Professor G-Z Pan and colleagues from the Department of Gastroenterology at the Chinese Academy of Medical Sciences in Beijing, China, were interested to find out more about the pathogenesis of post-infective irritable bowel syndrome (IBS), about which little is known.
Therefore, they investigated the incidence of IBS and functional bowel disease (FBD) in a Chinese patient population who had recovered from bacillary dysentery.
They also examined the relationship between mast cells and intestinal nerves, as well as examining neuroimmunological changes in interleukins, mast cells and neuropeptides, in order to further understand its pathogenesis.
The researchers studied a cohort of 295 patient who had recovered from bacillary dysentery, 71.4% of whom had shigella identified from stool samples, as well as 243 control subjects. These consisted of patient siblings or spouses who had not been infected with bacillary dysentery.
Using questionnaires, all subjects were followed-up for 1 to 2 years in order to identify the incidence of FBD and IBS, as defined by the Rome II criteria.
|Bacillary dysentery is a causative factor in post-infective IBS|
In 56 cases of IBS, both post-infective and non post-infective, the numbers of mast cells in biopsy specimens from the intestinal mucosa were counted under light microscopy, following staining with anti-tryptase antibody.
In addition, the relationship of mast cells to neurone specific enolase (NSE), substance P (SP), 5-hydroxytryptamine (5-HT), or calcitonin gene related peptide positive nerve fibers was observed using double staining with alcian blue and neuropeptide antibodies.
In 30 cases of IBS (half of which were post-infective), taken randomly from the 56 cases of IBS in total, expression of interleukin (IL)-1, IL-1ß, and IL-1 receptor antagonist (IL-1ra) mRNAs in intestinal mucosa were identified using reverse transcription-polymerase chain reaction.
All the results were compared with 12 non-IBS controls.
The results showed that in the group of bacillary dysentery-infected patients, the incidences of FBD and IBS were 22.4% and 8.1%. In those who had provided stool samples positive for shigella, the incidence of IBS rose to 10.2%.
In the control group the levels of FBD and IBS were considerably lower, at 7.4% and 0.8% respectively.
The researchers found that a longer duration of diarrhea (7 days) was associated with a higher risk of developing FBD, while expression of IL-1ß mRNA in the terminal ileum and rectosigmoid mucosa was significantly higher in post-infective IBS patients.
The number of mast cells in the terminal ileum mucosa in post-infective IBS (11.19) and non-post-infective IBS patients (10.78) was significantly increased compared with that in control subjects (6.05).
Also, in the terminal ileum and rectosigmoid mucosa of IBS patients, the density of NSE, SP, and 5-HT positively stained nerve fibers increased and appeared in clusters, surrounding an increased number of mast cells compared with controls.
Commenting on their findings, Professor Pan said they showed that bacillary dysentery is a causative factor in post-infective IBS. He added that both the immune system and the nervous system may play important roles in the pathogenesis of post-infective IBS.