Interstitial Mononuclear Infiltration Research Articles

A potential defensive role of TIM-3 on T lymphocytes in the inflammatory involvement of diabetic kidney disease.

The aberrant mobilization and activation of various T lymphocyte subpopulations play a pivotal role in the pathogenesis of diabetic kidney disease (DKD), yet the regulatory mechanisms underlying these processes remain poorly understood. Our study is premised on the hypothesis that the dysregulation of immune checkpoint molecules on T lymphocytes disrupts kidney homeostasis, instigates pathological inflammation, and promotes DKD progression. A total of 360 adult patients with DKD were recruited for this study. The expression of immune checkpoint molecules on T lymphocytes was assessed by flow cytometry for peripheral blood and immunofluorescence staining for kidney tissue. Single-cell sequencing (scRNA-seq) data from the kidneys of DKD mouse model were analyzed. Patients with DKD exhibited a reduction in the proportion of CD3+TIM-3+ T cells in circulation concurrent with the emergence of significant albuminuria and hematuria (p=0.008 and 0.02, respectively). Conversely, the incidence of infection during DKD progression correlated with an elevation of peripheral CD3+TIM-3+ T cells (p=0.01). Both univariate and multivariate logistic regression analysis revealed a significant inverse relationship between the proportion of peripheral CD3+TIM-3+ T cells and severe interstitial mononuclear infiltration (OR: 0.193, 95%CI: 0.040,0.926, p=0.04). Immunofluorescence assays demonstrated an increase of CD3+, TIM-3+ and CD3+TIM-3+ interstitial mononuclear cells in the kidneys of DKD patients as compared to patients diagnosed with minimal change disease (p=0.03, 0.02 and 0.002, respectively). ScRNA-seq analysis revealed decreased gene expression of TIM3 on T lymphocytes in DKD compared to control. And one of TIM-3's main ligands, Galectin-9 on immune cells showed a decreasing trend in gene expression as kidney damage worsened. Our study underscores the potential protective role of TIM-3 on T lymphocytes in attenuating the progression of DKD and suggests that monitoring circulating CD3+TIM3+ T cells may serve as a viable strategy for identifying DKD patients at heightened risk of disease progression.

Sage (Salvia officinalis) alleviates trazadone induced rat cardiotoxicity mediated via modulation of autophagy and oxidative stress.

The antidepressant drug trazodone (TRZ) is commonly used for treating depression, anxiety, and insomnia, however, it causes cardiotoxicity, which is one of its limitations. The objective of this work was to investigate the impact of sage (Salvia officinalis) in rats against cardiotoxicity induced by TRZ and to investigate the mechanisms involved in its cardio-protective properties through autophagy and oxidative stress. Fifty male albino rats were split randomly into five experimental groups: control group, sage oil group (100 mg/kg), TRZ group (20 mg/kg), protective group, and curative group. Cardiac function biomarkers (aspartate aminotransferase [AST], creatine kinase-MB [CK-MB], and cardiac troponin T [cTnI]) were assessed in serum. Oxidative stress and inflammatory biomarkers in cardiac tissue (total antioxidant capacity, malondialdehyde, and tumor necrosis factor-α) were evaluated. Heart tissues were subjected to histological, immunohistochemical, and ultrastructural evaluations. DNA damage also evaluated. Significant rise in the levels of AST, CK-MB, and cTnI were observed with enhanced autophagy along with marked histopathological changes in the form of interrupted muscle fibers with wide interstitial spaces with areas of hemorrhage and extravasated blood and interstitial mononuclear cellular infiltration in TRZ group. DNA damage was also significantly increased in TRZ group. However, administration of sage in both protective and curative groups show marked improvement of the cardiac alterations. In conclusion, sage ameliorated the alterations in the heart induced by trazadone through modulation of autophagy and oxidative stress.

The Effect of Covid-19 on the Respiratory System

This study aims to assess the risk factors associated with COVID-19 patients at the General Basrah Hospital from June to October 2020. Since COVID-19 is related to acute respiratory distress syndrome, very few interstitial mononuclear inflammatory infiltrates were detected within the heart tissue samples during the research period [3]. The results of the study demonstrate that COVID-19 infections were more common in patients with cardiovascular diseases and acute respiratory. People aged >51 years showed a higher COVID-19 infection rate. Conclusions: The study demonstrates that COVID-19 infection rates were higher in patients with cardiovascular and acute respiratory diseases. Covid 19 posed a similar risk to males and women.

