Inflammatory Infiltrates In Patients Research Articles

Virological and histological evaluation of intestinal samples in COVID-19 patients.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the pathogen responsible for pandemic coronavirus disease 2019 (COVID-19). It is a highly contagious virus which primarily affects the respiratory tract, nevertheless, the lungs are not the only target organs of the virus. The intestinal tract could represent an additional tropism site for SARS-CoV-2. Several observations have collectively suggested that enteric infections can occur in COVID-19 patients. However, the detection of viral RNA in gastrointestinal (GI) tissue samples has not been adequately investigated and results are conflicting. To detect the presence of SARS-CoV-2 RNA in intestinal mucosa samples and to evaluate histological features. The COVID-19 patients hospitalized at an Italian tertiary hospital from April 2020 to March 2021 were evaluated for enrollment in an observational, monocentric trial. The study population was composed of two groups of adult patients. In the first group (biopsy group, 30 patients), patients were eligible for inclusion if they had mild to moderate disease and if they agreed to have a rectal biopsy; in the second group (surgical specimen group, 6 patients), patients were eligible for inclusion if they underwent intestinal resection during index hospitalization. Fifty-nine intestinal mucosal samples were analyzed. Viral RNA was not detectable in any of the rectal biopsies performed (0/53). Histological examination showed no enterocyte damage, but slight edema of the lamina propria with mild inflammatory lymphoplasmacytic infiltration. There was no difference in inflammatory infiltrates in patients with and without GI symptoms. SARS-CoV-2 RNA was detected in fecal samples in 6 cases out of 14 cases examined (42.9%). In the surgical specimen group, all patients underwent emergency intestinal resection. Viral RNA was detected in 2 surgical specimens of the 6 examined, both of which were from patients with active neoplastic disease. Histological examination also pointed out abundant macrophages, granulocytes and plasma cells infiltrating the muscular layer and adipose tissue, and focal vasculitis. Mild-moderate COVID-19 may not be associated with rectal infection by the virus. More comprehensive autopsies or surgical specimens are needed to provide histological evidence of intestinal infection.

P-300 Study of the composition of the inflammatory infiltrate in patients with colorectum cancer

Colorectal cancer is a real public health problem, it ranks third among cancers in terms of frequency the world and second in terms of mortality. Several environmental and genetic factors participate in the development and progression of this multifactorial disease. It develops from a colorectal adenoma. During of the evolution of tumor cells, the environment is crucial for their survival, growth and progression. The tumor microenvironment has become a privileged target to study new approaches for the treatment of cancers.

Spinal Cord Compression Due to Hypertrophic Dorsal Pachymeningitis in a Patient with ANCA + Vasculitis

Hypertrophic pachymeningitis is an infrequent cause of spinal cord compression, secondary to an intracanal and extramedullary inflammatory infiltrate in patients with Wegener’s disease, and it produces canal stenosis and spinal cord compression. We present the case of a patient with this rare entity, providing explanatory images, who was treated with corticosteroids with partial remission of the lesions.

Intestinal production of secreted protein acidic and rich in cysteine (SPARC) in patients with ulcerative colitis

BackgroundUlcerative colitis (UC) is an inflammatory disease of the intestine. The genetics factors play an important role in the pathogenesis of UC. SPARC exacerbates colonic inflammatory symptoms in dextran sodium sulphate-induced murine colitis. The aim of the study was to measure the gene expression and intestinal production of SPARC in patients with UC and controls as well as, to determine its correlation with histological activity. MethodsWe included 40 patients with confirmed diagnosis of UC, and 20 controls without endoscopic evidence of any type of colitis or neoplasia. The relative quantification of the gene expression was performed by real time PCR. GAPDH was used as housekeeping gene for normalization purposes and quality controls. Protein expression was determined by immunohistochemistry. ResultsThe gene expression of SPARC was increased in patients with active UC vs in remission UC and vs. controls (P = 0.005). There was no significant difference between patients with remission UC and controls. The overexpression of SPARC in patients with active UC correlated significantly with mild histological activity (P = 0.06, OR = 7.77, IC = 0.77–77.9) moderate (P = 0.06, OR = 8.1, IC 95%=0.79–82.73), and severe (P = 0.03, OR = 6.5, IC 95%=1.09–38.6). Double positive SPARC+/CD16+ cells were localized mainly in submucosa, muscular layer, and adventitia, and in perivascular inflammatory infiltrates in patients with active UC. ConclusionThe gene and protein expression of SPARC is increased in active UC. SPARC could be a marker of intestinal inflammation and its expression correlates with histological activity.

