RESUMO
There is clearly some form of inflammatory response to the heavy load of epithelially invasive whipworms in the colonic and rectal mucosa in the fully developed trichuris dysentery syndrome (TDS). We have shown by extensive immunohistochemical studies of caecal biopsies that there is no evidence that this is "immunologically medicated" (essentially, T-cell-controlled) inflammation with mucosal structural damage. One major difference between infected and control children shown by immunohistochemistry, however, was a 10-fold increase in lamina propria cells with surface IgE, presumably mast-cells (MacDonald et al, CCMRC, 1989). Children with TDS were studied before treatment, 3 days after the completion of worm-expulsive chemotherapy, and 3 or 6 weeks later when they had shown a height gain of >0.7 percent over a 3-week interval. On each of these 3 occasions rectal mucosa was placed in ice-cold Tyrode's buffer for in vitro histamine release studies, either spontaneous (at 37§C) or following challenge with rabbit anti-human IgE or T.trichiura excretory-secretory (ES) product. Residual tissue histamine concentration was also assayed. Spontaneous histamine release tended to be high on the first biopsy (maximum 81 percent of total in 20 mn), and was not then capable of being boosted by anti-IgE or Trichuris ES. However, following worm expulsion (max 16 percent) and on the third biopsy (max 6 percent) there was a clear trend for spontaneous histamine release to be diminishing. In some specimens at the 2nd and 3rd stages Trichuris ES antigen could then provoke a massive discharge of intracellular histamine into the supernatant. These studies of cell histamine release have advanced our understanding of the inflammatory mechanism of this disease (Type I hypersensitivity) and have shown in some children a persisting worm-sensitive state of the rectal mucosa (AU)