Pathohistological changes in aborted foetuses of cows due to neosporosis: Evidence from Ukraine

Neosporosis is a parasitic disease characterized by abortions and the birth of weak offspring in cows. The causative agent of Neospora caninum is an obligate, protozoan parasite that belongs to the type Apicomplexa. The relevance of the study is conditioned upon the adverse impact of neosporosis on the economy of Ukraine (loss of productivity, veterinary and diagnostic costs). Furthermore, the issue of neosporosis is understudied. In this regard, the purpose of this study was to establish pathohistological changes in aborted foetuses and the foetal part of placentas and to confirm the involvement of the parasite (Neospora caninum) in cases of abortions recorded in different regions of the country. Two methods were used to investigate this problem: histological and real-time polymerase chain reaction. In aborted foetuses positive for N. caninum, the following pathohistological changes were most often detected: focal gliosis and perivascular mononuclear infiltrates in the brain; focal or diffuse mononuclear infiltration in the heart and skeletal muscles; periportal mononuclear infiltrates in the liver; focal necrosis of the mucous membrane and mononuclear infiltration in the foetal part of the placenta. Changes were less often detected in the lungs – mononuclear infiltration of the interstitium and diffuse lymphocytic alveolitis, and in the kidneys – diffuse interstitial mononuclear infiltration. No changes were found in the spleen. Neospore-like cysts were found in one out of twelve foetuses. Lesions established of foetal organs and placentas are inherent in neosporosis. The results of histological studies substantially complement the data of other authors, confirm the involvement of N. caninum in the occurrence of abortions in cows in certain regions of Ukraine, and also represent practical value for the diagnosis and control of neosporosis in cattle

Spectrum of lung pathology in medicolegal autopsies at rural teaching hospital

Background: Lungs are the major organs involved by a number of infectious, inflammatory and occupational hazards. They are also involved secondarily by all forms of terminal events like cardiovascular events. Autopsy is a part of pathology that serves as an important tool to identify the cause and manner of death and to learn about methods to prevent them. Methods: This is a retrospective study conducted on the autopsy specimens received in the department of pathology from 1 January 2020 to 31 December 2021. Gross findings were noted at the time of autopsy and the specimen was subjected to routine histopathological processing and hematoxylin and eosin staining. Histopathological findings were noted. Results: Out of total 78 cases, 30.17% shows Congestion and oedema, 24.65% shows Pneumonia. 10.95% and 8.21% shows interstitial changes in the form of interstitial pneumonia or mononuclear interstitial infiltrate and Diffuse alveolar damage respectively, 6.84% shows emphysematous changes and 5.84% shows chronic passive venous congestion. 4.1% cases shows findings of tuberculosis and only 1 case was of lung abscess, metastatic papillary renal cell carcinoma and fibrin thrombi each. Highest number of cases (32) belonged to 16-30 age group. Least number of cases (2) were from >75 age group.

High phosphate-induced progressive proximal tubular injury is associated with the activation of Stat3/Kim-1 signaling pathway and macrophage recruitment.

Dietary phosphate intake in the Western population greatly exceeds the recommended dietary allowance and is linked to enhanced cardiovascular and all-cause mortality. It is unclear whether a chronic high phosphate diet (HPD) causes kidney injury in healthy individuals. Here, we show that feeding a 2% HPD in C57BL/6N mice for one up to six months resulted in hyperphosphatemia, hyperphosphaturia, increased plasma levels of fibroblast growth factor (FGF) 23, and parathyroid hormone (PTH) compared to mice on a 0.8% phosphate diet. Kidney injury was already noted after two months of HPD characterized by loss of proximal tubular (PT) cell polarity, flattened epithelia, disruption of brush border membranes, vacuolization, increased PT cell proliferation, marked interstitial mononuclear infiltration, and progressive accumulation of collagen fibers. HPD increased Stat3 activation and Kim-1 expression in PT epithelial cells and enhanced renal synthesis of chemokines recruiting monocytes and macrophages as well as macrophage related factors. Enhanced recruitment of F4/80+ macrophages around injured PT lesions was timely associated with increased Kim-1 synthesis, tubular MCP-1 expression, and degree of PT injury score. Likewise, tubulointerstitial fibrosis was associated with activation of Stat3/Kim-1 signaling pathway. The stimulation of human proximal tubular cells with high phosphate activated Stat3 signaling and induced HAVCR1 and CCL2 expression. We conclude that high phosphate results in progressive proximal tubular injury, indicating that high dietary phosphate intake may affect kidney health and therefore represents an underestimated health problem for the general population.