Brain-derived neurotrophic factor is associated with coronary macrophage infiltrates in patients with acute coronary syndrome

Abstract Background Brain-derived neurotrophic factor (BDNF) is a neurotrophine that plays a key role in the regulation of both central and peripheral nervous system. Moreover, BDNF is secreted in multiple tissues and exerts systemic, autocrine, and paracrine effects in the cardiovascular system. Of importance, BDNF expression was enhanced in macrophages and smooth muscle cells in atherosclerotic coronary arteries and may be involved in thrombus formation. Thus, BDNF has been suggested as an important link between inflammation and thrombosis, potentially involved in the pathogenesis of acute coronary syndrome (ACS). Purpose In our study we aimed at assessing serum levels of BDNF in patients with ACS, evaluating differences according to clinical presentation [ST-segment elevation myocardial infarction (STEMI) vs. Non-ST-segment elevation ACS (NSTE-ACS)]. Moreover, we assessed the presence of optical coherence (OCT)-defined macrophage infiltrates (MØI) in the culprit vessel of ACS patients and evaluated their relationship with BDNF levels. Methods ACS patients were prospectively selected. Blood samples were collected at admission and serum levels of BDNF were subsequently assessed. Presence of OCT-defined MØI along the culprit vessel was assessed. Results 166 ACS patients were enrolled [mean age 65.3±11.9 years, 125 (75.3%) male, 109 STEMI, 57 NSTE-ACS]. Serum levels of BDNF were higher among STEMI patients compared with NSTE-ACS [median (IQR) 2.48 pg/mL (1.54–3.34) vs. 2.12 pg/mL (1.34–2.47), p=0.007], while C-reactive protein levels did not differ between the two groups. OCT assessment was performed in 53 patients and MØI were detected in 27 patients. Of importance, patients with MØI in the culprit vessel had higher levels of BDNF compared with patients without MØI [median (IQR) 2.23 pg/mL (1.38–2.53) vs. 1.41 pg/mL (0.93–2.07), p=0.023], while C-reactive protein levels did not differ between the two groups. Of note, at multivariate regression analysis BDNF levels were independent predictor of MØI [OR: 2.20; 95% CI (1.02–4.74), p=0.043]. Conclusions Serum levels of BDNF may reliable identify the presence of local macrophage inflammatory infiltrates in patients with ACS. Moreover, BDNF levels are higher in patients with STEMI compared with NSTE-ACS. Taken together, these data suggest that BDNF may represent an interesting link between local inflammatory activation and enhanced thrombosis in ACS. BDNF serum levels Funding Acknowledgement Type of funding source: None

Computer-Assisted Definition of the Inflammatory Infiltrates in Patients With Different Categories of Banff Kidney Allograft Rejection.

Currently, the diagnosis of kidney allograft rejection relies on individual histological assessments made by expert pathologists according to the Banff classification. In this study, we applied new Computer-Assisted System Technology (newCAST™) by Visiopharm® with the aim of identifying and quantifying the immune cells in inflammatory infiltrates. We searched for distinctive cellular profiles that could be assigned to each rejection category of the Banff schema: antibody-mediated rejection (active and chronic active), borderline, T cell-mediated rejection (TCMR), and mixed rejection. This study was performed with 49 biopsy samples, 42 from patients with rejection and 7 from patients with clinical signs of dysfunction but an absence of histological findings of rejection. Plasma cells, B and T lymphocytes, natural killer cells, and macrophages, with a special focus on the M1 and M2 subsets, were studied. A major difference among the Banff rejection groups was in the total amount of cells/mm2 tissue. Principal component analysis identified some distinctive associations. The borderline category grouped with CD4+ lymphocytes and M1 macrophages, and active antibody-mediated rejection (aAMR) clustered with natural killer cells. Despite these findings, the search for characteristic profiles linked to the rejection types proved to be a very difficult task since the cellular composition varied significantly among individuals within the same diagnostic category. The results of this study will be analyzed from the perspective of reconciling the classic way of diagnosing rejection and the immune situation “in situ” at the time of diagnosis.

