Neonatal maternal deprivation promotes Nippostrongylus brasiliensis infection in adult rats.

Neonatal stress is known to alter immune responses in adults and parasitic infection is modulated by the immune status of the host. The present study aimed to establish whether neonatal maternal deprivation affects the time course of Nippostrongylus brasiliensis infection and associated intestinal alterations in adult rats. Rat pups were separated from their dam 3h daily during postnatal days 2-14, or left undisturbed. At 12 weeks of age, N. brasiliensis infection was induced by subcutaneous administration of 3000 L3 larvae. At 7 and 12 days after primary infection, the number of intestinal adult worms, fecal egg output, jejunal paracellular permeability, and myeloperoxidase (MPO) activity were measured. On days 7 and 12 after a secondary infection, numbers of adult worms and egg production were determined. Maternal deprivation increased the number of jejunal adult worms and fecal eggs and larvae on day 7 after primary infection, and exacerbated the increase in jejunal MPO activity induced by the infection. On day 12, adult worms were only observed in deprived rats. N. brasiliensis infection did not potentiate the increase in jejunal paracellular permeability induced by maternal deprivation. After the second infection, no egg was detected in both control and deprived rats. In conclusion, maternal deprivation in rats facilitates primary infection by N. brasiliensis and enhances the inflammatory response of the jejunum, but does not induce severe breakdown of immunity to N. brasiliensis.

Alteration of CCK-induced satiety in post-Nippostrongylus brasiliensis-infected rats.

In rats, the nematode Nippostrongylus brasiliensis induces an intestinal inflammation, but after the inflammation had resolved and the worm burden eliminated, morphological alterations of the intestinal wall, mainly consisting of mast cell hyperplasia and enteric nerve remodeling, persist for several weeks. Intestinal signals reaching the brain through the vagus nerve and involving neuropeptides such as CCK, play a role in the control of food intake. Our hypothesis was that neuroimmune alterations of the intestine may alter this control. This work was aimed to evaluate whether post-infection alterations of the intestinal wall may affect the satiety effects of CCK and further, the role of mast cells and their mediators, histamine and serotonin, in post-N. brasiliensis-infected rats. In basal conditions, food intake was not different in control and post-infected groups of rats. Post-infected rats were characterized by prolonged satiety effects of both CCK and histamine but not serotonin. The prolonged effect of CCK was reduced when mast cells were previously stabilized by ketotifen, which had no effect per se on food intake. No difference was observed in the increase of food intake induced by CCK-A and CCK-B receptor antagonists in both control and post-infected rats. Mast cell degranulation with compound 48/80 induced severe anorectic effects that lasted for less than 24h in post-infected rats and as long as 6 days in controls. Thus, in our experimental conditions, i.e., within 30-50 days post-N. brasiliensis infection, we observed an enhancement of the anorectic effect of exogenous CCK involving mast cell degranulation and histamine.