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The incidence and prevalence of inflammatory bowel disease has increased over and typically attributed to gut inflammation and its complications and various extraintestinal manifestations that can be severe. However, the cause-and-effect relationships of such manifestations are remain not fully understood, and the functional state of enterocytes requires detailed study under conditions of experimental glomerulonephritis (EG). Gold nanoparticles (AuNPs) have recently been actively used in different spheres of nanomedicine. Nanoparticles synthesized with polymers as stabilizing agents. Polymer/AuNP systems can become a new preventive and therapeutic agent in the treatment of these disorders. The aim of this study was to establish the regulated cell death of enterocytes of the iliac section small intestine under conditions of experimental glomerulonephritis and treatment with polymer/AuNPs systems in mice. Experiments have been conducted on male Albino white laboratory mice (25-30 g). The animals were divided into following experimental groups: I - control (injected with saline), II -D-g-PAA(PE)/AuNPs was introduced intravenously once a day, five times (at a dose of 9.78 mg/kg, 0,3 ml into the tail vein), III - EG was reproduced by immunizing animals with kidney homogenate, four times intraperitoneally according to the scheme of the experiment, IV - EG + D-g-PAA(PE)/AuNPs - after EG was introduced polymer/AuNPs systems (at a dose of 9.78 mg/kg, 0,3 ml into the tail vein) intravenously once a day, five times. Cell viability was studied using the method of intravital double staining with fluorescent nucleic acid dyes Hoechst 33342 and propidium iodide. For the statistical analysis of the results, Graph Pad Prism, version 8.0.1.244 for Windows (Graph Pad Software, USA) were used. The application of D-g-PAA(PE)/AuNPs caused decrease the number of living cells by 6,73% (р<0.05, n=8). Under conditions of EG the number of living cells decreased by 20,62 %, the number of cells with signs of necroptosis increased by 2,82 times and apoptosis by 2,61 times, compared to the corresponding values in the control (p<0.05, n=8). The treatment with D-g-PAA(PE)/AuNPs under conditions of EG the share enterocytes with apoptosis increased by 22.69% (p<0.05, n=8). Our data suggest that treatment with gold nanoparticles in the polymer matrix D-g-PAA(PE) change regulated cell death of enterocytes under conditions of experimental glomerulonephritis in mice. The obtained data open new perspectives for research on inflammatory bowel diseases an d kidney diseases. [ABSTRACT FROM AUTHOR]

Abstract. Pathogenesis of acute post-streptococcal glomerulonephritis (APSGN), a major complication of group A streptococcal (GAS) throat or skin disease, remains unclear. Over years, various theories were based on distinct streptococcal extracellular factors, as well as immunological mimicry of streptococci for renal tissue antigens was considered. Previously we reported that a lot of clinical GAS isolates with proven nephritogenic ability show a non-immune binding of monomeric or aggregated IgG. Moreover, using a rabbit model of APSGN, we obtained evidence for important causative role of streptococcal IgG Fc-binding proteins (IgG FcBPs) belonging to the M family surface proteins. I.e., rabbits injected by whole IgG FcBP-positive streptococci showed induction of renal glomerular changes, with deposition of IgG and complement C3, resembling the picture recorded in human APSGN. These typical renal changes were always preceded by development of circulating anti-IgG antibodies. Present study was performed in the same rabbit model. Both purified IgG FcBPs isolated from type M22 GAS were found to elicit glomerular degenerative damage of renal glomeruli comparable to those caused by whole bacteria, as well as induce anti-IgG antibodies, deposition of IgG and C3 complement and production of proinflammatory cytokines (IL-1β, TNFα, IL-6) by glomerular mesangial and endothelial cells. By contrast, rabbits injected with proteins A or G, IgG FcBPs of S. aureus and group G streptococci, respectively, exhibited only low levels of circulating anti-IgG and reversible glomerular changes. In these settings, we have not observed any features of membranousproliferative glomerulonephritis (GN) resembling morphological traits of acute post-streptococcal GN in humans. These data correlated with results obtained after injection of intact Staphylococcus aureus (Cowan 1 strain) or group G streptococci (G148 strain). Both microbial types are known to harbor IgG Fc-binding proteins (А and G, respectively). These results support the idea that GAS IgG FcBPs are unique in their ability to initiate strong post-streptococcal glomerular changes and could be considered as important factors in pathogenesis of APSGN similar to acute post-streptococcal GN in humans.