Bronchopneumonia in sheep associated with Providencia stuartii

Bacteria of the genus Providencia are opportunistic pathogens in humans, widely distributed in the environment and associated with greater resistance to antibiotics, and this being uncommon the association with clinical diseases. This study reports the isolation of P. stuartii in two sheep that presented clinical signs of pneumonia. At necropsy there was severe and acute fibrinopurulent bronchopneumonia. Histologically, there were infiltrated neutrophils and fibrin in the alveolar lumen, and the alveolar septa presented multifocal thickening with moderate proliferation of pneumocytes and mononuclear interstitial infiltrate. Providencia sp. was isolated in the microbiological tests of the lung and tracheal secretions. The isolate was subjected to DNA extraction, polymerase chain reaction (PCR) for the 16SrRNA gene and sequencing of genomic DNA, which demonstrated 100% homology with P. stuartii. This is the first report of the presence of this microorganism as a cause of interstitial and fibrinopurulent bronchopneumonia in sheep. Therefore, it is suggested that epidemiological surveillance strategies should be carried out in animals to better understand their role in the dissemination of this pathogen.

BIRD FANCIER'S DISEASE: A CASE OF HYPERSENSITIVITY PNEUMONITIS

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: The immunologic lung disease through inhalation and sensitization of an aerosolized antigen is termed hypersensitivity pneumonitis (HP). Here we describe a case of HP from exposure to avian antigen. CASE PRESENTATION: A 42 y/o F presented with progressively worsening dyspnea at rest & exertion, pleuritic chest pain, dry cough for past 2 months. She denied sick contacts or recent travel. On exam BP: 122/76mmHg, HR 107bpm, RR 30bpm, SpO2 82% on room air. Physical exam, significant for b/l crackles. Labs: WBC 16.33 k/mm3, ABG PaO2 of 45mmHg. CXR showed b/l airspace opacities & CT-thorax showed b/l diffuse GGO. ECHO showed LVEF 55% with normal global systolic function with mildly elevated PASP. Treatment was initiated with hi-flo oxygen and her SpO2 improved to 97%. QuantiFERON Gold, urine legionella, Mycoplasma IgM, and respiratory multiplex viral panel were negative. Cardiac CT revealed patent coronaries. Spirometry revealed severe restrictive ventilatory defect. Further questioning revealed that patient got parakeets a few months prior to onset of symptoms. She was then started on methylprednisolone for possible HP. Bronchoscopy with BAL and transbronchial biopsies showed no bacterial/fungal/viral growth. Cytology was unremarkable and biopsies revealed mild inflammatory changes with lymphocytes and aggregates of intralaveolar foamy macrophages. The CD4:CD8 ratio was 0.89. Patient clinically improved with steroid therapy and gradually weaned from supplemental oxygen. She was discharged on oral prednisone with close follow up where she continued to improve after removal of her parakeets DISCUSSION: HP an immune-mediated response from repeated inhalation, sensitization, & hyperresponsiveness to various organic particles which can be mammalian or avian proteins, fungi, bacterial, or chemicals. Based on duration of exposure & symptoms onset, HP can be divided into acute, subacute, or chronic. Acute HP presents as flu-like illness, subacute HP has insidious onset of symptoms, dyspnea on exertion or reduced exercise capacity. Physical exam reveals inspiratory crackles. Imaging usually demonstrates GGO, mosaic attenuation and centrilobular nodules. BAL reveals lymphocytic predominant cells with CD8 alveolitis. Histopathology usually demonstrates cellular bronchiolitis with predominant lymphocytic or plasmocytic infiltrates. It can also present as interstitial mononuclear infiltrates or loosely-formed granulomas. Treatment for HP is avoidance of antigen exposure. Role of steroids in treating HP is not well known, however general practice is slow tapering steroid regimen for about 3-6 months duration. Prognosis is usually good with complete recovery in most patients; a few may progress to chronic fibrosing HP. CONCLUSIONS: A high level of suspicion should be present in diagnosing HP with a thorough history and prompt management must be initiated to prevent progression of disease. REFERENCE #1: Selman M, Pardo A, King TE Jr. Hypersensitivity pneumonitis: insights in diagnosis and pathobiology. Is J Respir Crit Care Med. 2012; 186:314-24. REFERENCE #2: Costabel U, Bonella F, Guzman J. Chronic hypersensitivity pneumonitis. Clin Chest Med. 012; 33:15163. REFERENCE #3: Camarena A, Juárez A, Mejía M, Estrada A, Carrillo G, Falfán R, Zuñiga J, Navarro C, Granados J, Selman M. Major histocompatibility complex and tumor necrosis factor-alpha polymorphisms in pigeon breeder's disease. Am J Respir Crit Care Med. 2001;163:1528-33. DISCLOSURES: no disclosure on file for Jagadish Akella; No relevant relationships by Alex Diaz, source=Web Response no disclosure on file for Iqbal Javed; No relevant relationships by Raghavendra Sanivarapu, source=Web Response

