scholarly journals Decreased Expression of Colonic Slc26a3 and Carbonic Anhydrase IV as a Cause of Fatal Infectious Diarrhea in Mice

2009 ◽  
Vol 77 (9) ◽  
pp. 3639-3650 ◽  
Author(s):  
Diana Borenshtein ◽  
Katherine A. Schlieper ◽  
Barry H. Rickman ◽  
Jeannie M. Chapman ◽  
Clifford W. Schweinfest ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Intestinal Transport ◽  
Inbred Strains ◽  
Fluid Loss ◽  
Infectious Diarrhea ◽  
Chloride Absorption ◽  
Inbred Strains Of Mice ◽  
C3h Mice ◽  
Electrolyte Loss ◽  
Carbonic Anhydrase Iv

ABSTRACT Citrobacter rodentium causes epithelial hyperplasia and colitis and is used as a model for enteropathogenic and enterohemorrhagic Escherichia coli infections. Little or no mortality develops in most inbred strains of mice, but C3H and FVB/N mice exhibit fatal outcomes of infection. Here we test the hypothesis that decreased intestinal transport activity during C. rodentium infection results in fatality in C3H/HeOu and FVB/N mice. Susceptible strains were compared to resistant C57BL/6 mice and to inbred strains SWR and SJL of Swiss origin, which have not been previously characterized for outcomes of C. rodentium infection. Mortality in susceptible strains C3H/HeOu and FVB/N was associated with significant fluid loss in feces, a remarkable downregulation of Slc26a3 and carbonic anhydrase IV (CAIV) message and protein expression, retention of chloride in stool, and hypochloremia, suggesting defects in intestinal chloride absorption. SWR, SJL, and C57BL/6 mice were resistant and survived the infection. Fluid therapy fully prevented mortality in C3H/HeOu and FVB/N mice without affecting clinical disease. Common pathogenic mechanisms, such as decreased levels of expression of Slc26a3 and CAIV, affect intestinal ion transport in C. rodentium-infected FVB and C3H mice, resulting in profound electrolyte loss, dehydration, and mortality. Intestinal chloride absorption pathways are likely a potential target for the treatment of infectious diarrhea.

scholarly journals The problem of dehydration in pediatrics

2021 ◽  
Vol 16 (4) ◽  
pp. 296-303
Author(s):  
S.O. Kramarov ◽  
V.V. Yevtushenko ◽  
О.М. Yevtushenko ◽  
Ye.A. Maevska ◽  
V.V. Babak
Keyword(s):  
Clinical Symptoms ◽  
Cyclic Vomiting Syndrome ◽  
Fluid Loss ◽  
Infectious Diarrhea ◽  
Oral Rehydration ◽  
Diabetic Ketosis ◽  
Pathological Conditions ◽  
Significant Difference ◽  
Electrolyte Loss ◽  
Cyclic Vomiting

Dehydration syndrome often complicates the course of various diseases in children. The article covers the main pathological conditions that are accompanied by fluid loss, such as infectious diarrhea, cyclic vomiting syndrome, non-diabetic ketosis and ketoacidosis. The pathophysiological mechanisms that lead to water and electrolyte loss are described, as well as methods for correc­ting dehydration in pediatrics. We presented the results of a clinical study of Reogel, which was used for oral rehydration in children with acute infectious diarrhea receiving inpatient treatment. According to the results of this observation, we did not find a significant difference in the duration of the main clinical symptoms of the disease, such as diarrhea, vomiting and dehydration symptoms, as well as the frequency and duration of parenteral rehydration between groups of children receiving Reogel and standard oral rehydration. The results of this study give grounds to consider Reogel as an alternative to traditional oral rehydration in children with infectious diarrhea, accompanied by mild and moderate dehydration.

scholarly journals Nematospiroides dubius: stimulation of acquired immunity in inbred strains of mice

1977 ◽  
Vol 51 (3) ◽  
pp. 167-175 ◽  
Author(s):  
Jerzy M. Behnke ◽  
D. Wakelin
Keyword(s):  
Primary Infection ◽  
Inbred Mice ◽  
Cell Activity ◽  
Inbred Strains ◽  
Acquired Immunity ◽  
Systematic Analysis ◽  
Inbred Strains Of Mice ◽  
C3h Mice ◽  
Nematospiroides Dubius ◽  
Stimulation Of

ABSTRACTThe development of immunity to Nematospiroides dubius was studied in three strains of inbred mice (BALB/c, C3H and NIH). Although a primary infection in NIH mice persisted for two months without evidence of a reduction in worm numbers, female mice of this strain readily developed resistance to reinfection. The degree of resistance was enhanced when an immunizing infection of 600 larvae was administered as 6 separate doses of 100 larvae given between days 0 and 11, and the worms removed by anthelmintic treatment given on days 15, 21, 28 and 35. Immunity in mice immunized in this way was manifest both as a reduction in worm recoveries on days 9–14 after challenge and also as an expulsion of established worms from the intestine. BALB/c mice were initially less resistant, but expelled most of the worms which became established; C3H mice showed no evidence of expulsion. The finding that inbred NIH and BALB/c mice acquire resistance to N. dubius offers possibilities for the systematic analysis of lymphoid cell activity in initiating and expressing immunity to this parasite.

