong, F. K., Wakeham, A. C., et al. (2025) · Immunity · doi:10.1016/j.immuni.2025.04.002 · Cited by 29
Therapy with antibody to tumor necrosis factor in sepsis
Pennington, J. E. (1993) · Clinical Infectious Diseases · doi:10.1093/clinids/17.supplement_2.s515 · Cited by 26
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Metadata
- Authors
- Tracey, K. J., Beutler, B., Lowry, S. F., Merryweather, J., Wolpe, S., Milsark, I. W., Hariri, R. J., Fahey, T. J., Zentella, A., Albert, J. D., Shires, G. T., & Cerami, A.
- Affiliations
- Weill Cornell Medical Center (US)
- Department of Surgery, New York Hospital-Cornell Medical Center, New York, NY 10021.
- Venue
- Science
- Published
- 1986-10-24
- Volume
- 234
- Issue
- 4775
- Pages
- 470-474
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1968713831
- Cited by
- 2,549
- References
- 45
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 16 · 2023: 12 · 2022: 13 · 2021: 18 · 2020: 19 · 2019: 18 · 2018: 21 · 2017: 21 · 2016: 28 · 2015: 19 · 2014: 30 · 2013: 38 · 2012: 29
- FWCI
- 107.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Sepsis Diagnosis and Treatment
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- TNF-α, endotoxin, septic shock, tissue damage, hypotension, metabolic acidosis, hemoconcentration, respiratory arrest, hyperglycemia, hyperkalemia, pulmonary hemorrhage, acute tubular necrosis, gastrointestinal bleeding, macrophages
- MeSH terms
- Animals, Blood Glucose, Endotoxins, Female, Glycoproteins, Humans, Potassium, Recombinant Proteins, Shock, Sodium, Tumor Necrosis Factor-alpha, Rats
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