Intestinal Mast Cell Numbers Research Articles

Characterization of Nippostrongylus brasiliensis Infection in Different Strains of Mice

Five mouse strains, CBA/J, BALB/c, C3H/HeJ, A/J, and C57Bl/6J-bg-bg, all showed similar expulsion kinetics for Nippostrongylus brasiliensis (infective dose = 500 L3). Typically, parasite recovery was maximal on day 2 in the lungs and by day 4 in the small intestine. Few worms (less than 5% infective dose) were recovered on day 14 in all strains. These same mouse strains exhibited immune depression on day 5 of infection with mesenteric lymph node cells (MLN) showing reduced (10-30% normal) IgM, IgG, and IgA responses against heterologous antigen. The intestinal mast cell numbers and tissue histamine levels were examined in CBA/J mice. Mast cell numbers increased (normal = less than 1/villous crypt unit; VCU) from day 5 and peaked on day 12 (greater than 15/VCU). Intestinal histamine levels did not completely correlate with mast cell numbers with maximum concentrations (240 +/- 73 ng/g, 2-fold over normal) reached by day 8. Histamine concentrations in the intestine returned to normal levels by day 20.

Kinetics of expulsion of the nematode, Nippostrongylus brasiliensis, in mast-cell deficient W/WV mice.

Mucosal mast-cell hyperplasia is frequently observed in intestinal nematode infections and it has been suggested that mast-cell responses to parasite antigens are involved in worm expulsion (self cure). To evaluate the importance of this mechanism, the course of infection and expulsion of Nippostrongylus brasiliensis was compared in mast-cell deficient W/WV and normal (+/+) mice. Initial infectivity rates were similar, but the subsequent kinetics of expulsion of adult worms differed principally in that the onset of expulsion in mast-cell deficient mice appeared to occur 24-36 h later than that in normal mice. Expulsion was complete by the 14th day post infection in both W/WV and normal mice. Worm fertility (as estimated by faecal egg output) also differed in W/WV and normal mice, with maximal egg output in W/WV mice occurring 24 h later than that in normal mice. Although a few mast cells were present in the intestinal mucosa and tongue of W/WV mice, their numbers did not change during the course of infection with N. brasiliensis. In contrast, worm expulsion in normal mice was associated with a moderate increase in numbers of intestinal mast cells, commencing at the onset of expulsion and peaking several days after expulsion was completed.

Nippostrongylus brasiliensis infection in the rat: effects of surgical removal of Peyer's patches, mesenteric lymph nodes and spleen.

The influence of the surgical removal of Peyer's patches, mesenteric lymph nodes and spleen has been examined on the host response to Nippostrongylus brasiliensis infection in the rat. In animals subjected to these procedures, no effects were observed on whole blood or plasma histamine levels, peripheral blood leucocytosis or reaginic antibody levels, intestinal mast cell numbers or histamine content, nor on faecal egg output.

Intestinal mast cell response in thymectomised and normal mice infected with [formula omitted

In NIH mice, expulsion of Trichinella spiralis from the small intestine and increase in intestinal mast cells were each dependent on the presence of T-lymphocytes. Both changes were deficient in thymectomised mice but could be largely restored by reconstitution of thymectomised mice with syngeneic mesenteric lymph node cells. In both NIH and BALB/C mice the majority of the increased number of mast cells occurred within the intestinal epithelium. In NIH mice increase in the number of intestinal mast cells coincided roughly with expulsion of the parasites. In BALB/C mice increase in the numbers of intestinal mast cells did not appear to be connected with the location or expulsion of parasites and it is concluded that mast cell proliferation, accumulation and discharge per se do not result in or from worm expulsion.

Pathology of Taenia taeniaeformis infection in the rat: Gastrointestinal changes

The development of morphological changes in the stomach and small intestine of rats was observed for 75 days post infection (DPI) after oral infection with 1000 or 2000 eggs of Taenia taeniaeformis. Increases in size of both organs, due to mucosal hyperplasia, occurred earlier and tended to be more extreme in rats with the heaviest hepatic metacestode infections, although this was not always the case. Stomach weight increased up to 20-fold. Irregular proliferation of mucous epithelium and stroma of the lamina propria produced dramatic papillary and cystic thickening of the gastric mucosa with excessive mucus production. Weight and mucosal thickness of the small intestine doubled with little change in architecture or villus-crypt ratio of 2:1. Intestinal mast cell numbers increased throughout the observation period and were highest in the duodenum of heavily infected rats. In contrast, intestinal eosinophil numbers reached a peak between 30 and 40 DPI and then declined, in parallel with peripheral blood eosinophil counts. The implications of these gastrointestinal changes caused by a hepatic metacestode are discussed in terms of the possible mechanisms whereby they are produced and their significance in the host-parasite relationship.