Fatal lymphocytic cardiac damage in coronavirus disease 2019 (COVID-19): autopsy reveals a ferroptosis signature.

AimsCardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID‐19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism in COVID‐19 lethal cardiogenic shock.Methods and resultsWe report on a 48‐year‐old male COVID‐19 patient with cardiogenic shock; despite extracorporeal life support, dialysis, and massive pharmacological support, this rescue therapy was not successful. Severe acute respiratory syndrome coronavirus 2 RNA was detected at autopsy in the lungs and myocardium. Histopathological examination revealed diffuse alveolar damage, proliferation of type II pneumocytes, lymphocytes in the lung interstitium, and pulmonary microemboli. Moreover, patchy muscular, sometimes perivascular, interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in the cardiac tissue. The lymphocytes ‘interlocked’ the myocytes, resulting in myocyte degeneration and necrosis. Predominantly, T‐cell lymphocytes with a CD4:CD8 ratio of 1.7 infiltrated the interstitial myocardium, reflecting true myocarditis. The myocardial tissue was examined for markers of ferroptosis, an iron‐catalysed form of regulated cell death that occurs through excessive peroxidation of polyunsaturated fatty acids. Immunohistochemical staining with E06, a monoclonal antibody binding to oxidized phosphatidylcholine (reflecting lipid peroxidation during ferroptosis), was positive in morphologically degenerating and necrotic cardiomyocytes adjacent to the infiltrate of lymphocytes, near arteries, in the epicardium and myocardium. A similar ferroptosis signature was present in the myocardium of a COVID‐19 subject without myocarditis. In a case of sudden death due to viral myocarditis of unknown aetiology, however, immunohistochemical staining with E06 was negative. The renal proximal tubuli stained positively for E06 and also hydroxynonenal (4‐HNE), a reactive breakdown product of the lipid peroxides that execute ferroptosis. In the case of myocarditis of other aetiology, the renal tissue displayed no positivity for E06 or 4‐HNE.ConclusionsThe findings in this case are unique as this is the first report on accumulated oxidized phospholipids (or their breakdown products) in myocardial and renal tissue in COVID‐19. This highlights ferroptosis, proposed to detrimentally contribute to some forms of ischaemia–reperfusion injury, as a detrimental factor in COVID‐19 cardiac damage and multiple organ failure.

Adverse effects of sympathetic activation should not be neglected during the coronavirus disease 2019 pandemic.

Adverse effects of sympathetic activation should not be neglected during the coronavirus disease 2019 pandemic.

High Prevalence of Concurrent Gastrointestinal Manifestations in Patients With Severe Acute Respiratory Syndrome Coronavirus 2: Early Experience From California

High Prevalence of Concurrent Gastrointestinal Manifestations in Patients With Severe Acute Respiratory Syndrome Coronavirus 2: Early Experience From California

Compound K inhibits priming and mitochondria-associated activating signals of NLRP3 inflammasome in renal tubulointerstitial lesions.

