Experimental Pyelonephritis: A New Method for Inducing Pyelonephritis in the Rat

Miller, Thomas E.; Robinson, K. B.

doi:10.1093/infdis/127.3.307

Cited by 56 publications

(19 citation statements)

References 2 publications

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“…In the experimental group 100 pi of a 105 Escherichia coli suspension was inoculated directly into the left renal cortex under general anesthesia according to the method of Miller et al [14] and Miller and Robinson [17], TheE. coli strain used for inoculation was derived from the urine of a patient with radiologically proven pyelonephritic scars.…”

Section: Experimental Pyelonephritismentioning

confidence: 99%

Interstitial Myof ibroblasts in Experimental Renal Infection and Scarring

Hewitson

Becker

1995

Am J Nephrol

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We have examined the temporal and spatial distribution of myofibroblast-like cells, a phenotype with fibroblast and smooth muscle features, in an experimental model of renal infection. Escherichia coli organisms (10⁵) were inoculated directly into the renal cortex of Sprague-Dawley rats weighing 270 g. Saline was substituted in a control group. The animals were sacrificed at five time points up to day 24 (E. coli n = 8, controls n = 3 each interval). Myofibroblasts were identified by morphology and immunohistochemistry for alpha smooth muscle actin (Α-SMA) and compared with staining for monocytes (ED-1), collagen III, and bromodeoxyuridine incorporation. Histological changes included a focal lesion in E. coli infected animals. Interstitial Α-SMA staining was confined to spindle-shaped cells resembling myofibroblasts. The percent fractional area of Α-SMA staining in the lesion increased from 0.12 ± 0.09 at day 1 to 20.0 ± 7.1 at day 3 (p < 0.005), decreasing progressively to 2.0 ± 2.6 by day 24. This paralleled bromodeoxyuridine incorporation in myofibroblasts: 0.4 ± 0.5 cells/0.25 mm² at day 1, 105.0 ± 36.3 at day 3, and 2.6 ± 2.2 cells/0.25 mm² at day 24. ED-1-positive cells increased from 374 ± 200/ 0.25 mm² at day 1 to 894 ± 88 at day 3 (p < 0.01), declining to 230 ± 108/ 0.25 mm² by day 24. Intracellular collagen III and Α-SMA stainings were colocalized at day 3. The fractional area of collagen III increased by day 24 (p < 0.05). In conclusion, myofibroblasts accumulate transiently during renal interstitial fibrosis and are derived at least in part from local proliferation. Double labeling suggests that myofibroblasts may be synthetically active.

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Section: Experimental Pyelonephritismentioning

confidence: 99%

Interstitial Myof ibroblasts in Experimental Renal Infection and Scarring

Hewitson

Becker

1995

Am J Nephrol

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“…Pyelonephritis was induce(d bN (lirect inoculationi of E. coli into the surgically exposedl kidney. Details of this metho(d halve been given previoulsly (9 (Fig. 3).…”

Section: Methodsmentioning

confidence: 99%

Suppressor cell regulation of cell-mediated immune responses in renal infection in vitro modulation of suppressor cell activity.

Miller¹,

Marshall²

1980

J. Clin. Invest.

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Hospital, Aucklanid, News Zeala 11(d A B S T R A C T Infection-induced anergy is a fre(luent complication of bacterial, viral, and parasitic infection. A marked suppression of the thymus-derived (T) lymphocyte response to concanavalini A has been demonstrated in vitro during renal infection and the mechaniismiis by which suppressioni occurs have been investigated. In particular we have considered the possibility that suppressioni might result from the inhibitory effect of prostaglandins, secreted by activated macrophages with immunoregulatory potential. The experiments have shown that the T-lymphocyte effector status in experimentally-induced renal infection is determined by two suppressor cells, one infectioni-induced and the other naturally occurring. The inability to respond to mitogenic stimulation was reversible and restoration of immnune responsiveness to splenic lymphocytes from infected animals could be achieved in two stepwise manipulations; differential centrifugation removed the infection-induced suppressor cells, and the suppressor activity of the naturally occurring suppressor cells could then be inhibited by indomethacin. Thus the two suppressor cells were distinguishable on the basis of their physical characteristics and their response to indomethacin. The dominant factor determininig the immune responsiveness of splenic lymphocytes from the pyelonephritic animals was, however, the infection-induced suppressor cell. This cell has been characterized as a sedimentable cell (30 g) with suppressor activity demonistrable in coculture experiments. Plastic-adherent cells from the sedimentable fraction of pyelonephritic animals' splenic cells were shown to have suppressor activity that was not inhibited by indomethacin. The infection-induced and naturally occurring suppressor cells can be viewed as prototypes for the equivalent cells in man and may be useful models for studying the

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“…To in vestigate the importance of nonviablc bacte ria in the pathogenesis of renal tubular cell death, heat-killed bacteria and their compo nents have been experimentally introduced into the host's kidney [44], Direct inoculation of nonviable E. coli into the parenchyma re sulted in pyelonephritic-like lesions which were less severe in immunosuppressed ani mals [45]. This finding indicates that bacte rial antigenic components and the host's im mune response are both critical in the patho genesis of pyelonephritis.…”

Section: Immunobiology Of Gram-negative Bacteria and Their Antigenic mentioning

confidence: 99%

Medical Progress: Immunobiology and Genetic Factors in the Pathogenesis of Pyelonephritis

Hemstreet

Cruse

Feye

1984

Pathol Immunopathol Res

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Experimental Pyelonephritis: A New Method for Inducing Pyelonephritis in the Rat

Cited by 56 publications

References 2 publications

Interstitial Myof ibroblasts in Experimental Renal Infection and Scarring

Interstitial Myof ibroblasts in Experimental Renal Infection and Scarring

Suppressor cell regulation of cell-mediated immune responses in renal infection in vitro modulation of suppressor cell activity.

Medical Progress: Immunobiology and Genetic Factors in the Pathogenesis of Pyelonephritis

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