Abstract. In former studies, using an experimental rabbit model of acute post-streptococcal glomerulonephritis (GAS), we have proven a role of M-like Fc-binding streptococcal proteins (IgG FcBPs) for initiating destructive/degenerative lesions of renal glomeruli that are characteristic to membranous/proliferative and destructive glomerulonephritis. This activity was shown for the strains of types 1, 22 and 49. Their clinical isolates are able to bind Fc fragment of human and rabbit IgG, and are considered as an etiological agent of glomerulonephritis. It is well known that GAS strains of M12 serotype (commonly nephritogenic) are not able to interact with IgG monomers, and usually bind aggregated IgG, in spite of participation of IgG FcBPs in the both events.In present study, the GAS reference strain M12(1800) and twenty-one clinical strains of M12 type isolated from the patients with acute poststreptococcal glomerulonephritis (APSGN) were tested for binding with two artificial immune complexes (ICs): (i) peroxidase – antiperoxidase rabbit IgG (PAP) and (ii) tetanus toxoid – anti-tetanus human IgG (TAT). Streptococcal strain M12 (1800), as well as the majority of clinical isolates (19 strains) were strongly positive for the binding of both ICs tested. Using previously described model of experimental streptococcal glomerulonephritis rabbits were injected with heat-killed M12(1800) and each of two clinical isolates M12(257) and M12(305), positive and negative for the binding of ICs, respectively. Renal tissue material of rabbits injected with M12(1800) and M12(257), but not M12(305), showed strong inflammatory and degenerative changes compatible with pattern observed in APSGN. Streptococcal strains M12(1800) and M12(257), in contrast to strain M12(305), induced circulating anti-IgG, tissue deposition of IgG and C3 as well as secretion of IL-1β, Il-6 and TNF-α by the glomerular mesangial and endothelial cells. Our experimental data suggest that the IC-binding ability of type M12 streptococci should be of importance for the nephritogenic potential of these GAS serotype strains.

Se estudió el efecto del ozono por vía rectal a diferentes dosis sobre variables de función renal y la presión arterial sistólica en un modelo de glomerulonefritis tóxica experimental por adriamicina. La glomerulonefritis experimental es causa de insuficiencia renal, caracterizada por un daño renal progresivo. Existen diferentes esquemas de tratamiento, los cuales son muy caros y producen inmunosupresión, que afecta la calidad de vida del paciente. Para desarrollar este trabajo se utilizaron 40 ratas hembras Wistar de 200 g de peso, divididas en 4 grupos, uno control, otro control positivo, que recibieron adriamicina durante un período de 10 semanas, y otros 2 que recibieron terapia con ozono. A todos se les determinó la proteinuria, presión arterial sistólica y diuresis de 24 h. Los resultados mostraron que la terapia con ozono a una dosis de 0,3 mg/kg tuvo efecto renoprotectorThe effect of ozone by rectal route at different doses on variables of renal function and systolic arterial pressure was studied in a model of experimental toxic glomerulonephritis due to adriamicine. Experimental glomerulonephritis causes renal failure and it is characterized by a progressive renal damage. There are different treatment schemes that are very expensive and produce immunosupression, affecting the patient’s quality of life. To develop this work, 40 Wistar rats of 200 g of weight were used. They were dividided into 4 groups: a control group and a positive control group that were administered adriamicine during 10 weeks, and other 2 that received ozone therapy. Proteinuria, systolic arterial pressure and 24-hour diuresis were determined in all of them. The results showed that ozone therapy at a dosis of 0.3 mg/kg had a renal protective effect

