Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

Abstract

It is suggested that different neuropeptides regulate gastric mucosal integrity and participate in the development of chronic gastritis. The aim of this study was to examine the roles and changes of immunoreactive (IR) nerves and immunocompetent cells in human gastritis. Immunohistochemical, immunocytochemical, and confocal laser microscopic methods were used. All investigated nerve fibers were found in different quantities in the mucosa of both control and gastritis samples. The number of SP, NPY, and VIP IR nerve fibers increased significantly (P < 0.05) in gastritis. No IR immunocompetent cells (lymphocytes, plasma cells, mast cells) were found in the control, however, some showed NPY (16.8%) and SP (9.4%) immunoreactivity in chronic gastritis. The distance between nerve fibers and immunocompetent cells was 200 nm to 1 microm. In conclusion, the increased number of SP, NPY, and VIP IR nerves and IR immunocytes suggests that they participate in development of neurogenic inflammation, repairing processes of chronic gastritis.

Participation of Capsaicin-Sensitive Afferent Nerves in the Gastric Mucosa of Patients with Helicobacter pylori-Positive or-Negative Chronic Gastritis

“…These mediators can increase mucosal blood flow by vasodilatation [23], can activate mast cells and immunocells in the mucosa [24], and are involved in drug effects [25,26], and somatostatin can elicit systemic anti-inflammatory and analgetic "sensory functions." The immunodistribution of neuropeptides (SP, VIP, NPY, SOM, GAL, and TH) released from the sensory neurons and their neuroimmune function are known in H. pylori-positive gastritis but have not been examined in gastritis without this infection [27]. We suggest that the participation of capsaicin-sensitive afferent nerves depends on a causative factor to produce gastritis in patients, and of course Helicobacter pylori infection was especially considered as a causative factor to produce gastritis in patients.…”

Capsaicin as New Orally Applicable Gastroprotective and Therapeutic Drug Alone or in Combination with Nonsteroidal Anti-Inflammatory Drugs in Healthy Human Subjects and in Patients

“…The peripheral action of capsaicin is a dose-dependent action (Szolcsányi 1984;Mózsik et al 2001) (Table 9.5). Capsaicin releases CGRP and SP (Inui et al 1991;Dömötör et al 2005), which modifies the vascular reactions in the gastrointestinal mucosa (Sipos et al 2006) recently demonstrated that the existence of neuroimmune link between the CGRP, SP, and immune cells in the gastric mucosa of patients with chronic gastritis. Dömötör et al (2006b) demonstrated the increased release of glucagon during a sugar loading test in healthy human subjects, indicated a new step of capsaicin-induced changes taking place between the capsaicin-sensitive afferent nerves and neurohormonal regulation.…”

Neuropeptid Y és P anyag immunreaktív idegrostok és immunkompetens sejtek változása hepatitisben

“…A klinikai vizsgálatok már igazolták, hogy SP-antagonistákkal csökkenteni lehet a gyulladást a gyomor-bél csatornában [27,28]. Számos immunsejt expresszál NPY-t indukció hatására [29,30]. Morfológiai vizsgálatok bizonyították, hogy gyulladás során az NPY-idegrostok száma szignifi kánsan megemelkedett, és nagyon közeli kapcsolatban találha-tók a szintén NPY-pozitív immunsejtekkel.…”