PubMed Health⌕ Search

Biomedical subjects

G A Castro

Publications and source records attributed to G A Castro.

At least 55 records · Page 3Linked to original sources
PubMed1986

Anamnestic stimulus-specific myoelectric responses associated with intestinal immunity in the rat.

Changes in small intestinal motility reflective of local anaphylaxis are hypothesized to be associated with the rapid, immune-mediated rejection of infective larvae of the nematode Trichinella spiralis. This hypothesis was tested by comparing intestinal myoelectric activity in primarily and secondarily infected rats; the latter group represented immunized hosts, i.e., immunized by initial contact with the parasite. Patterns of slow waves, action potentials, interdigestive migrating myoelectric complexes, and migrating action-potential complexes induced by secondary infection differed from those associated with primary infection. Patterns in both cases differed from those in uninfected rats. Secondary but not primary infection evoked changes in myoelectric patterns within 15 min after administration of infective larvae. These changes could not be elicited by inoculation with dead larvae, larval excretory-secretory antigens, or a heterologous parasite, Eimeria nieschulzi. Results indicate that altered smooth muscle contractile activity is part of an anamnestic, stimulus-specific response to T. spiralis in immunized rats. These changes may represent the in vivo equivalent of the anaphylactically mediated intestinal smooth muscle contraction elicited in vitro in the Schultz-Dale reaction.

Action Potentials↗
PubMed1985

Phosphatidylethanolamine methylation in intestinal brush border membranes from rats resistant to Trichinella spiralis.

Methylation of phospholipids is proposed as a mechanism to explain changes in properties of intestinal brush border membrane that coincide with development of immunity to the intraepithelial parasite, Trichinella spiralis. Methylation was measured by the incorporation of the [3H]methyl group from S-adenosyl-L-[3H]methyl methionine into phospholipids. At least two enzymatic components were detected that converted phosphatidylethanolamine to phosphatidylcholine. The first, designated methyltransferase I, catalyzed the formation of phosphatidylmonomethylethanolamine from phosphatidylethanolamine and had a low Km for S-adenosyl-L-methyl-methionine (5 microM). The second, designated methyltransferase II, which catalyzed the methylation of phosphatidylmonomethylethanolamine to phosphatidyldimethylethanolamine and phosphatidyldimethylethanolamine to phosphatidylcholine, had a high Km for S-adenosyl-L-methyl methionine (167 microM). Both enzymes had two pH optima, were most active at 37 degrees C and were Mg2+ dependent. A decrease in methylation activity was present in brush border membranes from rats immunized against T. spiralis. Although the synthesis of phosphatidylcholine was not significantly altered there was a substantial decrease in the formation of phosphatidylmonomethylethanolamine and phosphatidyldimethylethanolamine as compared with nonimmunized rats. Since phospholipid composition influences membrane fluidity and cell function, it is proposed that altered methylation activity may influence the characteristics of brush border membrane in the immune host.

Animals↗
PubMed1985

Anaphylactic-like reaction of small intestinal epithelium in parasitized guinea-pigs.

Antigens derived from Trichinella spiralis were used to challenge, in vitro, sensitized jejunum from infected guinea-pigs while monitoring ion transport properties of the tissue. Antigen challenge resulted in dose-dependent increases in trans-epithelial electrical potential difference and short circuit current. Both antigen-stimulated electrical alterations and Schultz-Dale contractions were demonstrated in small intestinal tissue after the passive transfer of immune serum containing anti-trichinella homocytotropic antibodies.

Anaphylaxis↗
PubMed1984

Trichinella spiralis: rapid, immunologically influenced reduction of intestinal, sodium-coupled sugar transport in the rat.