Renal tubulointerstitial lesions (TILs), a key pathological hallmark for chronic kidney disease to progress to end-stage renal disease, feature renal tubular atrophy, interstitial mononuclear leukocyte infiltration and fibrosis in the kidney. Our study tested the renoprotective and therapeutic effects of compound K (CK), as described in our US patent (US7932057B2), on renal TILs using a mouse unilateral ureteral obstruction (UUO) model. Renal pathology was performed and renal draining lymph nodes were subjected to flow cytometry analysis. Mechanism-based experiments included the analysis of mitochondrial dysfunction, a model of tubular epithelial cells (TECs) under mechanically induced constant pressure (MICP) and tandem mass tags (TMT)-based proteomics analysis. Administration of CK ameliorated renal TILs by reducing urine levels of proinflammatory cytokines, and preventing mononuclear leukocyte infiltration and fibrosis in the kidney. The beneficial effects clearly correlated with its inhibition of: (i) NF-κB-associated priming and the mitochondria-associated activating signals of the NLRP3 inflammasome; (ii) STAT3 signalling, which in part prevents NLRP3 inflammasome activation; and (iii) the TGF-β-dependent Smad2/Smad3 fibrotic pathway, in renal tissues, renal TECs under MICP and/or activated macrophages, the latter as a major inflammatory player contributing to renal TILs. Meanwhile, TMT-based proteomics analysis revealed downregulated renal NLRP3 inflammasome activation-associated signalling pathways in CK-treated UUO mice. The present study, for the first time, presents the potent renoprotective and therapeutic effects of CK on renal TILs by targeting the NLRP3 inflammasome and STAT3 signalling.

Role of Different Doses of Vitamin E in Protection Against Isoproterenol-Induced Myocardial Damage in Adult Male Albino Rat: A Light and Electron Microscopic Study

Introduction: Cardiovascular diseases are one of the most common diseases in the world. It is essential to find an efficient natural protective agent against the myocardial damage.Aim: To determine the protective role of different doses of vitamin E against isoproterenol-induced myocardial damage.Material and Methods: Fifty adult male albino rats were divided into four main groups: Control group (I), vitamin E-treated group (II) equally divided into 2 subgroups; subgroup (IIa) received Vit E (50mg/kg) and subgroup (IIb) received Vit E (100mg/kg) for one month, isoproterenol-treated group (III) received 3ml normal saline orally for one month and isoproterenol (150mg/kg) intraperitoneally (IP) in the last two days of that month. Vitamin E and isoproterenol-treated group (IV) equally divided into two subgroups; Subgroup (IVa) received vitamin E (50mg/kg) orally for one month and isoproterenol (150mg/kg) IP in the last two days of that month and subgroup (IVb) received vitamin E (100mg/kg) orally for one month and isoproterenol (150mg/kg) IP in the last two days of that month. Heart specimens were processed for light and electron microscopic studies.Results: Rats injected by isoproterenol developed structural changes in the myocardium in the form of fragmentation of the myofibrils, vacuolated destroyed mitochondria, dilated SER, intracellular and extracellular edema and interstitial mononuclear cellular infiltration. Animals pretreated with vitamin E at a dose of 50mg/kg before injection of isoproterenol revealed minimal protection as they showed myocardial damage similar to isoproterenol-treated group. While animals pretreated with vitamin E at a dose of 100 mg/kg before injection of isoproterenol showed minimal microscopic alterations of the myocardium with preservation of the normal structure of the cardiac myocytes.Conclusion: Vitamin E at a high dose (100mg/kg) has a protective role on myocardium against isoproterenol- induced myocardial damage.

Molecular effect of human umbilical cord blood CD34-positive and CD34-negative stem cells and their conjugate in azoospermic mice.

Currently, azoospermia is one of the most common diseases of male infertility. Stem cell research is the new hope for novel therapy with a higher degree of safety and lower cost. This study aimed to investigate the effect of umbilical cord blood-derived stem cells (" and mesenchymal "UCB-MSCs") and mono-cell layer implanted into the induced azoospermic mice testis. Stem cells were isolated from umbilical cord blood and CD34+ve cells were separated from negative one by Mini MACs column. At 5th week after single injection of busulfan, stained mesenchymal (CD34-ve), hematopoietic stem cells (CD34+ve) and their conjugate (mono-cell layer) were injected locally into testis. At the end of the study, MSCs group showed that mRNA levels of genes related to meiosis (Vasa, SCP3, and PgK2) were increased with significant decrease of FSH and LH levels, compared to control group. Histologically, most of the tubules restored normal architecture. In contrast, HSCs and mono-cell layer groups showed statically insignificant change of FSH, LH, and gene expression, compared to control group. Histologically, distorted seminiferous tubules, with reduction in sperm content, and interstitial mononuclear cellular infiltration were seen. There was significant increase in the optical density of PCNA immune reaction in MSCs group than azoospermia, HSCs, and mono-cell layer, while there was non-significant difference between MSCs and control group. The present study suggested that injection of MSCs into chemotherapeutic-induced azoospermia in mice improved testicular failure; histologically and functionally, by restoration of spermatogenic gene expression while HSC and mono-cell layer showed no effect on spermatogenesis added to that mono-cell layer may induce testicular tissue damage.