A comparison of the prognostic value of the adaptive, T-lymphocyte and generalised inflammatory infiltrate in patients with primary operable colorectal cancer

A comparison of the prognostic value of the adaptive, T-lymphocyte and generalised inflammatory infiltrate in patients with primary operable colorectal cancer

Th1 and Th17 cytokines drive inflammation in Takayasu arteritis.

Takayasu arteritis (TAK) is a large-vessel vasculitis that induces damage to the aorta and its branches. Glucocorticoids remain the gold standard of therapy for TAK. The nature of the T cells driving vascular inflammation and the effects of glucocorticoids on the systemic components of TAK are not understood. The aim of this study was to analyze T cell homeostasis and cytokine production in peripheral blood and inflammatory lesions of the aorta in patients with TAK. T cell homeostasis and cytokine production in peripheral blood and inflammatory lesions of the aorta were analyzed using Luminex analysis, flow cytometry, and immunohistochemical analysis. The study included 41 patients fulfilling the American College of Rheumatology 1990 criteria for the classification of TAK (17 patients with active TAK and 24 patients with disease in remission), 30 patients with giant cell arteritis and 39 patients with Behçet's disease (disease controls), and 20 age- and sex-matched healthy control subjects. We observed a marked increase in the expression of Th1 and Th17 cells, which correlated with TAK disease activity. The addition of serum from patients with active TAK to sorted CD4+ T cells from healthy donors in culture medium induced significant production of interferon-γ (IFNγ) and interleukin-17A (IL-17A). We demonstrated the presence of IFNγ-, IL-6-, and IL-17A-producing T cells in vascular inflammatory infiltrates in patients with TAK. Corticosteroid therapy was associated with decreased levels of circulating Th1 cytokines in corticosteroid-treated patients with TAK compared with steroid-free patients with TAK (for IL-2, mean ± SD 5,079 ± 5,300 versus 7,359 ± 3,197 pg/ml; for IFNγ, 2,592 ± 3,072 versus 8,393 ± 3,392 pg/ml; for tumor necrosis factor α, 847 ± 724 versus 1,491 ± 392 pg/ml). However, glucocorticoids had essentially no effect on the frequency of Th17 cytokines (IL-1 receptor, IL-17, and IL-23). The Th17 and Th1 pathways contribute to the systemic and vascular manifestations of TAK. Glucocorticoid treatment suppresses Th1 cytokines but spares Th17 cytokines in patients with TAK.

Immunophenotype in orofacial granulomatosis with and without Crohn's disease.

Objectives: The aim of this investigation was to characterise and compare the inflammatory infiltrates in patients with orofacial granulomatosis solely (OFG-S) and OFG with coexisting Crohn’s disease (OFG+CD). Study Design: Biopsy specimens with granulomas were obtained from patients with OFG-S (n=11) and OFG+CD (n=11) and immunostained with antibodies against CD1a, CD3, CD4, CD8, CD11c, CD20, CD68 and mast cell tryptase, followed by quantitative analysis. Results: Analyses of the connective tissue revealed a significantly higher number of CD3-expressing T cells and CD11c-expressing dendritic cells in the connective tissue of patients with OFG-S compared to patients with OFG+CD. Mast cells displayed a high level of activation, although no significant difference was detected when comparing the two groups. Conclusions: The results show a different composition of the inflammatory infiltrate in patients with OFG-S compared to patients with OFG+CD. The present observations support that partly divergent immune mechanisms are involved in these two different subcategories of OFG. Key words:Granulomas, autoimmunity, T cells, B cells, dendritic cells, children, adults.

