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Updated: Jun 22, 2026
A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
Published on: February 20, 2021
Increased serum endotoxin and elevated CD14 and IL-1beta expression in a rat model of cerebrogenic multiple organ
Chuanqiang Qu1, Shougang Guo, Hongzhi Guo
1Department of Neurology, Qilu Hospital, Shandong University, Jinan, 250021, China.
Objectives:
To study the mechanisms underlying cerebrogenic multiple organ dysfunction syndrome (CMODS) through investigation of endotoxin levels and the expression of endotoxin receptor CD14 and interleukin IL-1beta mRNAs in a rat CMODS model.
Methods:
Acute cerebral hemorrhage was induced in Wistar rats by focal intracerebral injection of collagenase into the caudate nucleus. Serum endotoxin levels were quantitated using a chromogenic limulus lysate method; CD14 endotoxin receptor mRNA and IL-1beta mRNA levels in lung and intestine were determined by in situ hybridization.
Results:
Serum endotoxin levels increased after 12 h, reaching a peak after 24 h, and declined to control levels at 72 h. The increase was statistically significant (P<0.05) compared to unoperated controls and the sham-operated group respectively. CD14 mRNA in lung and intestine increased after 12 h, peaked after 24-36 h, and then declined after 48 h. IL-1beta mRNA levels were also increased in lung and intestine (P<0.05), peaking at 36 h and declining thereafter. Expression levels of both CD14 and IL-1beta mRNAs correlated significantly with serum endotoxin levels (Plt;0.01). We conclude that acute cerebral hemorrhage results in endotoxemia and widespread increases in CD14 and IL-1beta expression. We suggest that acute cerebrovascular challenge leads to a stress/shock response that compromises the intestinal mucosal barrier. In turn, this allows endotoxin translocation into the body that provokes the release of pro-inflammatory lymphokines, leading to a systemic inflammatory response syndrome (SIRS) that culminates in multiple organ dysfunction.
Insights
Acute cerebral hemorrhage triggers endotoxemia and increases CD14 and IL-1beta mRNA in organs. This suggests a compromised gut barrier leads to systemic inflammation and multiple organ dysfunction.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Cerebrogenic multiple organ dysfunction syndrome (CMODS) is a critical condition following brain injury.
- The precise mechanisms linking brain injury to systemic organ dysfunction require further elucidation.
Purpose of the Study:
- To investigate the role of endotoxin and its receptor CD14, along with interleukin-1beta (IL-1beta), in the development of CMODS.
- To establish a rat model of CMODS to study these molecular changes.
Main Methods:
- Acute cerebral hemorrhage was induced in rats via intracerebral collagenase injection.
- Serum endotoxin levels were measured using a chromogenic limulus lysate assay.
- Messenger RNA (mRNA) expression of CD14 and IL-1beta in lung and intestine was quantified using in situ hybridization.
Main Results:
- Serum endotoxin levels significantly increased post-hemorrhage, peaking at 24 hours.
- CD14 and IL-1beta mRNA expression in the lung and intestine showed a time-dependent increase, correlating with endotoxin levels.
- These molecular changes indicate a systemic inflammatory response initiated by the brain injury.
Conclusions:
- Acute cerebral hemorrhage leads to endotoxemia and elevated expression of CD14 and IL-1beta.
- A compromised intestinal barrier following cerebrovascular events may facilitate endotoxin translocation.
- This process likely triggers a systemic inflammatory response syndrome (SIRS), culminating in multiple organ dysfunction.
