Bridges between nervous and immune systems: their disconnection and clinical consequences.

Nervous and immune systems are connected by several mutual links, thus constituting a diffuse functional network in the body. In particular, neurohormones, neuropeptides, and cytokines represent the major mediators of the so-called psychoneuroendocrinoimmune axis. In this review, special emphasis is placed on certain pathologies characterized by a disconnection of the existing bridges between nervous and immune systems. For instance, spinal cord injury (SCI) is a clinical condition in which loss of neurons and very poor axon growth represent the main features. The role played by infiltrating and resident immunocompetent cells is still debated in SCI. However, to enhance axon growth in SCI, current therapeutic attempts are based on the stimulation of the immune response within the central nervous system, thus triggering either cell-mediated or humoral immune responsiveness.

New insights into the biological and clinical significance of fecal calprotectin in inflammatory bowel disease.

Nowadays, calprotectin, a cytoplasmatic protein, released by activated neutrophilic polymorphonuclear cells (PMN) and/or monocytes-macrophages (MØ), is considered a good indicator of inflammation in several diseases. Accordingly, fecal calprotectin represents a good predictor of clinical relapse in ulcerative colitis (UC) patients, whereas conflicting results have been reported in Crohn's disease (CD) patients. In our study, in 76 IBD patients (29 CD and 47 UC) fecal calprotectin has been evaluated by a commercial ELISA kit. Results demonstrate that levels of this protein in the stool are significantly more elevated in active CD and UC patients than in normal volunteers. In quiescent CD and UC a trend to higher levels of calprotectin than in the normal counterpart is, however, evident. These data suggest that a low-grade inflammation of the intestinal wall is always present in CD and UC patients, which may predict a clinical relapse risk. In the same group of patients calprotectin levels also were analyzed according to sex and age. A trend to higher values of calprotectin was present in male patients with active or quiescent CD than in their female counterparts. Only in UC patients in remission a trend to calprotectin increase was more marked in the male group than in the female counterpart. When CD and UC patients were divided up according to age, calprotectin positivity peaked between 30-39 years in active CD patients, while in quiescent CD maximum positivity was between 40 and 49 years. However, in both active and quiescent UC patients, calprotectin positivity increased with age. The more precocious detectability of fecal calprotectin in CD patients, as a marker of intestinal mucosa inflammation, may be related to the different histopathology of the two diseases (CD versus UC). However, reduced PMN and/or MØ trafficking from peripheral blood to intestinal mucosa with age by effects of chronic treatment should not be ignored in CD patients.