It is well known that tissue factor starts the extrinsic coagulation pathway, which activates factor X to Xa, and factor V is a membrane-bound potent cofactor for the terminating stage of prothrombin activation by factor Xa. In a previous in vitro study, factor V was induced in cultured mesangial cells by inflammatory stimulation and increased expression of factor V promoted fibrin generation on the cultured mesangial cell surface. We report that extracellular matrix (ECM) accumulation is increased in association with coagulation in the mesangial area through factor V expression in mesangioproliferative glomerulonephritis (MsPGN). Wistar rats were intravenously injected with rabbit anti-rat thymocyte serum accompanied with or without simultaneous injection of rabbit anti-factor V antibody. Time course study in immunohistochemistry revealed that factor V expression was prominent on day 3 and fibrin-related antigen (FRA) deposition, then ECM accumulation, followed from day 3 to day 8. Massive fibronectin depositions and transforming growth factor (TGF)-β expression were also noted in glomeruli from the disease control group, markedly higher than those in the normal group, and these depositions and expressions were significantly decreased in the anti-factor V neutralizing antibodyinjected group. Northern blot analysis revealed that factor V mRNA expression was prominent on day 3 and was weak on day 8. Doublelabeling experiments revealed the frequent colocalization of α-smooth muscle actin with factor V, FRA, and fibronectin in the same mesangial areas of glomeruli. TGF-β, connective tissue growth factor (CTGF), collagen type IV, and fibronectin mRNA were upregulated in the disease control group, and anti-factor V-neutralizing antibody injection suppressed these mRNA expressions in glomeruli. The present results suggest that ECM components accumulation may progress in accordance with coagulation in the mesangial area through mesangial factor V expression and upregulated expression of TGF-β and CTGF in MsPGN. [ABSTRACT FROM AUTHOR]

Isotretinoin alleviates renal damage in rat chronic glomerulonephritis. Background. Retinoids, derivatives of vitamin A, have strong anti-inflammatory and antiproliferative properties. We previously demonstrated that the pan-agonists all-transretinoic acid (RA) and isotretinoin (13-cis RA) alleviate renal damage in rat acute glomerulonephritis (GN) induced by anti-Thy-1.1 mAb OX-7. Methods. The present study examined the effects of low dose and high dose treatment with isotretinoin in the chronic glomerulonephritis model, Thy-GN. Thy-GN was induced by a single intravenous injection of monoclonal antibody (mAb) 1-22-3 in uninephrectomized Wistar rats (N = 7 to 10 per group). Control and nephritic groups were treated with vehicle (veh), low dose isotretinoin (2 mg/kg body wt), or high dose isotretinoin (10 mg/kg body wt). The experiment was terminated 60 days after induction of Thy-GN. Results. In animals with Thy-GN, isotretinoin abrogated the increase in blood pressure and significantly reduced albuminuria. Glomerulosclerosis index, glomerular and interstitial cell counts, as well as the area of the interstitial space were significantly lower in nephritic rats treated with low and high dose isotretinoin compared to vehicle-treated nephritic controls. Treatment with isotretinoin also significantly reduced the number of glomerular and interstitial macrophages. The increase of transforming growth factor (TGF)-β1, TGF receptor II and prepro-endothelin-1 gene expression in vehicle-treated nephritic rats was significantly attenuated by isotretinoin. Conclusions. Treatment with isotretinoin significantly reduces glomerular and interstitial damage in rats with chronic glomerulonephritis as indicated by different functional and histological markers. Retinoids may provide a novel therapeutic option for the treatment of glomerulonephritis. [ABSTRACT FROM AUTHOR]

The localization of annexin V, a calcium binding protein, was immunochemically and immunohistologically studied in experimental rat glomerulonephritis using annexin V polyclonal antibody. Plasma and urinary annexin V levels were measured by a sandwich enzyme-linked immunosorbent assay (ELISA). Urinary annexin V level, which was correlated with urinary l-lactate dehydrogenase activity, N-acetyl-β- d-glucosaminidase activity and protein level, increased time-dependently after the injection of nephritogenic antigen (bovine glomerular basement membrane), progressively increasing to attain a peak level at 4 weeks of 51.5±11.3 ng/h. However, plasma annexin V level showed no increase during the study period. Normal kidneys showed strong staining for annexin V in distal tubules, being particularly strong in tubules of the inner stripe of the outer medulla, but could not be detected in proximal tubules. Annexin V was seen in visceral epithelial cells, Bowman's capsule of the glomerulus, the vascular endothelium of arterioles and interlobular arteries, and vascular smooth muscle. In nephritis, the lumen of distal tubules and the luminal cell membrane were deeply stained, with leakage of annexin V being observed from tubular cells. In the present study, renal annexin V was markedly excreted into urine, and its urinary level reflected the severity of damage of renal tissue and the progression of nephritis. These changes of annexin V in the distal tubule and visceral epithelial cells may be of significance in cell injury of the kidney. [ABSTRACT FROM AUTHOR]

