| First Author | Verma-Gandhu M | Year | 2006 |
| Journal | Gastroenterology | Volume | 130 |
| Issue | 6 | Pages | 1721-8 |
| PubMed ID | 16697736 | Mgi Jnum | J:124915 |
| Mgi Id | MGI:3722949 | Doi | 10.1053/j.gastro.2006.01.045 |
| Citation | Verma-Gandhu M, et al. (2006) CD4+ T-cell modulation of visceral nociception in mice. Gastroenterology 130(6):1721-8 |
| abstractText | BACKGROUND & AIMS: Although inflammatory and immune cells are present in the gut in the absence of pathology, their presence does not result in sensitization of sensory nerves, implying the existence of a local antinociceptive influence. We hypothesized that a component of the immune system exerts an antinociceptive influence, thus enabling the gut to function in the absence of undue pain or discomfort. METHODS: Visceromotor responses to colorectal distention were measured in mice with severe combined immune deficiency (SCID) and their wild-type controls. RESULTS: SCID mice exhibited significantly lower pain thresholds. Transfer of CD4(+) T, but not B lymphocytes, normalized visceral pain in these mice. The restoration of normal visceral nociception following T-cell reconstitution in SCID mice was blocked by naloxone methiodide. Using an enzyme immunoassay and immunohistochemistry for beta-endorphin, we showed that in vitro stimulation of T lymphocytes induced the synthesis and release of beta-endorphin and that transfer of T cells into SCID mice increased the expression of beta-endorphin in the enteric nervous system. CONCLUSIONS: These findings indicate that the immune system is a critical determinant of visceral nociception and that T lymphocytes provide an important opioid-mediated antinociceptive influence in the gut. |