Comparison of visual and automated assessment of tumour inflammatory infiltrates in patients with colorectal cancer

BackgroundCancer-associated inflammation is increasingly recognised to be an important determinant of oncological outcome. In colorectal cancer, the presence of peri-tumoural inflammatory/lymphocytic infiltrates predicts improved survival. To date, these infiltrates, assessed visually on haematoxylin and eosin (H&E) stained sections, have failed to enter routine clinical practice, partly due to their subjective assessment and considerable inter-observer variation. The present study aims to develop an automated scoring method to enable consistent and reproducible assessment of tumour inflammatory infiltrates in colorectal cancer. Methods154 colorectal cancer patients who underwent curative resection were included in the study. The local inflammatory infiltrate was assessed using the method described by Klintrup–Makinen. H&E tumour sections were uploaded to an image analysis programme (Slidepath, Leica Biosystems). An image analysis algorithm was developed to count the inflammatory cells at the invasive margin. The manual and automated assessments of the tumour inflammatory infiltrates were then compared. ResultsThe automated inflammatory cell counts assessed using the freehand annotation method (p<0.001) and the rectangular box method (p<0.001) were significantly associated with both K–M score (p<0.001) and K–M grade (p<0.001). The inflammatory cell counts were divided using quartiles to group tumours with similar inflammatory cell densities. There was good agreement between the manual and automated scoring methods (intraclass correlation coefficient (ICC)=0.82). Similar to the visual K–M scoring system, the automated K–M classification of the inflammatory cell counts, using quartiles, was significantly associated with venous invasion (p<0.05) and modified Glasgow Prognostic Score (mGPS) (p⩽0.05). On univariate survival analysis, both automated K–M category (p<0.05) and automated K–M grade (p<0.005) were associated with cancer-specific survival. ConclusionThe results of the present study demonstrate that automated assessment effectively recapitulates the clinical value of visual assessment of the local inflammatory cell infiltrate at the invasive margin of colorectal tumours. In addition, it is possible to obtain an objective assessment of tumour inflammatory infiltrates using routinely stained H&E sections. An automated, computer-based scoring method is therefore a workable and cost-effective approach to clinical assessment of local immune cell infiltrates in colorectal cancer.

Effect of smoking on neutrophil apoptosis in chronic periodontitis: An immunohistochemical study

Periodontal disease is caused by chronic infection inducing an inflammatory reaction leading to breakdown of tooth-supporting tissues. There are various risk factors for the disease, and smoking is one of them. Apoptosis plays a critical role in the regulation of inflammation and host immune response which helps in tissue homeostasis, and a disturbance in this is often associated with disease. The imbalance between the apoptosis and proliferation in the periodontal tissue results in periodontal disease. Neutrophils play an important role in the defense mechanism and are the most abundant immune cells in gingival inflammatory infiltrate in patients suffering from periodontal disease. Neutrophil disorders are associated with rapid destruction of periodontal tissues. To study the influence of smoking on apoptosis of neutrophils by quantifying them in the gingival connective tissue of smoking and nonsmoking subjects suffering from chronic periodontitis. Thirty gingival biopsies were harvested from 15 smoking and 15 nonsmoking subjects who suffered from chronic periodontitis. The apoptosis of neutrophils was assessed and quantified using p53 monoclonal mouse antihuman antibody. Chi-square/Fisher's exact test was used to find the significance of study parameters on a categorical scale between the two groups. Neutrophil apoptosis was significantly more in the group of nonsmokers. There was no statistical difference between plaque and bleeding index, but there was a significant increase in clinical attachment loss among smokers. The study reveals that smoking plays a significant role in the inhibition of neutrophil apoptosis, thereby contributing to the destruction of periodontal tissues in periodontitis.