Tolvaptan suppresses monocyte chemotactic protein-1 excretion in autosomal-dominant polycystic kidney disease

Background: Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by multitudes of expanding renal cysts associated with mononuclear interstitial infiltrates. Monocyte chemotactic protein-1 is produced in the kidneys and excreted in the urine (uMCP1) of these patients in increased amounts. In the TEMPO 3:4 trial, tolvaptan slowed the rate of increase in total kidney volume (TKV) and the rate of decline in estimated glomerular filtration rate (eGFR). In a sub-analysis, we determined whether tolvaptan administration for up to 3 years changed the urinary excretion of MCP-1 referenced to creatinine in 869 treated subjects compared with 438 placebo subjects. Methods: Treatment group differences of uMCP1 at 0.75, 12, 24 and 36 months were evaluated by ANCOVA with factor of treatment and covariate baseline. Results: At baseline, mean uMCP1 was 429 ± 224 pg/mg in the tolvaptan and 434 ± 233 pg/mg in the placebo groups, ∼4-fold greater than normal. Log uMCP1 associated positively with log TKV (r = 0.2645, P < 0.0001) and negatively with eGFR (r = −0.1555 P < 0.0001) and fasting urine osmolality (r = −0.1933, P < 0.0001). Tolvaptan reduced uMCP1 13.8 ± 4.4% (P < 0.0001) below placebo-treated subjects at 24 months and 14.4 ± 3.7% (P < 0.0001) at 36 months, and to the same extent in females and males. The effect of tolvaptan on uMCP1 excretion at 36 months extended across CKD Stage 1 (11.1 ± 6.4%, P = 0.0595), CKD 2 (13.9 ± 5.4%, P = 0.0050) and CKD 3 (21.4 ± 8.0%, P = 0.0020). Conclusion: Tolvaptan, administered for 3 years to patients with ADPKD, caused a sustained reduction in the urinary excretion of MCP-1 relative to placebo.

Effect of mild aerobic training on the myocardium of mice with chronic Chagas disease.

BackgroundChronic chagasic heart disease represents extensive remodeling of the cardiovascular system, manifested as cardiac denervation, interstitial mononuclear infiltrate, myocyte and vascular degenerative changes, fibrosis, and hypertrophy. Moreover, aerobic exercises are widely indicated for the treatment of various disorders of the cardiovascular system.PurposeTo evaluate the right and left ventricles of BALB/c mice with chronic Chagas disease, undergoing mild exercise, by using morphometric and stereological methods.Materials and methodsA total of 20 male mice at 4 months of age were used for experiments. The animals were divided into four groups (n=5 in each group): untrained control, trained control, untrained infected (UI), and trained infected (TI). Animals of UI and TI groups were inoculated with 1,000 trypomastigote forms of Trypanosoma cruzi (Y strain), and after 40 days, animals entered chronic phase of the disease. Physical exercise, which included swimming, was performed for 30 minutes daily, five times a week for 8 consecutive weeks at a bath temperature of 30°C. After the trial period, euthanasia and subsequent withdrawal of the heart were done. The organ was prepared by histological staining procedures with hematoxylin–eosin and picrosirius red.ResultsWe found that the physical training used in our experimental model promoted increase in volume density of capillaries and decrease in volume density of collagen fibers and cross-sectional area of cardiomyocytes in chagasic animals (TI group). By histopathological analysis, we found differences in the inflammatory infiltrate, which was lower in animals of TI group. The training program promoted a recovery of these parameters in the TI group.ConclusionOur results suggest that low-intensity aerobic exercise acts on morphological and morphometric parameters of the left and right ventricles in mice infected with T. cruzi, reducing the changes caused by the organism and making the results comparable to those of the uninfected control group.

