White Blood Cell Infiltration Research Articles

Characterization of cardiac involvement in patients with LMNA splice-site mutation-related dilated cardiomyopathy and sudden cardiac death.

Introduction: LMNA splicing mutations occur in 9.1% of cases with cardiac involvement cases, but the phenotype and severity of disease they cause have not yet been systematically studied. The aim of this study was to understand the clinical and pathogenic characteristics of the LMNA splice-site mutation phenotype in patients with LMNA-related dilated cardiomyopathy (DCM) and sudden cardiac death (SCD). Methods and Results: First, we reported a novel family with LMNA-related DCM and SCD, and the clinical characteristics of all current patients with LMNA splicing mutations were further summarized through the ClinVar database. Seventeen families with a total of 134 individuals, containing a total of 15 LMNA splicing mutation sites, were enrolled. A total of 42 subjects (31.3%) had SCD. Compared without with the non-DCM group (n = 56), the patients within the DCM group (n = 78) presented a lower incidence of atrioventricular block (AVB) (p = 0.015) and a higher incidence rates of non-sustained ventricular tachycardia (p = 0.004),) and implantable cardioverter defibrillator (ICD) implantation (p = 0.005). Kaplan‒Meier survival analysis showed that the patients with pacemaker (PM) implantation had a significantly reduced the occurrence of SCD compared to patientswith those without PM implantation (log-rank p < 0.001), while there was no significant difference in ICD implantation between the two groups (log-rank p = 0.73). Second, we identified the family that we reported with a mutation in an LMNA c.513+1 G>A mutation in the reported family, and pathogenic prediction analysis showed that the mutation site was extremely harmful. Next, we conducted gene expression levels and cardiac pathological biopsy studies on the proband of this family. We found that the expression of normal LMNA mRNA from the proband was significantly downregulated in peripheral blood mononuclear cells than incompared with healthy individuals. Finally, we comprehensively summarized the pathological characteristics of LMNA-related DCM, including hypertrophy, atrophy, fibrosis, white blood cell infiltration, intercalated disc remodeling, and downregulation of desmin and connexin 43 (Cx43) expression. Discussion: Above all, Cardiaccardiac involvement in patients with LMNA splice-site mutation presented with a high rate of SCD. Implanting a pacemaker significantly reduced the SCD rate in non-DCM patients with AVB. The pathogenic characterization was not only haveinvolved suppressed the expression of the healthy LMNA allele, but was also associated with abnormal expression and distribution of desmin and Cx43.

Microglia-Mediated Neurovascular Unit Dysfunction in Alzheimer's Disease.

The neurovascular unit (NVU) is involved in the pathological changes in Alzheimer's disease (AD). The NVU is a structural and functional complex that maintains microenvironmental homeostasis and metabolic balance in the central nervous system. As one of the most important components of the NVU, microglia not only induce blood-brain barrier breakdown by promoting neuroinflammation, the infiltration of peripheral white blood cells and oxidative stress but also mediate neurovascular uncoupling by inducing mitochondrial dysfunction in neurons, abnormal contraction of cerebral vessels, and pericyte loss in AD. In addition, microglia-mediated dysfunction of cellular components in the NVU, such as astrocytes and pericytes, can destroy the integrity of the NVU and lead to NVU impairment. Therefore, we review the mechanisms of microglia-mediated NVU dysfunction in AD. Furthermore, existing therapeutic advancements aimed at restoring the function of microglia and the NVU in AD are discussed. Finally, we predict the role of pericytes in microglia-mediated NVU dysfunction in AD is the hotspot in the future.

Optical microscopy and cross anatomy for the intestinal wall of sheep infected with Tap worm

Ten intestinal mucosa of sheep intestine were obtained for cross and microscopy examination, the specimens from those intestinal wall were taken at pieces half cm and washed well by running water, then processed by histological technique according to Bancoft &amp; Steven 1987 including fixation, dehydration, clearing and embedding with paraffin wax also sectioning at six micrometer by microtome, finally stained by Hematoxylin and Eosin after that mounted with D. P. X and after drying in dry cabinet for 24 hour examined by light microscope , The intestinal wall was congested and patches of blood hemorrhage were seen. The histological examination revealed to sloughing of the intestinal villi from the luminal surface with presence of hyper secretion of mucus from the goblet cells and intestinal glands in the lamina properia also infiltration of white blood cells in the lamina properia in between the intestinal glands. In conclusion; the intestinal wall was damages after infection with Tape worm due to its effect on the villi of mucosa which are vital structures for absorption of nutritional elements in a animals.

