Experimental Escherichia coli ascending pyelonephritis in rats: active peroral immunization with live Escherichia coli

Mattsby‐Baltzer, Inger; Hanson, Lars Å.; Olling, S; Kaijser, B

doi:10.1128/iai.35.2.647-653.1982

Cited by 35 publications

(5 citation statements)

References 29 publications

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“…characterized and monoclonal antibodies to Ta antigens and different T-cell subsets are available, experimental UTI in this species would seem to be a suitable model for the study of cellular immune response in the urinary tract. Ascending UTI in rats has proved to be a useful experimental model in several applications bearing on specific immune response to bacterial antigen (16,17), and it was shown in this study that the attack rate and antibody response seemed to correlate reasonably well with previous findings (13,17), indicating that a humoral immune response that must have a cellular basis has taken place in the animals. Some differences in distribution of lymphoid cells between bladder and kidney tissues were observed.…”

Section: Discussionsupporting

confidence: 74%

Local cellular immune response in ascending urinary tract infection: occurrence of T-cells, immunoglobulin-producing cells, and Ia-expressing cells in rat urinary tract tissue

Hjelm¹

1984

Infect Immun

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The local immune response was studied in rats with ascending urinary tract infection that was induced by Escherichia coli 06K13H1. The occurrence in urinary tract tissue of cells reacting with monoclonal antibodies to T-cell markers and Ia antigen and with antibodies to immunoglobulin G (IgG), IgM, and IgA was studied by immunohistochemical methods. Serum antibody response and antibody coating of bacteria in the urine were also followed. Infection increased the number of irregular Ia-expressing cells in both bladder submucosa and the intertubular space in the kidney. The epithelial cells of some tubules were induced to express Ia antigens. A slight increase of what were most probably T-"helper" cells in the bladder was noted during the initial phase of infection. These cells soon disappeared, and there was instead an increase in irregular W3/25-reactive cells that may be identical to the observed Ia-positive cells. In the pyelonephritic lesions there were large amounts of T-cells, mainly T-helper cells, Ia-expressing cells, both rounded and irregular, and also IgGand IgM-producing cells. IgA-producing cells were demonstrated in the infected bladders. The results indicate that distinct differences exist between the immune reactions in bladder and kidney tissue which may be important for the development of infections in these organs.

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Section: Discussionsupporting

confidence: 74%

Local cellular immune response in ascending urinary tract infection: occurrence of T-cells, immunoglobulin-producing cells, and Ia-expressing cells in rat urinary tract tissue

Hjelm¹

1984

Infect Immun

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“…The differences observed here between nasal and oral vaccination are too small for us to state that the two routes differ in their capacity to evoke an antibody response in the male urogenital tract. Mattsby-Baltzer et al demonstrated protection against urinary tract infection after oral immunization in rodent models (19), and placebo-controlled clinical trials with patients with recurrent urinary tract infection have shown that membrane proteins of gram-negative bacteria given orally are effective in decreasing the incidence of infectious episodes (11). The mechanism is supposed to be production of antibodies on the epithelium of the urinary tract inhibiting the binding of the bacteria to the cells (33).…”

Section: Discussionmentioning

confidence: 99%

Antibody Responses in the Lower Respiratory Tract and Male Urogenital Tract in Humans after Nasal and Oral Vaccination with Cholera Toxin B Subunit

1999

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Nasal vaccine delivery is superior to oral delivery in inducing specific immunoglobulin A (IgA) and IgG antibody responses in the upper respiratory tract. Although an antibody response in the nasal passages is important in protecting against primary colonization with lung pathogens, antibodies in the lungs are usually required as well. We immunized 15 male volunteers twice nasally or orally with cholera toxin B subunit (CTB) and determined the specific antibody levels in serum, bronchoalveolar lavage (BAL) fluid, and urine before and 2 weeks after immunization. Nasal immunization induced fivefold increases in the levels of specific IgA antibodies in BAL fluid of most volunteers, whereas there were no significant specific IgA responses after oral immunization. The specific IgG antibody level increased eightfold in BAL fluid in the nasally vaccinated subjects, and the major part of IgG had most probably been transferred from serum. Since the specific IgG response in serum was lower in the individuals vaccinated orally, the IgG response in BAL fluid in this group was also lower and not significant. In conclusion, nasal immunization is also preferable to the oral route when vaccinating against lower respiratory tract infections, and a systemic immune response is considerably more important in the lower than in the upper respiratory tract. Moreover, both nasal and oral immunizations were able to stimulate 6- to 10-fold specific IgA and IgG responses in urine in about half of the individuals, which indicates that distant mucosal vaccination might be used to prevent adhesion of pathogens to the urogenital tract.

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“…Bacterial Strains. The pyelonephritogenic E. coli strain ARD6, serotype O6K13H1 [12] was used in this study. Some of the common uropathogenic virulence factors have been found in E. coli ARD6, including CNF1, •-hemolysin, type 1C pili and afimbrial adhesin; type 1 (fim A) and P-fimbriae were not detected.…”

Section: Methodsmentioning

confidence: 99%

Prenatal Exposure to High Level of Glucocorticoids Increases the Susceptibility of Renal Proximal Tubular Cells to Apoptosis Induced by Uropathogenic <i>Escherichia coli</i> Toxins

Chen

Bao²,

Ceccatelli³

et al. 2004

Am J Nephrol

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Prenatal exposure to excessive glucocorticoids may alter the developing fetus inducing metabolic and endocrine imbalance in various organs, including the kidney. This study aimed at evaluating whether prenatal exposure to high levels of glucocorticoids adversely affects renal cell survival and predisposes to renal cell death. Pregnant rats were injected with 0.1 mg/kg dexamethasone (DEX) i.p. from day 1 of gestation. Renal proximal tubular cells (PTCs) were prepared from 20-day-old offspring in the DEX (DEX cells) and control groups (CON cells). After 4 days’ culture, cells were exposed to uropathogenic Escherichia coli ARD6 toxins at concentrations known to induce apoptotic cell death. We found that cell death rate was significantly higher in DEX than in CON cells. Cells exhibited morphological and biochemical features of apoptosis. Conversely, the activity of the antioxidant enzyme catalase was significantly increased in renal cortex homogenate from 20-day-old DEX rats. The antioxidant vitamin E did not prevent apoptosis. These results indicate that prenatal exposure to high levels of glucocorticoids induces alterations in renal PTCs rendering them more sensitive to E. coli toxins via nonoxidative stress. With the increasing use of multiple doses of glucocorticoids in preterm infants, the possibility that antenatal glucocorticoids may lead to renal adverse consequences is of clinical relevance.

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Experimental Escherichia coli ascending pyelonephritis in rats: active peroral immunization with live Escherichia coli

Cited by 35 publications

References 29 publications

Local cellular immune response in ascending urinary tract infection: occurrence of T-cells, immunoglobulin-producing cells, and Ia-expressing cells in rat urinary tract tissue

Local cellular immune response in ascending urinary tract infection: occurrence of T-cells, immunoglobulin-producing cells, and Ia-expressing cells in rat urinary tract tissue

Antibody Responses in the Lower Respiratory Tract and Male Urogenital Tract in Humans after Nasal and Oral Vaccination with Cholera Toxin B Subunit

Prenatal Exposure to High Level of Glucocorticoids Increases the Susceptibility of Renal Proximal Tubular Cells to Apoptosis Induced by Uropathogenic <i>Escherichia coli</i> Toxins

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