AVALIAÇÕES HISTOLÓGICA E HISTOMORFOMÉTRICA DE TESTÍCULOS DE BOVINOS COM DERMATITE DIGITAL

The infection of the digital area is the most common cause of lameness in cattle, leading to the rejection of high-production animals destined to reproduction. This study aimed at histological and histomorphometric evaluations of the testis of bovines with digital dermatitis. Different portions of testis from 20 Nellore animals, ten healthy and ten with digital dermatitis, between 25 and 30 months of age, were analyzed. All analyzed testis showed some degree of degeneration of the seminiferous epithelium. Mononuclear interstitial infiltrate was observed in testis of both healthy bovines and the ones with digital dermatitis. Bovines with digital dermatitis presented higher height of seminiferous tubular epithelium in all regions of testis, larger area of the tubular lumen, and larger tubular diameter. We concluded that young Nellore bovines show different degrees of testicular degeneration, as well as chronic nonspecific interstitial orchitis, unrelated to digital dermatitis. The testis histomorphometric changes of these animals are not related with foot disease. KEYWORDS: morphometry; podal disease; testicular changes.

Acute interstitial nephritis due to proton pump inhibitors

Proton pump inhibitors (PPI) are commonly prescribed for dyspepsia and acid peptic disease. Acute interstitial nephritis (AIN) is an uncommon though important side-effect of these classes of drugs. We describe four cases: three females and one male. PPIs implicated were pantoprazole in two, omeprazole and esomeprazole in one each. AIN developed after an average period of 4 weeks of drug therapy. The symptoms were vomiting, loin pain, and oliguria. Minimal proteinuria with pyuria were seen and the mean serum creatinine was 4.95 ± 4 mg/dl. Two patients required hemodialysis. Renal biopsy showed interstitial mononuclear, plasma cell and eosinophilic infiltrates in all cases. PPI was stopped and steroids were started in all. Renal recovery was total in two and partial in two. A high index of suspicion is required to diagnose PPI induced AIN. Renal biopsy for confirmation followed up by prompt steroid therapy results in renal functional improvement.

Delayed Graft Function and Cotrimoxazole

Acute interstitial nephritis is an infrequent cause of early allograft dysfunction. Prophylactic trimethoprim sulfamethoxazole (cotrimoxazole) is frequently prescribed early in the course of kidney transplantation. Herein we have reported a case of delayed graft function associated with eosinophilia in which the renal biopsy showed interstitial mononuclear infiltrates with abundant eosinophils. An initial methylprednisolone course failed to lower the serum creatinine, but renal function and eosinophilia persistently improved following cotrimoxazole withdrawal and a second course of steroids. Cotrimoxazole acute interstitial nephritis is an infrequent but treatable cause of kidney allograft dysfunction, which should be included in the differential diagnosis of delayed renal allograft function.

Histopathology of the reproductive system of male sheep experimentally infected with Toxoplasma gondii

The aim of this study was to investigate the histopathological changes in reproductive system (testicles, epididymis, seminal vesicles, and prostate) of small male ruminants after Toxoplasma gondii infection. Eight sheep were inoculated with T. gondii: group I, four sheep (2.0 × 10(5) P-strain oocysts); group II, four sheep (1.0 × 10(6) RH-strain tachyzoites); and group III, two uninfected sheep maintained as control. Infection with T. gondii was confirmed by seroconversion (indirect fluorescent antibody test-IgG) in all the infected animals beginning on post-inoculation day (PID) 7. On PID 70, all the animals were euthanized and tissue samples (testicles, epididymis, seminal vesicles, and prostate) were collected and processed for histological analysis. The main changes detected were a focal mononuclear interstitial inflammatory infiltrate in the prostate and seminal vesicles; diffuse testicular degeneration associated with calcification foci and a multifocal mononuclear interstitial inflammatory infiltrate; and a mononuclear interstitial infiltrate and focal necrotic areas of the muscle fibers surrounding the seminal vesicles. The histopathological findings of this work, along with the detection of T. gondii in the examined parenchyma tissues (immunohistochemistry) and the results obtained by other authors examining different tissues, suggest that histological changes diagnosed in the reproductive system of rams infected with T. gondii are strongly suggestive of toxoplasmatic infection.