Cardiac Inflammation in Adult-Onset Genetic Dilated Cardiomyopathy.

Dilated cardiomyopathy (DCM) has a genetic cause in up to 40% of cases, with differences in disease penetrance and clinical presentation, due to different exogeneous triggers and implicated genes. Cardiac inflammation can be the consequence of an exogeneous trigger, subsequently unveiling a phenotype. The study aimed to determine cardiac inflammation in a cohort of genetic DCM patients and investigate whether it associated with a younger disease onset. The study included 113 DCM patients with a genetic etiology, of which 17 had cardiac inflammation as diagnosed in an endomyocardial biopsy. They had a significant increased cardiac infiltration of white blood, cytotoxic T, and T-helper cells (p < 0.05). Disease expression was at a younger age in those patients with cardiac inflammation, compared to those without inflammation (p = 0.015; 50 years (interquartile range (IQR) 42-53) versus 53 years (IQR 46-61). However, cardiac inflammation was not associated with a higher incidence of all-cause mortality, heart failure hospitalization, or life-threatening arrhythmias (hazard ratio 0.85 [0.35-2.07], p = 0.74). Cardiac inflammation is associated with an earlier disease onset in patients with genetic DCM. This might indicate that myocarditis is an exogeneous trigger unveiling a phenotype at a younger age in patients with a genetic susceptibility, or that cardiac inflammation resembles a 'hot-phase' of early-onset disease.

Yinma Jiedu Granule attenuates LPS-induced acute lung injury in rats via suppressing inflammation level.

Yinma Jiedu Granule (YMJD) is a traditional Chinese patent medicine (CPM), which has been proved to have anti-inflammatory effects and therapeutical effects on obstructive pulmonary disease. The purpose of the current investigation is to find out if YMJD can alleviate acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats and its underlying mechanisms. Rats were treated with either vehicle or YMJD for 14 consecutive days, and 2h after the last administration, the rat model of ALI was induced by the intratracheal instillation of LPS. High performance liquid chromatography (HPLC) was applied for the fingerprint analysis of YMJD. The efficacy and molecular mechanisms were investigated. The results showed that treatment with YMJD improved the general state of rats, reduced weight loss and serum lactate (LA) levels, attenuated pulmonary edema and pathological damage of the lung tissue. Moreover, we found that YMJD effectively decreased the infiltration of white blood cells (WBC), lymphocytes (LYM), mononuclear cells (MON) and neutrophils (NEUT) in bronchoalveolar lavage fluid (BALF), reduced the concentration of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in the lung tissue. Additionally, we found that YMJD could significantly increase the activity of superoxide dismutase (SOD) and reduce the malondialdehyde (MDA) level in the lung tissue. By employing RNA-sequencing, we have identified that JAK2/STAT1 is an important pathway that is involved in the lung protection of YMJD, and further Western blot assay verified that YMJD could effectively inhibit the activation of the JAK2/STAT1 pathway. YMJD could attenuate LPS-induced ALI through suppressing inflammation and oxidative stress in the lung tissue of rats, associating with the inhibition of JAK2/STAT1 activation. These findings provide evidence for the clinical use of YMJD for treatment of inflammatory pulmonary diseases like ALI.

Retracted: Unilateral Sciatic Nerve Crush Induces White Blood Cell Infiltration of the Contralateral Nerve.

[This retracts the article DOI: 10.1155/2022/1101383.].

