The distribution and chemical coding of enteroendocrine cells in Trypanosoma cruzi-infected individuals with chagasic megacolon.

Chagas disease is caused by the parasite, Trypanosoma cruzi that causes chronic cardiac and digestive dysfunction. Megacolon, an irreversible dilation of the left colon, is the main feature of the gastrointestinal form of Chagas disease. Patients have severe constipation, a consequence of enteric neuron degeneration associated with chronic inflammation.

Effects of a health education program on cytokines and cortisol levels in fibromyalgia patients: a randomized controlled trial.

Background: Fibromyalgia (FM) is a syndrome characterized by widespread chronic pain associated to other symptoms, such as: fatigue, anxiety, depression and sleep disorders. Health education programs (HEP) have emerged as good non-pharmacological strategies to treat it. However, it is still not clear if the benefits are only subjective, or it has also objective impacts on immune and or neuroendocrine systems.

Evaluation of the immunoreactivity of nerve growth factor and tropomyosin receptor kinase A in the esophagus of noninfected and infected individuals with Trypanosoma cruzi.

Megaesophagus is one of the major manifestations of the chronic phase of Chagas disease. Its primary symptom is generally dysphagia due to disturbance in the lower esophageal sphincter. Microscopically, the affected organ presents denervation, which has been considered as consequence of an inflammatory process that begins at the acute phase and persists in the chronic phase.

Mast cell-nerve interaction in the colon of Trypanosoma cruzi-infected individuals with chagasic megacolon.

Chagas disease is an infection caused by the parasite Trypanosoma cruzi that affects millions of people worldwide and is endemic in Latin America. Megacolon is the most frequent complication of the digestive chronic form and happens due to lesions of the enteric nervous system. The neuronal lesions seem to initiate in the acute phase and persist during the chronic phase, albeit the mechanisms involved in this process are still debated.

Analysis of enteroendocrine cell populations in the human colon.

Recent studies have shown that patterns of colocalisation of hormones in enteroendocrine cells are more complex than previously appreciated and that the patterns differ substantially between species. In this study, the human sigmoid colon is investigated by immunohistochemistry for the presence of gastrointestinal hormones and their colocalisation. The segments of colon were distant from the pathology that led to colectomy and appeared structurally normal.

Mast cells in the colon of Trypanosoma cruzi-infected patients: are they involved in the recruitment, survival and/or activation of eosinophils?

Megacolon is frequently observed in patients who develop the digestive form of Chagas disease. It is characterized by dilation of the rectum-sigmoid portion and thickening of the colon wall. Microscopically, the affected organ presents denervation, which has been considered as consequence of an inflammatory process that begins at the acute phase and persists in the chronic phase of infection.

The involvement of melatonin in the clinical status of patients with fibromyalgia syndrome.

Objectives: The aim of this study was to evaluate the levels of 6-sulphatoxymelatonin (6-SMT) in the urine of patients with fibromyalgia (FM) and correlate them with the score obtained by these patients in four clinical assessment instruments.

Methods: Fifty-eight women with primary FM and 39 healthy women matched for age and body mass index were included in the study sample. The levels of 6-SMT were evaluated in urine collected from 8 pm until 8 am the next day by the immunosorbent assay.

Neuroimmunopathology of Trypanosoma cruzi-induced megaoesophagus: Is there a role for mast cell proteases?

Tryptase and chymase are mast cell (MC)-specific proteases, which influence in the activation of inflammatory cells. In this study, we quantified tryptase- or chymase-expressing MCs in the oesophaguses of Chagas patients, and searched for a correlation between those data with area of nerve fibres that expressed either PGP9.5 (pan-marker) or vasoactive intestinal polypeptide (VIP), which is a neuromediator that has anti-inflammatory activity.

An imbalance between substance P and vasoactive intestinal polypeptide might contribute to the immunopathology of megaesophagus after Trypanosoma cruzi infection.

