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. 2021 May 9;10(9):2021.
doi: 10.3390/jcm10092021.

The Short-Term Kinetics of sICAM-1 after Induction of Acute Experimental Pain in Healthy Volunteers

Philipp Lüke  1   2 , Eduard Kraft  3 , Shahnaz Christina Azad  1   2
Affiliations

The Short-Term Kinetics of sICAM-1 after Induction of Acute Experimental Pain in Healthy Volunteers

Philipp Lüke et al. J Clin Med. .

Abstract

Intercellular adhesion molecule-1 (ICAM-1) mediates extravasation of leukocytes, releasing proinflammatory cytokines or endogenous opioids in the inflamed tissue. Thus, ICAM-1 is a crucial component of peripheral antinociception. Previously, we demonstrated a significant correlation between the soluble form of ICAM (sICAM-1) in serum and pain intensity reported by chronic pain patients. The present study examines the role and kinetics of sICAM-1 in experimentally induced acute pain. Three groups of 10 subjects were exposed to 10 min of high (capsaicin-enhanced) or low-intensity heat pain or cold pain, respectively. Thermal stimuli were induced using a device for quantitative sensory testing. Topical capsaicin significantly increased heat pain intensity without the risk of thermal tissue damage. Pain intensity was recorded every minute during testing. sICAM-1 concentrations in serum were determined by ELISA before, immediately after, and 60 min after test termination. Among all experimental groups, sICAM-1 significantly decreased immediately after pain induction. After 60 min, sICAM-1 concentrations returned towards initial values. Interestingly, a linear correlation was found between the extent of sICAM-1 changes and the initial concentrations. Whereas high initial values led to a distinct decrease of sICAM-1, low concentrations tended to increase. There was no statistically significant correlation between levels or alterations of serum sICAM-1 and pain intensity reported by the test subjects. In contrast to our previous findings in chronic pain patients, the present results show that sICAM-1 values do not correlate with the intensity of acute experimental pain. However, we were able to detect short-term changes of sICAM-1 after induction of nociceptive thermal stimuli, suggesting that this marker is part of a demand-oriented homeostatically controlled system.

Keywords: QST; acute pain model; biomarker; cold pain; heat pain; sICAM-1.

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Conflict of interest statement

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Average pain intensity induced by three different pain models developed by our research group. Thermal nociceptive stimuli were applied by a device for quantitative sensory testing [25]. The red line represents the average perceived pain intensity, the gray lines show the standard deviation.
Figure 2
Figure 2
Soluble ICAM-1 serum concentrations as a function of test duration among all test participants are shown as a box plot diagram. Outliers are not shown. The difference in mean sICAM-1 concentration before and immediately after induction of pain was statistically significant (p = 0.003).
Figure 3
Figure 3
Soluble ICAM-1 serum concentrations as a function of test duration in the low-intensity heat pain group are shown as a box plot diagram. Outliers are not shown. The difference in sICAM-1 concentration before and immediately after heat induction was statistically significant (p = 0.037).
Figure 4
Figure 4
Soluble ICAM-1 serum concentrations as a function of test duration in the high-intensity heat pain group are shown as a box plot diagram.
Figure 5
Figure 5
Soluble ICAM-1 serum concentrations as a function of test duration in cold pain group are shown as a box plot diagram. Outliers are not shown.
Figure 6
Figure 6
Illustration of the gradient of the decline in the sICAM-1 concentration after passing through the experimental setup in relation to the initial sICAM-1 concentration. The values of all test participants are shown.
See this image and copyright information in PMC

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