In-vivo thermodynamic exploration of gas-based intraperitoneal hyperthermia

BackgroundWhile hyperthermic intraperitoneal (i.p) applications are highly efficient in treating peritoneal metastases (PM), they are currently limited to temperatures of 41 – 43° Celsius (C). First data on gas-based i.p. hyperthermia is promising, as this novel method allows a significant temperature rise in superficial peritoneal layers without increasing core temperatures. Until now, key mechanisms of this novel tool, e.g. thermodynamic energy transfer, have not been investigated. This study aims to explore the volume of thermodynamic energy transfer during gas-based i.p. hyperthermia at 48-50°C and its peritoneal effects.MethodsFor this study, three swine were subjected to gas-based i.p. hyperthermia at varying temperatures (48°, 49° and 50°C) in a diagnostic laparoscopy setting with a high-flow air stream. Temperatures of the i.p. cavity, in- and outflow airstream at the trocar were measured and the thermodynamic energy transfer was calculated. Tissue samples were collected on postoperative day 7 for histopathologic analyses.ResultsAccording to our data, temperatures within the intraabdominal cavity and at the outflow site remain relatively stable at < 40°C. An increase in thermodynamic energy transfer is observed with increasing applied temperatures. Gas-based i.p. hyperthermia induced capillary coagulation and white blood cell infiltration within peritoneal layers.ConclusionsGas-based i.p. hyperthermia is an innovative approach which enables the i.p. delivery of specific amounts of thermodynamic energy. Following this procedure, our data indicate remarkable histologic changes on the superficial peritoneal layer most likely attributable to the applied thermodynamic energy. Further studies are required to investigate how these findings can be applied in PM management.

Free-cell therapeutics and mechanism of exosomes from adipose-derived stem cells in promoting wound healing: current understanding and future applications.

Free-cell therapeutics and mechanism of exosomes from adipose-derived stem cells in promoting wound healing: current understanding and future applications.

Resolution and Re-ossification of Orbital-Wall Langerhans Cell Histiocytosis Following Stereotactic Needle Biopsy.

Introduction Langerhans cell histiocytosis (LCH) is a rare disease that encompasses a spectrum of clinical syndromes. It is characterized by the proliferation and infiltration of white blood cells into organs or organ systems. Reports of management of these lesions have included biopsy, resection, curettage, radiation, and/or chemotherapy. Case Presentation A 40-year-old man presented with a history of right proptosis and retro-orbital pain and was found to have a lytic mass involving the greater wing of the sphenoid extending into the right orbit. A stereotactic needle biopsy using neuronavigation demonstrated this to be LCH. After no further treatment, the mass spontaneously resolved, with virtual normalization of the orbital magnetic resonance imaging at 10 months following the needle biopsy. The bony defect of the temporal bone caused by the mass also re-ossified following the needle biopsy. Discussion This report highlights the potential for an isolated LCH lesion to regress after simple needle biopsy, an outcome only rarely reported previously. Thus, expectant management of such lesions following biopsy or initial debridement should be considered prior to proceeding with additional treatment.

BMI1 Silencing Induces Mitochondrial Dysfunction in Lung Epithelial Cells Exposed to Hyperoxia.

Acute Lung Injury (ALI), characterized by bilateral pulmonary infiltrates that restrict gas exchange, leads to respiratory failure. It is caused by an innate immune response with white blood cell infiltration of the lungs, release of cytokines, an increase in reactive oxygen species (ROS), oxidative stress, and changes in mitochondrial function. Mitochondrial alterations, changes in respiration, ATP production and the unbalancing fusion and fission processes are key events in ALI pathogenesis and increase mitophagy. Research indicates that BMI1 (B cell-specific Moloney murine leukemia virus integration site 1), a protein of the Polycomb repressive complex 1, is a cell cycle and survival regulator that plays a role in mitochondrial function. BMI1-silenced cultured lung epithelial cells were exposed to hyperoxia to determine the role of BMI1 in mitochondrial metabolism. Its expression significantly decreases in human lung epithelial cells (H441) following hyperoxic insult, as determined by western blot, Qrt-PCR, and functional analysis. This decrease correlates with an increase in mitophagy proteins, PINK1, Parkin, and DJ1; an increase in the expression of tumor suppressor PTEN; changes in the expression of mitochondrial biomarkers; and decreases in the oxygen consumption rate (OCR) and tricarboxylic acid enzyme activity. Our bioinformatics analysis suggested that the BMI1 multifunctionality is determined by its high level of intrinsic disorder that defines the ability of this protein to bind to numerous cellular partners. These results demonstrate a close relationship between BMI1 expression and mitochondrial health in hyperoxia-induced acute lung injury (HALI) and indicate that BMI1 is a potential therapeutic target to treat ALI and Acute Respiratory Distress Syndrome.

Unilateral Sciatic Nerve Crush Induces White Blood Cell Infiltration of the Contralateral Nerve.