Effects of Foster Nursing on Alcohol Selection in Inbred Strains of Mice

1972 ◽  
Vol 33 (2) ◽  
pp. 494-503 ◽  
Author(s):  
Setsuo Komura ◽  
Masao Ueda ◽  
Toshikiyo Kobayashi
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice

Duplications and deletions of Vh genes in inbred strains of mice

1988 ◽  
Vol 28 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Adele Tutte ◽  
Roy Riblet
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Vh Genes

scholarly journals THE GENETIC DIVERGENCE OF SUBLINES AS ASSESSED BY HISTOCOMPATIBILITY TESTING

Genetics ◽  
1973 ◽  
Vol 75 (4) ◽  
pp. 671-677
Author(s):  
Willys K Silvers ◽  
David L Gasser
Keyword(s):  
Genetic Divergence ◽  
Inbred Strains ◽  
Skin Grafts ◽  
Inbred Strains Of Mice ◽  
Inbred Rats

ABSTRACT The degree of genetic divergence which has occurred between a number of inbred strains of mice and between two sublines of inbred rats was assessed by determining the fate of inter-subline skin grafts. Sublines which had been separated for 29 and 42 generations possessed no detectable incompatibility, while three combinations of sublines judged to have been maintained apart for from 123 to 129 generations showed slight degrees of histoincompatibility. One pair of sublines which had been separated for 119 generations demonstrated a marked degree of incompatibility, and an F2 test suggested that mutations had occurred at four or five histocompatibility loci.

scholarly journals A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse.

1990 ◽  
Vol 171 (2) ◽  
pp. 519-531 ◽  
Author(s):  
A Matsuzawa ◽  
T Moriyama ◽  
T Kaneko ◽  
M Tanaka ◽  
M Kimura ◽  
...  
Keyword(s):  
Recessive Gene ◽  
Mutant Gene ◽  
Inbred Strains ◽  
Lymphoid Hyperplasia ◽  
Lymphoid Cells ◽  
Autoantibody Production ◽  
Genetic Studies ◽  
Inbred Strains Of Mice ◽  
Backcross Populations ◽  
Generalized Lymphadenopathy

Several mice with generalized lymphadenopathy were found in the CBA/KlJms (CBA) colony maintained at our institute. A new mutant strain of mice that develop massive lymphoid hyperplasia at 100% incidence within 5 mo after birth was established by crossing these diseased mice. Genetic studies on lymphadenopathy were conducted in F1, F2, and backcross populations from crosses between mutant CBA (CBA-m) and various inbred strains of mice. The results supported the control of lymphadenopathy by a single autosomal recessive gene. Since C3H/He-gld/gld (C3H-gld), MRL/MpJ-lpr/lpr (MRL-lpr), and C3H/HeJ-lpr/lpr (C3H-lpr) mice develop the same type of lymphoid hyperplasia, allelism of the mutant gene with gld or lpr was tested by investigating lymphadenopathy in F1 and backcross populations from crosses between CBA-m and C3H-gld, MRL-lpr, or C3H-lpr mice. The gene was confirmed to be allelic with lpr but not with gld. Interestingly, however, the mutant gene interacted with gld to induce less severe lymphadenopathy. Thus, the mutant gene was named lprcg, an lpr gene complementing gld in induction of lymphoproliferation. The genetic conclusion was supported by the same profile of surface markers of lymphoid cells with gld/gld, lpr/lpr, lprcg/lprcg, lprcg/lpr, and +/gld +/lprcg genotypes, as well as by massive lymph node hyperplasia and high titers of autoantibodies in the first four genotypes, but slight hyperplasia and insignificant autoantibody production in the last. The discovery of lprcg provided strong genetic evidence for the parallels between anomalous phenotypes of gld and lpr, and CBA/KlJms-lprcg/lprcg mice will contribute to elucidation of the mechanism of induction of the same abnormal differentiation and functions of lymphocytes by gld and lpr.

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