Epithelium of isolated small intestinal segments were studied in Ussing-type chambers to detect physiological changes associated with rapid, immune rejection of Trichinella spiralis infective larvae. Electrophysiological parameters associated with Na+-coupled hexose transport were measured. Changes in transepithelial electrical potential difference (PD), resistance, and short circuit current (Isc) due to the addition of actively absorbed beta-methyl-D-glucoside (BMG) to the mucosal solution were determined. Measurements were made prior to and 30 min after primary and secondary infections. Animals were infected by intraduodenal inoculation. As the infective larval dose in primarily infected (nonimmunized) rats increased from 50 to 2000 larvae the magnitude of the rise in Isc elicited by BMG decreased in a dose-dependent fashion, with 50 larvae per rat having no effect. In previously infected (immunized) rats challenged with a secondary inoculum, all doses, ranging from 50 to 2000 larvae per rat, decreased the BMG-stimulated change in Isc by approximately 50%. The effect of 50 worms per rat in immunized hosts was equivalent to that produced by approximately 1600 worms in nonimmunized animals. Measurements of 14C-BMG mucosa-to-serosa flux confirmed that Na+-BMG cotransport was responsible for observed changes in Isc. Results support the conclusion that changes in intestinal epithelial function are associated with larval challenge of immune rats.

Animals↗
PubMed1984

Trichinella spiralis: intestinal myoelectric activity during enteric infection in the rat.

The objective was to characterize changes in the host's small intestinal smooth muscle contractile activity caused by the enteric stages of the nematode, Trichinella spiralis, during primary infection. Myoelectric activity was recorded from electrodes permanently implanted on the seromuscular surface of the small bowel in conscious, unrestrained rats during the first 2 weeks postinfection (PI). Several myoelectric parameters examined collectively indicated that smooth muscle function of the small bowel was altered by infection. A decrease in contractile activity was indicated by reductions in electrical slow wave and spike potential frequencies that were maximal 6-12 days postinfection. Normal coordinated contractile behavior was also impaired, as evident from a reduction in the frequency of migrating myoelectric complexes. An infection-induced qualitative change occurred designated as a migrating action potential complex. This unusual spiking activity swept down the bowl rapidly, occurred with greatest frequency 2-6 days PI, and coincided with the disruption of the normal migrating myoelectric complex. It is concluded that recordings of intestinal myoelectric activity provide sensitive, quantifiable correlates of contractile patterns throughout the intestinal phase of trichinellosis in a single host.

Action Potentials↗
PubMed1984

Local and systemic effects on inflammation during Eimeria nieschulzi infection.

Rats infected with Eimeria nieschulzi, a coccidium that inhabits intestinal epithelium, have a lower basal inflammatory state in their intestinal mucosa eight days postinoculation as reflected by a drop in mucosal peroxidase activity and a decrease in the number of granulocytes in the lamina propria. The reduction of systemic inflammation in infected rats was assessed from a reduction in the formation of granulation tissue around a sterile cotton string implanted under the abdominal skin of the hosts. This reduced inflammatory response, both locally and systemically, occurs during the development of gamonts by the parasite and the release of oocysts from the host. These results plus the presence of normal or slightly elevated numbers of granulocytes in peripheral blood lead to the conclusion that the parasite does not affect hematopoiesis but interferes with some phase in the directed migration of leukocytes to specific sites.

Animals↗
PubMed1983

Sialic acid deficiency in lectin-resistant intestinal brush border membranes from rats following the intestinal phase of trichinellosis.

Maximal binding (Bmax) of the lectin, wheat germ agglutinin, by small intestinal brush border membrane is significantly reduced in rats infected with Trichinella spiralis. Wheat germ agglutinin specificity is for N-acetylglucosamine and sialic acid. Whereas total hexosamine and N-acetylglucosaminidase-labile N-acetylglucosamine were comparable in membranes from uninfected as compared with infected rats, the total sialic acid content and neuraminidase-released sialic acid were significantly higher in BBM from uninfected hosts. N-Acetylglucosaminidase treatment of membranes reduced Bmax for wheat germ agglutinin in both hosts. Neuraminidase treatment reduced Bmax in uninfected hosts, but tended to increase it in infected rats. Membranes from uninfected rats incorporated more N-acetylglucosamine from UDP-N-[14C]acetylglucosamine into oligosaccharide-lipid than did membranes from infected hosts. However, lipid and protein fractions were labeled at the same rate in both sets of membranes. Sialic acid was incorporated into protein at a slightly faster rate in brush border membrane from uninfected rats, indicative of a higher level of sialotransferase activity. These results suggest that the reduction in Bmax for wheat germ agglutinin in gut epithelial cell membranes from infected rats is related to a reduced level of sialic acid available for lectin binding as well as specific interactions between N-acetylglucosamine and sialic acid.