Nerve injury leads to the accumulation of white blood cells derived from the bone marrow in the lesioned nerve, but it is still unknown whether there are similar responses in unlesioned nerves. To address this question, sciatic nerves of mice expressing enhanced green fluorescent protein (EGFP) in their bone marrow were crushed unilaterally to observe the invasion of bone marrow-derived cells into the contralateral unlesioned nerve. Two days after surgery, EGFP+ cells began to infiltrate both the damaged and undamaged nerves. These cells gradually amplified to the highest point within 14 days and slowly lowered. In ipsilateral (lesioned) and contralateral (unlesioned) nerves, the time course of infiltration of EGFP+ cells was similar, but the magnitude was much less for the unlesioned one. Through CD68 staining, some cells were identified as macrophages. Transmission electron microscopy revealed slight demyelination and phagocytosing macrophages in the contralateral nerve. The data showed that infiltration by white blood cells is a response to nerve injury, even in uninjured nerves.

M261 EARLY DIAGNOSIS OF EOSINOPHILIC FASCIITIS IN A 16 YEAR-OLD FEMALE

Eosinophilic fasciitis (EF) is an uncommon scleroderma-like disorder resulting from infiltration of eosinophils and other white blood cells into the fascia. The etiology of EF is frequently idiopathic, but triggers have included trauma, medications, infection, and autoimmune conditions.

Open-Source Automatic Biomarker Measurement on Slit-Lamp Photography to Estimate Visual Acuity in Microbial Keratitis.

PurposeTo assess clinical applicability of automatic image analysis in microbial keratitis (MK) by evaluating the relationship between biomarker measurements on slit-lamp photography (SLP) and best-corrected visual acuity (BCVA).MethodsSeventy-six patients with MK with SLP images and same-day logarithm of the minimum angle of resolution (logMAR) BCVA were evaluated. MK biomarkers (stromal infiltrate, white blood cell infiltration, corneal edema, hypopyon, epithelial defect) were segmented manually by ophthalmologists and automatically by a novel, open-source, deep learning–based segmentation algorithm. Five measurements (presence, maximum width, total area, proportion of the corneal limbus area affected, centrality) were calculated. Correlations between the measurements and BCVA were calculated. An automatic regression model estimated BCVA from the measurements. Differences in performance between using manual and automatic measurements were evaluated using William's test (for correlation) and the paired-sample t-test (for absolute error).ResultsMeasurements had high correlations of 0.86 (manual) and 0.84 (automatic) with true BCVA. Estimated BCVA had average (mean ± SD) absolute errors of 0.39 ± 0.27 logMAR (manual, median: 0.30) and 0.35 ± 0.28 logMAR (automatic, median: 0.30) and high correlations of 0.76 (manual) and 0.80 (automatic) with true BCVA. Differences between using manual and automatic measurements were not statistically significant for correlations of measurements with true BCVA (P = .66), absolute errors of estimated BCVA (P = .15), or correlations of estimated BCVA with true BCVA (P = .60).ConclusionsThe proposed algorithm measured MK biomarkers as accurately as ophthalmologists. Measurements were highly correlated with and estimative of visual acuity.Translational RelevanceThis study demonstrates the potential of developing fully automatic objective and standardized strategies to aid ophthalmologists in the clinical assessment of MK.

Development of Phospholipids Vesicular Nanocarrier for Topical Delivery of Tea Tree Oil in Management of Atopic Dermatitis Using BALB/c Mice Model

AbstractThis work aims to develop and evaluate the efficacy of tea tree oil (TTO) ethosomal cream with improved deposition in skin layers for treatment of atopic dermatitis (AD). Ethosomes of TTO are developed using phosphatidylcholine (2% and 3% w/v) and ethanol (20%, 30%, and 40% w/v). Ethosomes are evaluated for percent entrapment efficiency (%EE), vesicle size, zeta potential, and in vitro drug diffusion. Ethosomal creams with optimized ethosomal dispersion are developed and evaluated for physicochemical parameters, thermal stability, ex vivo permeation, skin retention, and in vitro cytotoxicity using HaCat skin cell lines in comparison to conventional creams of TTO. In vivo investigations of optimized creams are performed using BALB/c mice model. The %EE, vesicle size, and zeta potential for optimized ethosomes are found to be 76.19 ± 3.26%, 333.6 nm, and –35.3 mV, respectively. Ethosomal creams showed higher deposition in the epidermis and dermis. The optimized creams are non‐cytotoxic to HaCat cell lines. The creams significantly reduce the inflammatory response by decreasing the clinical score and infiltration of white blood cells, eosinophils, and IgE antibodies. Overall efficacy of ethosomal cream is higher than conventional cream. In conclusion, optimized ethosomal cream of TTO shows good efficacy for treatment of AD.Practical applications: The method used for the formulation of ethosomes is simple and can be easily scaled up on the industrial level. The loading of TTO within ethosomes can increase the efficiency by enhanced drug deposition in the epidermis and might also improve its stability against oxidative degradation. Topical ethosomal cream of TTO can improve patient compliance by avoidance of adverse effects linked with corticosteroids and could be a possible complementary or alternative therapy in management of AD.

