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Updated: Aug 8, 2026
Isolation and Flow Cytometric Characterization of Murine Small Intestinal Lymphocytes
Published on: May 8, 2016
Effects of somatostatin on human intestinal lamina propria lymphocytes. Modulation of lymphocyte activation
S Fais1, B Annibale, M Boirivant
1Cattedra di Gastroenterologia, Università La Sapienza, Rome, Italy.
Insights
Somatostatin (SOM) significantly inhibits immune cell activation in the human gut. Intestinal immune cells show higher affinity SOM receptors, suggesting a key role for SOM in regulating mucosal immunity.
Area of Science:
- Immunology
- Neuroendocrinology
- Gastroenterology
Background:
- Somatostatin (SOM) is a neuropeptide with known immunomodulatory functions.
- The intestinal mucosa harbors a complex immune system influenced by neural signals.
Purpose of the Study:
- To investigate the effect of SOM on mitogen-induced activation of human intestinal lamina propria mononuclear cells (LPMNC) and peripheral blood lymphocytes (PBMNC).
- To characterize SOM receptors on these immune cells.
Main Methods:
- Cell isolation from human intestinal mucosa and peripheral blood.
- Mitogen stimulation assays to assess immune cell activation.
- Flow cytometry to quantify interleukin-2 receptor (IL-2R)-positive cells.
- SOM receptor binding studies.
Main Results:
- SOM significantly reduced IL-2R expression on LPMNC and PBMNC in a dose-dependent manner.
- LPMNC exhibited SOM receptors with 1000-fold higher affinity than PBMNC.
- SOM inhibited immunoglobulin production in both cell types, with a more pronounced effect on IgA in PBMNC.
Conclusions:
- Human intestinal immune cells possess high-affinity somatostatin receptors.
- SOM plays a crucial role in modulating the immune response within the human intestinal mucosa.
- Neural-immune interactions involving SOM are important for mucosal immune regulation.
Abstract:
We have investigated the effect of somatostatin (SOM) on the mitogen-induced activation of lamina propria mononuclear cells isolated from the human intestinal mucosa (LPMNC) and of the autologous peripheral blood lymphocytes (PBMNC). The occurrence of specific SOM receptors and their biological characteristics were also investigated. The counts of interleukin-2 receptor (IL-2R)-positive cells after mitogen stimulation were significantly lower in the presence of SOM. This effect of SOM appeared to be dose dependent, with SOM concentrations ranging between 1 pM and 1 microM. The amount of SOM required for the 50% inhibition of this expression was 1000 times lower in the LPMNC population than in the PBMNC. Binding studies showed that human LPMNC bear specific receptors for SOM and demonstrated that the affinity of these receptors was 1000 times higher than that of the SOM receptors present on the PBMNC (Kd 2.1 +/- 0.34 nM vs. 910 +/- 46 nM, respectively). The inhibitory effect of SOM on the proliferative response appeared to be restricted to PBMNC, with a maximal inhibition at 1 nM SOM, while LPMNC proliferative response was poorly affected. SOM inhibited the in vitro immunoglobulin production of both PBMNC and LPMNC over a wide range of concentrations, with a maximal inhibition at 1 nM. At this concentration the effect of SOM on IgA was more pronounced in the PBMNC than in the LPMNC. Our results lend support to the concept that in humans SOM plays a role in the modulation of the immune response at the level of the intestinal mucosa where cell-to-cell interactions between SOM releasing nerve fibers and cells and the immune system occur.