Intestinal mast cell response in rats and chickens to coccidiosis, with some properties of chicken mast cells.

The response of intestinal mast cells to infection with coccidian protozoa in rats and chickens was compared with the well-known increase in the numbers of these cells which follows helminth infections. In <i>Eimeria</i>-infected chickens and rats given a moderate primary infection, there was an initial fall in the numbers of intestinal mast cells, small and insignificant in the rats, but more marked in the chickens. This was followed, towards the end of infection, by a return to (chicken) or an increase above (rat) normal levels. In birds given a large challenge inoculum of oocysts there was, within hours of dosing, an initial increase in numbers followed by a return to normal by day 2 and this response was similar in both immunised and susceptible birds. This rapid recruitment of cells was not seen in immune rats similarly challenged: in this species numbers were not increased until day 2 at the earliest. A marked increase in vascular leakage after the large challenge inoculum was apparent only in immunised birds. Thus this could not be correlated with the increase in numbers of mast cells which occurred equally in both immune and susceptible and was probably related to the invasion of host cells by the parasite. The mast cells of chickens are not degranulated by polymyxin B or compound 48/80, both of which affect rat mast cells. In the rat, connective tissue and intestinal mast cells differ in various ways including their dye-binding properties, but this was not seen with chicken mast cells.

Increased permeability of gut mucosa in rats infected with Nippostrongylus brasiliensis

The permeability of the gut mucosa to macromolecules has been examined in 4 different strains of rats infected with Nippostrongylus brasiliensis (N. brasiliensis). There is a marked increase in mucosal permeability during the infection. In addition, a considerable strain difference is observed in both worm burden kinetics and the kinetics of intestinal permeability. The dose-response and drug treatment experiments in outbred Wistar rats suggest that increased mueosal permeability is a function of the worm burden. However, the increased permeability is related neither to the rapid phase of worm expulsion nor to the rise in intestinal mast cell numbers.

Adoptive transfer of the intestinal mast cell response in rats infected with Nippostrongylus brasiliensis

The intestinal mast cells (IMC) were examined in normal and adoptively immunized rats infected with Nippostrongylus brasiliensis. An increase in the numbers of IMC was observed in infected recipients of thoracic duct lymphocytes (TDL) obtained from donor rats which had themselves been infected 10 days previously (Day 10 TDL). The increase in the number of IMC in the mucosa was related to the number of Day 10 TDL transferred into infected recipients. When TDL were fractionated into populations of cells either bearing (sIg +) or lacking (sIg −) surface immunoglobulin, only sIg − cells were able to confer the IMC response. Antigenic stimulation was necessary for the differentiation of intestinal mast cells. There was a marked difference between different strains of rats with regard to worm burden and intestinal mast cell kinetics although the increase in intestinal mast cells was always closely related to the final stage of the rapid phase of worm expulsion. These results are compatible with the concept that intestinal mast cells are derived from T cells and suggest that sIg + cells do not influence IMC differentiation. Alternatively, the possibility that the transferred TDL regulate the differentiation of cells of host origin into IMC cannot be excluded.

Immunological unresponsiveness to helminth parasites: II. Antibody response and hypersensitivity reaction associated with Nippostrongylus brasiliensis infection in young rats

We have previously shown that in rats infected when under 6 weeks of age with N. brasiliensis worm expulsion occurs only if more than 200 worms are established in the intestine. In such cases, worm expulsion starts later and proceeds at a slower rate than in comparatively infected adult rats stopping when a worm burden of 200 is reached. This relatively large residual infection persists into adult life. In the present paper the antibody status of rats infected when young was examined. Passive protection tests using the serum from such rats showed that protective antibody was produced by rats infected with more than 800 larvae, despite the fact that in these rats worm expulsion did not proceed to completion. It was also found that young rats produced reaginic antibody comparable in time of appearance and titer with similarly infected adults. Allergen production by the worms of the persistent infection was titrated and found to be produced in unreduced amount for at least 40 days after infection. Intestinal mast cell counts of the unresponsive rats were similar to those of infected adult rats. It was concluded that the incomplete expulsive reaction of rats infected when young cannot at present be explained by the absence of protective or reaginic antibodies or by a deficiency in the number of intestinal mast cells.