HISTOMORPHOLOGICAL ALTERATIONS IN THE LUNGS IN ACUTE COMBINED BACLOFEN AND ETHANOL POISONING

A generic Baclofen, also known under the brand name of Lioresal, is a derivative of gamma-aminobutyric acid. Due to its psychotropic effect it is often used as a drug of abuse and for criminal poisoning. An experimental study was carried out on 5 Wistar rats (versus 5 intact rats of the control group) exposed to combined Baclofen (at a dose of 85 mg/kg) and ethanol (7 ml/kg of 40% ethanol) poisoning. We have identified a complex of pathological changes in the lungs of the rats in the early period after the experiment. The outcomes included circulatory disorders of the pulmonary microvasculature (plethora of capillaries, venules), emphysema, atelectasis and dystelectasis, infiltration of white blood cells into intraalveolar septa and thickening of intraalveolar septa due to edema. To quantify the severity of histomorphological changes in the lungs a morphometric study is required.

Syringin alleviates ovalbumin-induced lung inflammation in BALB/c mice asthma model via NF-κB signaling pathway.

Asthma is an allergic chronic inflammatory disease of the pulmonary airways, characterized by the infiltration of white blood cells and release of inflammatory cytokines of complex pathways linked to its pathogenesis. Syringin extracted from various medicinal plants has been used extensively for the treatment of inflammatory diseases. Hence, this study was conducted to further explore the protective effects of the syringin in ovalbumin (OVA) induced-asthma mice model. OVA-sensitized BALB mice were treated intraperitonealy with three doses (25, 50 and 100 mg/kg) of the syringin which was validated by the alteration in the immunoglobulin E (IgE) levels, cytokines levels, histopathological evaluation inflammatory cell count, lung weight, nitrite (NO) levels, oxidative stress biomarkers and gene markers. The treatment of syringin intensely reduced the increased IgE, inflammatory cytokines, WBC count and restored the antioxidant stress markers OVA stimulated animals. In addition, a significant reduction in inflammation and mucus production was evidenced in histopathological analysis which was further validated by suppression NF-κB pathway activation by syringin. These results suggest that syringin may improve asthma symptoms in OVA-induced mice by modulating NF-κB pathway activation.

Histomorphological changes in the lungs induced by poisoning with baclofen and its combination with ethanol (experimental study)

Aim.Detection and assessment of histomorphological changes in the lungs in acute poisoning with Baclofen and its combination with ethanol three hours after poisoning.Material and methods.Experimental studies were conducted in 15 Wistar lineage rats divided into three groups. The control group included five intact animals, group 1 was treated with Baclofen at a dose of 85 mg/kg, group 2 with a combination of Baclofen (85 mg/kg) and ethanol (7 mL/kg of 40% ethanol).Results.No pathological changes were observed in the lungs of the controls. Both treated groups manifested the capillary and venous plethora, sludge syndrome, atelectases and dystelectases, emphysema and infiltration of white blood cells into the interalveolar septa. Bronchioles in the group 2 animals contained secretion.Conclusion.In the conducted trials, a complex of pathological changes was observed in the lungs of animal models shortly after the administration of Baclofen, including circulatory disorders in all departments of the microcirculatory bed (plethora of capillaries and venules), emphysema, atelectases and dystelectases, leucocyte infiltration into the interalveolar septa. Morphometric studies are necessary to quantify the severity of histomorphological changes in the lungs.

Measurement Reliability for Keratitis Morphology.

