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Intestinal absorption of macromolecules during viral enteritis: an experimental study on rotavirus-infected
Abstract:
Epithelial transport and degradation of horseradish peroxidase (HRP), a macromolecular tracer, was studied in conventional and germ-free suckling mice following an experimental infection with rotavirus. Conventional and germ-free mice developed diarrhea from days 2 to 8 postinfection (pi), with growth failure. In mucosal homogenates, infectious virus detected by immunofluorescence on MA 104 cells was present from day 2 through day 8 pi in germ-free mice, but persisted longer (day 13 pi) in conventional mice. Only mild histological lesions were observed during diarrhea, but obvious macrovacuolation of epithelial cells and increased cellular density occurred during the convalescence period (days 9 to 13 pi). Intact and degraded HRP fluxes from mucosa to serosa were measured in vitro on segments of jejunum mounted in Ussing chambers. Both groups of mice developed increased HRP permeability during the experimental period, but at different times after inoculation: during the diarrheal period (days 2 and 3 pi) conventional mouse epithelium absorbed five times more HRP than noninfected controls and during the convalescence period (days 9 to 13 pi) HRP absorption in germ-free mice rose 10-fold as compared to its level before infection. In both cases, this increase in HRP permeability was entirely due to an increase in intact HRP absorption, probably via a transcellular route, and occurred without any alteration in degraded HRP transport. These results indicate that in mice, rotavirus infection causes a transient rise in gut permeability to undegraded proteins. The intestinal microflora seems to affect the timing, magnitude, and duration of this increased permeability.
Insights
Rotavirus infection in mice transiently increases gut permeability to intact proteins. Intestinal microflora influences the timing and extent of this increased permeability, impacting protein absorption.
Area of Science:
- Gastroenterology
- Virology
- Immunology
Background:
- Rotavirus is a common cause of gastroenteritis in infants.
- Epithelial barrier function is crucial for intestinal health.
- Macromolecular transport across the gut epithelium can be altered during infection.
Purpose of the Study:
- To investigate the effect of rotavirus infection on epithelial transport and degradation of horseradish peroxidase (HRP).
- To compare the impact of rotavirus on gut permeability in conventional and germ-free mice.
- To determine the role of intestinal microflora in rotavirus-induced changes in gut permeability.
Main Methods:
- Experimental rotavirus infection in suckling conventional and germ-free mice.
- Detection of infectious rotavirus by immunofluorescence.
- Measurement of intact and degraded HRP fluxes across jejunal segments using Ussing chambers.
- Histological examination of intestinal tissues.
Main Results:
- Both conventional and germ-free mice exhibited diarrhea and growth failure post-infection.
- Increased HRP permeability was observed in both groups, but at different time points.
- Conventional mice showed increased HRP absorption during diarrhea (days 2-3 pi), while germ-free mice showed increased absorption during convalescence (days 9-13 pi).
- The increased permeability was primarily due to enhanced absorption of intact HRP, suggesting a transcellular route, without altering degraded HRP transport.
Conclusions:
- Rotavirus infection induces a transient increase in intestinal permeability to undegraded proteins in mice.
- The intestinal microflora significantly influences the timing, magnitude, and duration of rotavirus-induced gut hyperpermeability.
- These findings highlight the complex interplay between viral infection, host physiology, and the gut microbiome in modulating intestinal barrier function.