Immunomorphological analysis of renal tissue from rabbits immunized with group A streptococci differing in the expression of IgG Fc-binding proteins showed that only IgG Fc-positive streptococci induced destructive degenerative changes in the kidneys classified as membranous proliferative glomerulonephritis with symptoms of fibroplastic glomerulonephritis. These morphological changes in renal tissue are comparable to changes in patients with acute poststreptococcal glomerulonephritis. Depositions of IgG and C3 complement component on the basal membrane of renal glomeruli and secretion of antiinflammatory cytokines IL-1ß, IL-6, and TNF-α by mesangial cells were revealed. No destructive changes were found in the kidneys of rabbits immunized with IgG Fc-negative streptococcus strain or isogenic mutant completely devoid of genes responsible for the expression of IgG Fc-binding proteins. Thus streptococcal IgG Fc-binding proteins determine the development of experimental glomerulonephritis in rabbits. [ABSTRACT FROM AUTHOR]

FITC-labelled IgG obtained from patients convalescing from acute poststreptococcal glomerulonephritis (APSGN) stains glomeruli of patients with early APSGN. We previously reported a streptococcal antigen (preabsorbing antigen (PA-Ag)) that preabsorbed the stain out of sera from the convalescent patients and thus prevented glomerular staining. To confirm the nephritogenicity of PA-Ag, we administered up to 40 mg of this antigen to rabbits for 8 days and observed them for up to 9 weeks. Immunohistological analysis showed diffuse and global glomerular staining for C3 without notable staining for γ-globulin. Light microscopic examinations revealed slight to moderate proliferative glomerulonephritis with exudative change. Control rabbits, which received similar doses of bovine serum albumin, did not show significant staining for C3. A transient and significant decrease in CH50 was observed from weeks 3 to 7 (9.7 ± 0.3 U/ml at week 3; normal range 12.9 ± 0.6 U/ml). This experimental model showed a resemblance to immunological and immunohistological features of APSGN in humans. Although the precise mechanisms are yet to be determined, complement activation by PA-Ag seems to hold a key position in this model and in the human disease. [ABSTRACT FROM AUTHOR]

To investigate the role of cytokines in the pathogenesis of experimental glomerulonephrilis (GN), we examined interleukin I (IL-1) activity in isolated glomeruli of rats with an accelerated autologous form of nephrotoxic serum nephritis (NTSN). Glomeruli were isolated and explanted in tissue culture. The prominent feature of the glomerular outgrowth of the glomeruli in the NTSN was the presence of large numbers of type III cells (macrophages). In addition, there were significantly greater numbers of type II (mesangial) cells in culture from the NTSN rats as compared with glomeruli from normal rats, though the numbers of type I (epithelial) cells were the same. IL-1 bioactivity was significantly higher in culture supernatants generated by glomeruli isolated from NTSN animals versus normal animals early in the course of the disease. When glomerular culture supernatants and purified IL-I were pre-incubated with an anti-IL-1β antibody, a parallel decrease of the biological activity was found, suggesting that the biologically active binding sites of the culture supernatants and monocyte-produced IL-1 share some common structure. The administration of a rabbit anti-rat macrophage serum (AMS) prevented the outgrowths of type III cells (macrophages) and type II (mesangial) cells and reduced the production of IL-1 activity in the NTSN rats. In this experimental model IL-I synthesis, probably by multiple cell types, is present early in the disease process and perhaps may be an important mediator of glomerular immune injury. [ABSTRACT FROM AUTHOR]

Experimental immune complex glomerulonephritis was induced with human IgG (HIgG) in two strains of rats. Wistar-King-Aptekman (WKA) and spontaneously hypertensive rats (SHR). The rats were pre-immunized s.c. with 1 mg of HIgG in Freund's complete adjuvant, and 8 weeks later were given a daily i.v. 2 mg of HIgG injections for 4 weeks. Renal tissue, obtained at weekly intervals after the beginning of i.v. injections, was examined by light, immunofluorescence and electron microscopic tests. SHR developed an endocapillary proliferative glomerulonephritis with heavy proteinuria after the administration of HIgG for 4 weeks. They had massive depositions of HigG, rat IgG, and rat C3 both in the mesangial area and along the capillary wall. On the other hand, in WKA rats, the proliferative lesions were scarcely seen and the immune deposits were observed almost exclusively in the mesangium. Moreover, urinary protein excretion of these rats was within normal range. In comparison with bovine serum albumin (BSA) nephritis in SHR. HIgG-induced glomerular lesion was relatively mild. This difference seemed attributable to the nature of the HIgG, such as its molecular weight and immunogenicity. [ABSTRACT FROM AUTHOR]