To evaluate the reliability of manual annotation when quantifying cornea anatomical and microbial keratitis (MK) morphological features on slit-lamp photography (SLP) images. Prospectively enrolled patients with MK underwent SLP at initial encounter at 2 academic eye hospitals. Patients who presented with an epithelial defect (ED) were eligible for analysis. Features, which included ED, corneal limbus (L), pupil (P), stromal infiltrate (SI), white blood cell (WBC) infiltration at the SI edge, and hypopyon (H), were annotated independently by 2 physicians on SLP images. Intraclass correlation coefficients (ICCs) were applied for reliability assessment; dice similarity coefficients (DSCs) were used to investigate the area overlap between readers. Seventy-five MK patients with an ED received SLP. DSCs indicate good to fair annotation overlap between graders (L = 0.97, P = 0.80, ED = 0.94, SI = 0.82, H = 0.82, WBC = 0.83) and between repeat annotations by the same grader (L = 0.97, P = 0.81, ED = 0.94, SI = 0.85, H = 0.84, WBC = 0.82). ICC scores showed good intergrader (L = 0.98, P = 0.78, ED = 1.00, SI = 0.67, H = 0.97, WBC = 0.86) and intragrader (L = 0.99, P = 0.92, ED = 0.99, SI = 0.94, H = 0.99, WBC = 0.92) reliabilities. When reliability statistics were recalculated for annotated SI area in the subset of cases where both graders agreed WBC infiltration was present/absent, intergrader ICC improved to 0.91 and DSC improved to 0.86 and intragrader ICC remained the same, whereas DSC improved to 0.87. Manual annotation indicates usefulness of area quantification in the evaluation of MK. However, variability is intrinsic to the task. Thus, there is a need for optimization of annotation protocols. Future directions may include using multiple annotators per image or automated annotation software.

Titanium dioxide nanoparticles exaggerate respiratory syncytial virus-induced airway epithelial barrier dysfunction.

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in children worldwide. While most develop a mild, self-limiting illness, some develop severe acute lower respiratory infection and persistent airway disease. Exposure to ambient particulate matter has been linked to asthma, bronchitis, and viral infection in multiple epidemiological studies. We hypothesized that coexposure to nanoparticles worsens RSV-induced airway epithelial barrier dysfunction. Bronchial epithelial cells were incubated with titanium dioxide nanoparticles (TiO2-NP) or a combination of TiO2-NP and RSV. Structure and function of epithelial cell barrier were analyzed. Viral titer and the role of reactive oxygen species (ROS) generation were evaluated. In vivo, mice were intranasally incubated with TiO2-NP, RSV, or a combination. Lungs and bronchoalveolar lavage (BAL) fluid were harvested for analysis of airway inflammation and apical junctional complex (AJC) disruption. RSV-induced AJC disruption was amplified by TiO2-NP. Nanoparticle exposure increased viral infection in epithelial cells. TiO2-NP induced generation of ROS, and pretreatment with antioxidant, N-acetylcysteine, reversed said barrier dysfunction. In vivo, RSV-induced injury and AJC disruption were augmented in the lungs of mice given TiO2-NP. Airway inflammation was exacerbated, as evidenced by increased white blood cell infiltration into the BAL, along with exaggeration of peribronchial inflammation and AJC disruption. These data demonstrate that TiO2-NP exposure exacerbates RSV-induced AJC dysfunction and increases inflammation by mechanisms involving generation of ROS. Further studies are required to determine whether NP exposure plays a role in the health disparities of asthma and other lung diseases, and why some children experience more severe airway disease with RSV infection.

Pericytes Contribute to Dysfunction in a Human 3D Model of Placental Microvasculature through VEGF-Ang-Tie2 Signaling.

Placental vasculopathies are associated with a number of pregnancy‐related diseases, including pre‐eclampsia (PE)—a leading cause of maternal–fetal morbidity and mortality worldwide. Placental presentations of PE are associated with endothelial dysfunction, reduced vessel perfusion, white blood cell infiltration, and altered production of angiogenic factors within the placenta (a candidate mechanism). Despite maintaining vascular quiescence in other tissues, how pericytes contribute to vascular growth and signaling in the placenta remains unknown. Here, pericytes are hypothesized to play a detrimental role in the pathogenesis of placental vascular growth. A perfusable triculture model is developed, consisting of human endothelial cells, fibroblasts, and pericytes, capable of recapitulating growth and remodeling in a system that mimics inflamed placental microvessels. Placental pericytes are shown to contribute to growth restriction of microvessels over time, an effect that is strongly regulated by vascular endothelial growth factor and Angiopoietin/Tie2 signaling. Furthermore, this model is capable of recapitulating essential processes including tumor necrosis factor alpha (TNFα)‐mediated vascular leakage and leukocyte infiltration, both important aspects associated with placental PE. This placental vascular model highlights that an imbalance in endothelial–pericyte crosstalk can play a critical role in the development of vascular pathology and associated diseases.