Acetylglucosamine↗
PubMed1982

Intestinal epithelial membrane changes in rats immune to Trichinella spiralis.

Establishment of Trichinella spiralis infective larvae is blocked to a large degree in the immune rat as compared with the nonimmune host. The rapidity with which this response occurs indicates that most worms are either prevented from penetrating the intestinal epithelium or are rejected immediately after cell entry. It is proposed that interference with larval infectivity is due to alterations in the epithelial cell apical or brush border membrane. Alterations may result from prior infection or may reflect an acute change induced by challenge infection. In either case the establishment of normal populations of larvae in the mucosa is disturbed. Lectin binding capacity of brush border membranes was used to assess possible membrane alterations. This parameter in uninfected (control) rats was compared with that in infected rats, which acquire resistance to subsequent challenge, and in infected rats immediately after a challenge inoculum. Enriched brush border membrane preparations were characterized for their binding of wheat germ agglutinin, which attaches specifically to the carbohydrate, N-acetylglucosamine. Maximum specific binding of 125I-labeled wheat germ agglutinin occurred within 20 min. The spontaneous rate of dissociation was negligible for 90 min. Highest specific binding resulted at 24 degrees C, pH 6.0 and with 75 micrograms brush border membrane protein per assay tube. Results suggested the existence of multiple binding sites. 1 mg of membrane protein from uninfected rats and rats immunized by primary infection maximally bound 9.8 X 10(10) and 4.3 X 10(10) molecules of wheat germ agglutinin, respectively. Binding for the 'immune' brush border membrane, as compared with the 'uninfected' brush border membrane was reduced during the first 3 weeks of infection and remained low for at least 3 months. No further reduction in binding was observed for brush border membrane isolated within minutes after a secondary infection. These results reveal the induction by a primary infection of changes in brush border membrane structure and the persistence of these changes in the immune host. In view of the rapid turnover time of epithelial tissue the mechanism by which this change is perpetuated speculatively involves immune elements in the lamina propria.

Animals↗
PubMed1982

Immunological regulation of epithelial function.

The objective of this presentation is to develop a hypothesis through a survey of pertinent literature rather than to review an established area of physiology. The focal point is the mucosa of the small intestine. The major thesis is that lamina propria cells regulate functions of epithelial cells. Support for this comes from studies of the "immunophysiological" interplay that goes on in the mucosa and that has been amply revealed through investigations of host-parasite interactions. Immunological reactions in several intestinal helminth infections affect epithelial cell differentiation and development as well as secretory, absorptive, and digestive activities. Epithelial cells may be influenced indirectly as bystander cells during immunologically mediated inflammation or directly through their recruitment as effector components in immune reactions. Immune responses, by convention, are thought to be mediated by nonepithelial cells. Therefore, involvement of epithelial cells in effecting immunity or in responding to immunologically elicited signals implies a regulatory role for lamina propria cells in epithelial function. Confirmation of the capacity of epithelial cells to respond to the command of other cells with "memory" capabilities would imply the existence of a sensitive, locally organized, and highly specific adaptive mechanism in the host.

Animals↗
PubMed1982

Reduced hexose transport by enterocytes associated with rapid, noninjurious rejection of Trichinella spiralis from immune rats.