Bone marrow-derived inflammatory cells contribute to glomerular damage in experimental glomerulonephritis. The time sequential appearance and the pattern of inflammatory cells in the diseased glomerulus is, however, unclear. We therefore characterized the inflammatory cell infiltrate in a model of unilateral immune complex glomerulonephritis. The cellular infiltrate was specific for the diseased kidney and independent of changes in peripheral blood or spleen. We found an influx of leukocyte common antigen (LCa)-positive and EDI-positive (monocytes/macro-phages) cells in isolated glomeruli as early as 24 h after induction of the disease. Lymphocytes of the CD4-, CD8- and CD20-positive phenotypes were present in diseased glomeruli at Day 10. Complement depletion prevented the influx of monocytes/macrophages at 24 h in the glomerulus, which indicates that complement activation is important for the glomerular cell infiltrate at this early time point. The results demonstrate that the inflammatory cell infiltrate is regulated at the glomerular level and not accompanied by similar changes in peripheral blood and spleen cells. [ABSTRACT FROM PUBLISHER]

Mesangial cells (MC) of renal glomeruli respond to immune-inflammatory injury by accelerated proliferation and generation of reactive oxygen metabolites (ROM). We studied in vivo and in vitro roles of cAMP-protein kinase A (PKA) signaling in modulation of these pathobiologic processes with focus on PDE isozymes. Mitogenic synthesis of DNA in mesangial cells grown in primary culture was blocked by forskolin and dibutyryl cyAMP. Incubation of MC with PDE-3 inhibitors, cilostamide and lixazione, inhibited (>50%) mitogenesis, whereas inhibitors of PDE-4, rolipram and denbufylline, caused little or no inhibition. Conversely, inhibitors of PDE-4 suppressed generation of ROM in MC, whereas inhibitors of PDE-3 had no effect. Incubation of mesangial cells with cilostamide or with rolipram increased in situ activity of PKA, and effects of the two inhibitors were additive. PDE inhibitors also decreased activity of mitogen-activated protein kinase. The efficacy of PDE isozyme inhibitors (IC50) to suppress mitogenesis or ROM generation paralleled IC50 for inhibition of cAMP hydrolysis by extracts from mesangial cells. Administration of lixazinone or lixazione in combination with rolipram to rats with mesangial proliferative glomerulonephritis induced by antithymic serum suppressed proliferation of mesangial cells and also reduced other histopathologic manifestations of the disease. Based on these observations, we propose that in MC, a cAMP pool that is hydrolyzed by PDE-3 inhibits by negative crosstalk via activation of PKA, mitogen-activated protein kinase (MAPK) pathway, and mitogenesis; whereas cAMP pool linked to PDE-4 inhibits, also via activation of PKA, ROM generation in mesangial cells. Results also suggest that PDE isozyme inhibitors, in particular inhibitors of PDE-3, should be investigated for potential use for “signal transduction pharmacotherapy” of glomerulonephritis. [ABSTRACT FROM AUTHOR]

Crescentic glomerulonephritis was induced in the rabbit with two intravenous injections of goat nephrotoxic serum (NTS). Prominent proliferative glomerulonephritis, characterized by intracapillary as well as extracapillary emigration of monocytes and fibrin deposition, developed 7 days after the first injection. The changes rapidly progressed to crescent formation. In order to observe alterations of the glomerular basement membrane (GBM) related to crescent formation, unfixed, isolated glomeruli were treated with Triton X-100. The GBM thus denuded was shown to have a number of microperforations, which subsequently became much larger holes or fissures. It is suggested that monocytes and fibrin deposits may play a role in the induction of the GBM change. [ABSTRACT FROM AUTHOR]