Megaesophagus is one of the major causes of morbidity in chronic Chagas disease, and extensive denervation, associated with an inflammatory process, is recognized as the key factor for alterations in motility and disease development. Here, we analyzed esophagus samples from necropsied, infected individuals--6 cases with megaesophagus and 6 cases without megaesophagus--for the relative areas of expression of 2 neuromediators, substance P and vasoactive intestinal peptide, which are known to activate or inhibit, respectively, local immune cells. Samples from 6 noninfected individuals were used as controls.

Characterization of enteroglial cells and denervation process in chagasic patients with and without megaesophagus.

Chagas disease is caused by infestation with the parasite Trypanosoma cruzi, and some patients who are serologically positive develop chronic megaesophagus, whereas others are symptom-free. Gastrointestinal form of Chagas disease involves an inflammatory invasion of the enteric plexuses and degeneration of enteric neurons and previous works related that enteroglial cells would be involved in enteric inflammatory responses. Because of this, the aims of this study were to determine the relation of enteroglial cells with the denervation process in chagasic patients with and without megaesophagus and seronegative individuals.

Cellular and genetic mechanisms involved in the generation of protective and pathogenic immune responses in human Chagas disease.

Perhaps one of the most intriguing aspects of human Chagas disease is the complex network of events that underlie the generation of protective versus pathogenic immune responses during the chronic phase of the disease. While most individuals do not develop patent disease, a large percentage may develop severe forms that eventually lead to death. Although many efforts have been devoted to deciphering these mechanisms, there is still much to be learned before we can fully understand the pathogenesis of Chagas disease.

Characterization of the presence and distribution of Foxp3(+) cells in chagasic patients with and without megacolon.

Patients with Chagas's disease in the chronic phase regularly present with the chagasic megacolon. This form is characterized by inflammation, neuronal destruction, and organ dilatation. Chagasic patients with megacolon always present with inflammatory process near the enteric plexuses of the colon, as previously demonstrated.

Glial fibrillary acidic protein and S-100 colocalization in the enteroglial cells in dilated and nondilated portions of colon from chagasic patients.

After acute immunoreactive infestation with the Chagas' disease parasite, Trypanosoma cruzi, some patients develop chronic megacolon, whereas others remain asymptomatic. Chronic chagasic patients with gastrointestinal involvement exhibit inflammation and degeneration of enteric neurons. Our hypothesis is that enteric glial cells may be involved in the modulation of enteric inflammatory responses or even control the colon's dilatation.

Substance P and NK1 receptor expression in the enteric nervous system is related to the development of chagasic megacolon.

Chagasic megacolon is one of the most important forms of Chagas disease. This form is characterized by inflammation, neuronal destruction and organ dilatation. The aim of this study is to characterize the expression of substance P and its main receptor, NK1 receptor, in dilated and non-dilated samples of colon from chagasic patients with megacolon.

Megacolon in Chagas disease: a study of inflammatory cells, enteric nerves, and glial cells.

After acute infestation with the Chagas disease parasite, Trypanosoma cruzi, some patients who are serologically positive develop chronic megacolon and megaesophagus, whereas others are symptom-free. Chagas disease with gastrointestinal involvement involves an inflammatory invasion of the enteric plexuses and degeneration of enteric neurons. It is known that glial cells can be involved in enteric inflammatory responses.

Vitamin E deficiency enhances pathology in acute Trypanosoma cruzi-infected rats.

Micronutrient malnutrition is usually highly prevalent in areas endemic for Chagas disease. Nevertheless, the contribution of micronutrient deficiency to the immunopathology of this infection is often overlooked. In the present work, we assessed the effects of vitamin E deficiency on acute Trypanosoma cruzi (Y strain) infection of Holtzman rats.

Chronic Chagas disease: presence of parasite DNA in the oesophagus of patients without megaoesophagus.

We have previously amplified Trypanosoma cruzi DNA by polymerase chain reaction (PCR) from the oesophagus of chagasic patients with megaoesophagus, whilst immunohistochemical analysis failed to detect T. cruzi antigen in the oesophagus of chagasic patients without megaoesophagus. During 2000-01, we tested for the presence of T.