Glucose Malabsorption and Intestinal Histopathology in Trichinella spiralis-Infected Guinea Pigs

Castro, Gilbert A.; Olson, L. J.; Baker, Richard G.

doi:10.2307/3276724

Cited by 39 publications

(8 citation statements)

References 18 publications

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“…However, mice reduce their food consumption during rejection of T. spiralis (Larsh, Goulson & Van Zandt, 1962;Goulson & Larsh, 1964) and it is well known that reduced intake of carbohydrates may retard the growth of hymenolepids (Read & Rothman, 1957 a). The reduction in growth of H. microstoma may, therefore, have been at least partially due to the altered dietary intake of the mouse, although it is also conceivable that a reduced intake might be offset by the malabsorption of nutrients associated with T. spiralis infection (Castro, Olson & Baker, 1967). However, it is unlikely that altered intake would markedly affect the initial establishment of the worms (Read & Rothman, 19576): the significant reduction in numbers of H. microstoma recovered that did occur in some groups was probably, therefore, caused by the inflammation associated with the rejection of T. spiralis.…”

Section: Discussionmentioning

confidence: 99%

The effect of concurrent infection with Trichinella spiralis on Hymenolepis microstoma in mice

et al. 1978

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Section: Discussionmentioning

confidence: 99%

The effect of concurrent infection with Trichinella spiralis on Hymenolepis microstoma in mice

et al. 1978

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“…Initially the adaptive immune response of vertebrates involves a covert afferent phase during which recognition of foreign invaders takes place and, eventually, this is translated into an effector phase during which the actual defences are unleashed. The latter can be pathogenic for the host and come at a cost (Castro, Olson and Baker, 1967; Mercer et al 2000), but it is during this effector phase that worms can be expelled from the host. We have been arguing for some time about whether a magic bullet exists within the complex array of effectors (Pemberton et al 2004; Anthony et al 2006; Artis, 2006; Artis et al 2004), but the fact is that once unleashed some components of the response to intestinal helminths, whether effective against the triggering species or not, can be detrimental to other species.…”

Section: The Immune Response As An Environmental Stressormentioning

confidence: 99%

Structure in parasite component communities in wild rodents: predictability, stability, associations and interactions .... or pure randomness?

Behnke

2008

Parasitology

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SUMMARYExperimental data establish that interactions exist between species of intestinal helminths during concurrent infections in rodents, the strongest effects being mediated through the host's immune responses. Detecting immune-mediated relationships in wild rodent populations has been fraught with problems and published data do not support a major role for interactions in structuring helminth communities. Helminths in wild rodents show predictable patterns of seasonal, host age-dependent and spatial variation in species richness and in abundance of core species. When these are controlled for, patterns of co-infection compatible with synergistic interactions can be demonstrated. At least one of these, the positive relationship betweenHeligmosomoides polygyrusand species richness of other helminths has been demonstrated in three totally independent data-sets. Collectively, they explain only a small percentage of the variance/deviance in abundance data and at this level are unlikely to play a major role in structuring helminth communities, although they may be important in the more heavily infected wood mice. Current worm burdens underestimate the possibility that earlier interactions through the immune system have taken place, and therefore interactions may have a greater role to play than is immediately evident from current worm burdens. Longitudinal studies are proposed to resolve this issue.

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“…Infective muscle-stage larvae were harvested from the skeletal muscle of T. spiralis-infected CF-1 mice (Charles River Laboratories) as previously described (11,21). Rats were fasted overnight and anesthetized with ketamine (80 mg/kg body wt im) and xylazine (13 mg/kg body wt im).…”

Section: Induction Of Nematode Infectionmentioning

confidence: 99%

“…These include decreased gastric emptying, increased intestinal motility, increased cholecystokinin release, and increased intestinal nutrient absorption (23,35,41). Enteric infections with the nematodes Nippostrongylus brasilien-sis and T. spiralis produce a range of gastrointestinal disturbances that include increased intestinal motility and propulsive behavior (1,7,21,33), increased mucosal secretion of water and electrolytes (9), decreased activities of enterocyte brush-border enzymes (11,22), altered responses to brain-gut peptides, including cholecystokinin, a satiety factor (14,15,32,38), and intestinal inflammation (8,10,11,12,25,38). Interleukin (IL)-1␤ and tumor necrosis factor-␣ (TNF-␣) are mediators of nematode-induced intestinal inflammation (26) and are known suppressors of food intake in rats (6,19,30,37,42).…”

mentioning

confidence: 99%

Suppression of food intake is linked to enteric inflammation in nematode-infected rats

Faro

Reidelberger

Palmer

2000

American Journal of Physiology-Regulatory, Integrative and Comp

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Our aim was to investigate the cause-effect relationship between intestinal inflammation induced by infection with enteric stages of Trichinella spiralis and decreased host food intake. A suppression of food intake in T. spiralis-infected rats occurred within the first 24 h postinfection (PI) and was maximized by day 6 PI. Food intake, cumulated over an 8-day PI period, decreased by 59% compared with uninfected animals. The anti-inflammatory glucocorticoid betamethasone 21-phosphate was orally administered to rats in their drinking water to suppress T. spiralis-induced jejunal inflammation. When treated with a low dose of glucocorticoid (5.2 microg/ml), food intake in infected rats was still significantly reduced, but only by 21% compared with glucocorticoid-treated, uninfected rats. At the highest glucocorticoid dose (10.4 microg/ml) administered, infection-induced reduction in food intake was not different from that of glucocorticoid-treated, uninfected counterparts. The elevation in jejunal myeloperoxidase activity caused by infection was also significantly blunted by oral glucocorticoid treatment. Our results suggest that suppressed host food intake during enteric T. spiralis infection is directly linked to intestinal inflammation.

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Glucose Malabsorption and Intestinal Histopathology in Trichinella spiralis-Infected Guinea Pigs

Cited by 39 publications

References 18 publications

The effect of concurrent infection with Trichinella spiralis on Hymenolepis microstoma in mice

The effect of concurrent infection with Trichinella spiralis on Hymenolepis microstoma in mice

Structure in parasite component communities in wild rodents: predictability, stability, associations and interactions .... or pure randomness?

Suppression of food intake is linked to enteric inflammation in nematode-infected rats

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