Intestinal Enzyme Profiles in Normal and Rotavirus-Infected Mice

Collins, Joanne; Starkey, W.; Wallis, Timothy S.; Clarke, G. J.; Worton, K. J.; Spencer, A. J.; Haddon, S. J.; Osborne, Michael P.; Candy, D. C. A.; Stephen, J.

doi:10.1097/00005176-198803000-00017

Cited by 65 publications

(53 citation statements)

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“…This would affect normal epithelial cell replacement and hence height of villi, and also crypt functions which by general consensus (Roggin et al, 1972;Field et-al., 1980;Welsh et al, 1982) are involved in normal secretion. Increased rates of villus base/crypt cell division are involved in the hypersecretory phase of rotavirus diarrhoea (Collins et al, 1988;Spencer et al, in press) and have been implicated in other bacterial toxin-induced diarrhoeas (Stephen and Osborne, 1988). Clearly N2M was not acting as a general cytotoxic agent, since it did not affect the numbers of long-lived lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

The role of leucocytes in the induction of fluid secretion by Salmonella typhimurium

Wallis

Vaughan

Clarke

et al. 1990

Journal of Medical Microbiology

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Summary. Nitrogen mustard (N2M) treatment of rabbits induced neutropenia, and, in ligated ileal loops, it inhibited fluid secretion induced by salmonella or by cholera toxin (CT). Pretreatment of rabbits with indomethacin almost abolished salmonellainduced fluid secretion and significantly reduced that induced by CT. Similar effects of N2M and indomethacin on fluid secretion induced by salmonella, but not by CT, have been reported by other workers and used to implicate prostaglandins, from the salmonella-induced inflammation, as mediators of fluid secretion. In contrast, we show that N2M treatment, in addition to reducing CT-induced secretion, caused severe morphological alterations to ileal mucosa. Irradiation techniques were developed for inducing neutropenia, but they did not totally inhibit salmonellainduced leucocyte influx into ileal mucosa. We propose an alternative mechanism for the inhibitory effect of N2M on salmonella-and CT-induced secretion, based on the known anti-mitotic activity of N2M. Also, the anti-secretory effect of indomethacin cannot be attributed uniquely to its anti-inflammatory activity because it depressed CT-induced secretion as well as salmonella-induced secretion. These results support the concept of pathophysiological secretion in infectious diarrhoea, developed previously for rotavirus and extended to bacterial infections.

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Section: Discussionmentioning

confidence: 99%

The role of leucocytes in the induction of fluid secretion by Salmonella typhimurium

Wallis

Vaughan

Clarke

et al. 1990

Journal of Medical Microbiology

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“…Similarly, Heyman et al (37), who measured transport of horseradish peroxidase in vitro in segments of mouse jejunum during and immediately after rotavirus infection, found a 5-fold rise in protein absorption during the diarrheal period (d 2 and 3 pi). The peak of rotavirus diarrhea also coincides with a peak in thymidine kinase activity (38), a marker of crypt cell proliferation, which in turn is correlated to changes in tight junction of crypt cells (39), suggesting that the leakiness of the epithelium might be increased during this stage of disease.…”

Section: Effect Of Litter Expansion On Nutrition and Viral Infectionmentioning

confidence: 95%

Effect of Rotavirus Infection and Malnutrition on Uptake of a Dietary Antigen in the Intestine

et al. 1990

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“…78,2004 MINIREVIEW 10215 face of infected enterocytes. For example, the activities of alkaline phosphatase, lactase, sucrase, and maltase are reduced (6,12,16). The expression of sucrase and isomaltase in cultured human intestinal epithelium was also reduced, probably as a result of perturbation of protein targeting and the microvillar cytoskeleton (33).…”

Section: The Molecular Basis Of Diarrhea Inductionmentioning

confidence: 99%

Pathogenesis of Intestinal and Systemic Rotavirus Infection

Ramig

2004

J Virol

311

230

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Rotaviruses are responsible for significant gastrointestinal disease, primarily in children Ͻ5 years of age and the young of other mammalian species. Each year rotaviruses cause approximately 111 million episodes of gastroenteritis in children, which result in 25 million visits to clinics, 2 million hospitalizations, and 352,000 to 592,000 deaths. On a worldwide basis, nearly every child experiences rotavirus gastroenteritis by age 5, 1 in 5 visits a clinic, 1 in 65 is hospitalized, and 1 in 293 dies. Children in the poorest countries account for 82% of rotavirus deaths (60). This disease burden underscores a need for interventions such as vaccines. A vaccine was developed and approved, but recommendation for its use was withdrawn because of vaccination-associated adverse events (57). Additional information about the molecular biology, immunology, and pathogenesis of rotavirus infection will inform ongoing vaccine development efforts.Our understanding of rotavirus-induced diarrheal disease is incomplete compared to that of several other pathogens (e.g., cholera). Rotavirus diarrhea has been attributed to several different mechanisms, including malabsorption secondary to enterocyte destruction, a virus-encoded toxin, stimulation of the enteric nervous system (ENS), and villus ischemia (13,45). Over the past several years, numerous studies have addressed mechanisms of diarrhea induction at the cellular and tissue levels, and a new understanding of the mechanisms is beginning to emerge. Here I will briefly outline the new data and present our current understanding of how rotaviruses induce diarrhea in the infected host.Recent studies confirm sporadic case reports that rotavirus infection is not confined to the intestine as was generally assumed. Although systemic sequellae to rotavirus infection are apparently rare, reports have continually appeared in the literature, and recent work with animal models has begun to shed light on how the virus spreads to extraintestinal sites. Our current understanding of extraintestinal spread and infection will also be considered below. GENERAL CHARACTERISTICS OF ROTAVIRUS INFECTION AND DISEASE IN HUMANS AND ANIMALSRotavirus. Rotaviruses comprise a genus within the family Reoviridae. The rotavirion has a nonenveloped, complex, triple-layered capsid structure that surrounds a genome composed of 11 segments of double-stranded RNA. There are six structural proteins and six nonstructural proteins, each encoded in a unique genome segment except for nonstructural proteins 5 and 6 (NSP5 and NSP6), which are encoded in overlapping reading frames of a single segment. The rotavirus genus is divided into serological groups (A to E). Groups A to C infect humans, and all groups infect animals. All the information presented here is in regard to group A virus infections.Pathophysiology of rotavirus diarrhea. The enterocytes lining the small intestine are generally divided into two types: enterocytes and crypt cells (Fig. 1). Villus enterocytes are mature, nonproliferating cells covering the vill...

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Intestinal Enzyme Profiles in Normal and Rotavirus-Infected Mice

Cited by 65 publications

References 0 publications

The role of leucocytes in the induction of fluid secretion by Salmonella typhimurium

The role of leucocytes in the induction of fluid secretion by Salmonella typhimurium

Effect of Rotavirus Infection and Malnutrition on Uptake of a Dietary Antigen in the Intestine

Pathogenesis of Intestinal and Systemic Rotavirus Infection

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