Rats immunized against Trichinella spiralis rejected larvae from a challenge infection within minutes. Infectivity of these once-rejected larvae for nonimmune rats following intestine-to-intestine transfer, infectivity for nonimmune mice following oral inoculation, and normal development in these mice indicated that the parasite did not sustain immediate or long term damage as a result of the host's immune response. Associated with rapid worm rejection was a change in host intestinal function - altered absorption. Uptake of a hexose, 14C-beta-methyl-D-glucoside, was studied in intestinal segments isolated from rats before and 30 min after primary and secondary infections. Larvae were administered intraintestinally. Absorption was measured using a tissue accumulation method, under conditions of substrate saturation (30 mMolar) and over a 5-min period. 3H-mannitol was used as a marker to measure extracellular water, hence, extracellular sugar. Following challenge infection of previously infected (immunized) hosts, there was a significant reduction (22%; P less than 0.05) in hexose absorption as compared to the uptake rate before challenge. In contrast, cellular uptake before and 30 min after primary infection was similar. These findings are presented in support of the hypothesis that the failure of T. spiralis larvae to infect immune hosts is the result, not of direct worm damage, but of functional changes in gut epithelium, the habitat of the parasite.

Animals↗
PubMed1980

Systemic anti-inflammatory effect associated with enteric trichinellosis in the rat.

The hypothesis tested was that enteric parasites that induce local inflammation in their host suppress inflammatory reactions at distant sites. A technique was developed to demonstrate, quantitatively, such an anti-inflammatory component. The systemic antiphlogistic effect produced by the intestinal stages of Trichinella spiralis was studied and compared with that caused by dexamethasone, a synthetic adrenocortical steroid. Inflammation was measured (dry weight, protein content, myeloperoxidase activity) as the amount of granulation tissue accumulated around a sterile cotton string implanted for 1 wk under the abdominal skin of rats. Based on this assay, T. spiralis infection had a systemic anti-inflammatory effect on the host which was directly dose related. Steroid treatment also had a dose-dependent suppressive effect on granuloma formation. The maximum dose (56 X 10(3) larvae/kg body weight) of T. spiralis used, had suppressive activity equivalent to 1.0 mg/kg body weight of steroid.

Animals↗
PubMed1979

Physiological characterization of a biphasic immune response to Trichinella spiralis in the rat.

Secondary infection with Trichinella spiralis in the rat was associated with a host response that prevented approximately 80% of the total number of larvae recovered after primary infection from embedding in the intestine. The host response occurred within 15 min after contract of the parasite with intestinal mucosa and was not associated with acute inflammatory cell infiltrates or with the pathophysiology of the primary infection. Eventual rejection of the residual population of embedded worms occurred between four and eight days after infection and involved tissue changes similar to those attending worm rejection during primary infection. Elimination of enteric stages of T. spiralis in primary infection probably involves a single response aimed at the expulsion of established worms. In contrast, immune rejection of worms in secondary infection involves physiologically and presumably immunologically distinct "early" and "late" responses, with each response having a different developmental stage of the parasite as its target.

Animals↗
PubMed1979

Altered intestinal fluid movement in response to Trichinella spiralis in immunized rats.

Net intestinal fluid movement was measured in immunized and non-immunized rats infected with the enteric stages of the nematode, Trichinella spiralis. Animals were studied 30 min, 5 days and 30 days after receiving infective larvae. Net water movement across the mucosal surface of the gut was measured in vivo by perfusing a cannulated segment (approximately 30 cm) of proximal small intestine with an isotonic solution containing a nonabsorbable marker, 14C polyethylene glycol, at a rate of 0.5 ml/min. Uninfected rats showed net absorption of water, 25 microliter/h per cm of intestine. This response was unaltered when rats were infected (7 x 10(3) larvae/rat) and examined 30 minutes later. Five days after primary infection net tissue-to-lumen fluid movement, ie. net secretion, occurred at a rate of 45 microliter/h per cm. When rats were studied 30 days after primary infection, net absorption equivalent to the preinfection level was observed once again. Previously infected (immunized) rats, when challenged (secondary infection, 7 x 10(3) larvae/rat) and examined within 30 min showed a significant decrease in net absorption rate as compared with non-immunized rats. Absorption returned to the preinfection level at both 5 and 30 days post challenge. Results support the conclusion that T. spiralis caused a decrease in net lumen-to-tissue fluid movement during primary and secondary infections. The response was initiated faster in previously infected hosts. The rapid induction of net fluid movement in the direction of secretion upon secondary contact with the parasite is associated temporarily with prevention of worm establishment.

Absorption↗