Renal Scarring Is Enhanced by Phorbol Myristate Acetate following Infection with Bacteria with Mannose-Sensitive Pili

Abstract

Renal scarring is considered to develop in the later stages of chronic pyelonephritis. In our experimental model of pyelonephritis, bacteria with mannose-sensitive (MS) pili on their surface promoted renal scarring following inoculation into the renal parenchyma. The administration of cyclophosphamide to induce leukopenia and of superoxide dismutase to inactivate superoxide released from polymorphonuclear leukocytes (PMN) at the infection site suppressed any renal scarring following the infection. Conversely, the administration of phorbol myristate acetate at an early stage of infection significantly enhanced the renal scarring. These findings suggest that the PMNs which infiltrate the infection site and the superoxide they release play an important role in any renal scarring following infection with MS-piliated bacteria.

The role of dexamethasone on decreasing urinary cytokines in children with acute pyelonephritis

“…This leads to a brisk migration of inflammatory cells such as polymorphonuclear leukocytes (PMN) and macrophages to the site of infection [26,27]. In fact, both macrophages and neutrophils may liberate a variety of cytokines, metabolites of arachidonic acid, and noxious inflammatory mediators such as oxygen radicals and lysosomal enzymes during the process of phagocytosis, which also may account for the deleterious effects to host cells, including tissue damage and scar formation [27][28][29][30]. By then, macroscopic and microscopic examinations demonstrate abscess formation with corresponding focal suppurative necrosis of kidney structures [21,26].…”

“…Inhibition of acute inflammation in experimental models by cyclophosphamide-induced neutropenia [29], antioxidant therapy with superoxide scavengers such as superoxide dismutase [33], ascorbic acid and ebselen [34], and even complement depletion with cobra venom factor [35] have all been reported to reduce kidney damage after infection. Other studies with oxytocin [28], melatonin [24,27], pentoxifylline [36], vitamin A [37], and montelukast [30] (a selective leukotriene CyslT1 receptor antagonist) showed the same result.…”

Experimental Study of Ascending <i>Candida albicans</i> Pyelonephritis Focusing on the Hyphal Form and Oxidant Injury

“…In this way, the pathogenicity of the hyphal form is thought to be marked [7][8][9][10][11], although this has not yet been clari fied by any experimental study reported in the literature. In addition, although the leukocytes appearing at sites of inflammation in bacterial [12,13] as well as Candida infections [14] exert a bacterio-and fungicidal action as part of the host's defense mechanism, the oxygen radicals generated at the same time in association with the respira tory burst of leukocytes may induce tissue injury [15,16]. However, few reports are available on oxidant injury in renal tissue in pyelonephritis [17] and none on oxidant injury in Candida pyelonephritis.…”