During the course of an accelerated form of anti-glomerular basement membrane nephritis in rats, the authors determined the temporal relationships between (a) glomerular hypercellularity, (b) kinetics of cell proliferation and (c) monocyte infiltration in glomeruli. Although glomerular hypercellularity was not appreciable or mild by qualitative histology, mean glomerular cell counts rose between days two and six of nephritis by up to 30% over controls. Cell proliferation in glomeruli was assessed 2 h after pulse label withH-thymidine by determining histoautoradiographic cell labeling indices (LI) and by measuring the total radioactivity of isolated glomeruli (TGA). On day one, mean LI of cells in Bowman's capsule was increased by 356% over controls and fell subsequently. LI values of tuft cells rose more gradually, reaching a maximum increment of 405% on day four. TGA also increased on day one and two, and peaked on day four. In additional rats, studied in parallel,H-thymidine incorporation was measured 48 h after the pulse in order to allow time for the labeling and glomerular influx of monocytes derived from dividing extra-renal precursors. In rats sacrificed on the first day of nephritis, the prolonged labeling time did not result in further gains of tuft LI or of TGA over values obtained 2 h after the pulse. On day four, by contrast, the 48-h labeling time was associated with markedly higher results for LI and TGA than the 2-h interval. These findings indicated that the glomerular influx of labeled blood-borne monocytes was not appreciable on day one but increased markedly between day two and day four. This was supported by histochemical studies for non-specific esterase which revealed a similar time course for the presence of monocytes in glomeruli by showing few esterase-positive monocytes in the early stage and many after day two. The results demonstrate that this model of glomerulonephritis is characterized by markedly enhanced replication of intrinsic glomerular cells, beginning on the first day of the injury at a time when the glomerular influx of monocytes is inconspicuous. Increases of glomerular cell prolifertion become most pronounced over the following days when they are associated with a sizeable monocytic infiltrate. The prominent cellular response in glomeruli is revealed by the applied quantitative methods in the absence of histologically impressive glomerular hypercellularity. [ABSTRACT FROM AUTHOR]

This paper describes the immunopathologic findings in acute malaria-associated glomerulonephritis in the rat. Young Sprague-Dawley rats were infected with Plasmodium berghei berghei. The subsequent parasitemia and elevation of circulating Clq-reactive immune complexes were transient while the appearance of anti-plasmodial antibody in the serum was persistent. Sequential examination of renal tissue and urine revealed the following glomerular alterations: (a) granular, predominantly mesangial deposits of IgG, IgM, and C 3, (b) electron dense deposits in the mesangial matrix, (c) glomerular deposition of plasmodial antigen(s) and of anti-plasmodial antibody as demonstrated by acid elution studies, (d) hypercellularity of the glomerular tufts and (e) increased urinary excretion of high molecular weight proteins. All renal abnormalities were transitory, disappearing within one to three months. The results indicate that this form of acute malarial glomerulonephritis in rats is mediated by immune complexes involving plasmodial antigen. The disease resembles the transient glomerular injury complicating cases of Plasmodium falciparum infection in humans. As an easily reproducible model, rat malarial glomerulonephritis appears most suitable for further immunopathologic and functional studies of post-infectious glomerular disease. [ABSTRACT FROM AUTHOR]

Experimental immune complex glomerulonephritis induced with bovine serum albumin (BSA) or sheep serum (SS) was studied under immunofluorescent, light and electron microscope. Immunofluorescent study revealed fine and coarse granular immunofluorescent deposits along the glomerular basement membrane (GBM). Electron microscopic examination showed humps of electron-dense deposits in the spaces between the processes of the podocyte external to the GBM. Light microscopic examination showed acute proliferative glomerulonephritis. Taking human immune complex glomerulonephritis into account, the results of the present Study are of considerable significance to the further study of etiology, pathogenesis, pathological changes, clinical manifestations, prevention and treatment of glomerulonephritis. In addition, similar results were obtained by using either BSA or SS. Under ordinary conditions, it is suitable to use SS instead of BSA, because the former is easy to get and cheaper. [ABSTRACT FROM AUTHOR]

A study was designed to investigate whether BCG could play a protective role in a rabbit model of mesangial proliferative glomerulonephritis. Fifteen rabbits were immunised with multiple injections of bovine serum albumin and their mononuclear phagocytic system was depressed by endotoxin from E. coli. The rabbits were divided into two groups: Group 1 (n = 7)received intravenous BCG from 3 weeks prior to the pathogenic immunisation and until the end of this period; Group 2 (n = 8) acted as a control and received normal saline.In the BCG group circulating immune complex (CIC) titres were significantly reduced, rabbit IgG deposition in glomeruli was significantly less, and mean glomerular cell counts were significantly less than those in the control group. We conclude that BCG stimulates the mononuclear phagocytic system to remove CIC and reduce the deposition of immune complexes in glomeruli, thereby mitigating the inflammatory response. [ABSTRACT FROM PUBLISHER]