Pulmonary involvement by chronic lymphocytic leukemia/small lymphocytic lymphoma is a specific pathologic finding independent of inflammatory infiltration

Pulmonary infiltrates in patients with chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL) are usually secondary to infection, but a subset is due to pathologic infiltration of malignant lymphocytes into the lung parenchyma. In cases with both CLL/SLL and inflammatory infiltrates, it is unknown whether the CLL infiltrate represents a nonspecific “passenger effect” secondary to ongoing inflammation or pathologic leukemic pulmonary infiltration (LPI). We reviewed 49 lung biopsies taken from 38 patients with CLL/SLL. LPI was found in 2 of 21 cases (9.5%) with acute inflammation, 0 of 10 cases of chronic inflammation and in 7 of 18 cases (38.8%) without any pathologic findings of acute or chronic inflammation (p = 0.01). These results demonstrate that LPI identified in biopsies with concurrent inflammation is uncommon, and that most inflammatory infiltrates in patients with CLL do not cause “passenger effect” CLL infiltration. Therefore, LPI usually represents a specific pathologic process. We conclude that bronchoscopy with transbronchial biopsy is an effective tool for guiding treatment decisions for symptomatic patients with CLL with pulmonary infiltrates. Moreover, LPI by CLL is not a bystander effect secondary to acute inflammation, but instead represents a distinct pathologic process in a subset of patients.

T1114 Comparative Study of Immunoexpression of Junctional Proteins (Claudin 1, 3 and 4), Cyclooxygenase-2 and Inflammatory Infiltrate in Patients With Erosive and Non-Erosive Gastroesophageal Reflux Disease

T1114 Comparative Study of Immunoexpression of Junctional Proteins (Claudin 1, 3 and 4), Cyclooxygenase-2 and Inflammatory Infiltrate in Patients With Erosive and Non-Erosive Gastroesophageal Reflux Disease

Clinical Variables Associated With the Presence of Inflammatory Infiltrates in Patients With Dilated Cardiomyopathy Undergoing Heart Transplantation

Introduction Idiopathic dilated cardiomyopathy (DCM) is, together with ischemic heart disease, the major cause of end-stage heart failure leading to heart transplantation. However, an unknown percentage of patients with this diagnosis has inflammatory foci found in the histopathological study of the explanted heart. This fact suggests an undetected process of acute myocarditis as the cause of cardiac dysfunction. Objective The objective of this study was to identify clinical and echocardiographic variables related to the presence of myocardial infiltrates, as a potential guide to determine which patients should undergo endomyocardial biopsy in DCM. Materials and Methods We retrospectively analyzed 161 patients who underwent heart transplantation with a diagnosis of DCM between 1987 and 2007. The presence of inflammatory infiltrates was considered significant when the histopathological study of tissue blocks from the left ventricle showed 1 or more foci per cm 2 of perivascular or interstitial mononuclear or polymorphonuclear cells, whether or not in the presence of cytolysis. Results Seventeen patients (11%) had these inflammatory histological findings; of them, 6 (35%) showed preponderance of eosinophils and 7 (41%) showed areas of cytolysis. The DCM group with inflammatory infiltrates showed significant differences in terms of younger age (45 ± 15 vs 50 ± 11 years; P < .01) and smaller ventricular diameters ( P < .05). Male gender was more frequent in this group, and the patients had a poorer clinical status and greater dependence on inotropic drugs. Conclusions Inflammatory infiltrates are frequently present in DCM explanted hearts. Although there are no relevant clinical variables to identify subclinical myocarditis, these patients are younger and have smaller ventricular diameters and poorer functional status at the time of transplantation.

A 32‐year‐old nursing student with hoarseness and dysphagia to solids

A 32‐year‐old nursing student with hoarseness and dysphagia to solids

Site-Specific Intraoperative Efficacy of Arthroscopic Knee Joint Synovectomy in Rheumatoid Arthritis

To assess the intraoperative reduction of inflammatory infiltrates achieved by arthroscopic knee joint synovectomy in patients with rheumatoid arthritis (RA) with special regard to the removal site, using preoperative and postoperative synovial tissue (ST) samples. A histologic and immunohistochemical study. Eleven patients with treatment-refractory RA knee synovitis underwent arthroscopic synovectomy. In each patient, ST specimens were obtained immediately before and after synovectomy from 9 defined sites covering the whole joint. The samples were graded using an acute synovitis score (ASS; presence of polymorphonuclear neutrophilic leukocytes [PMN] and fibrin) and a chronic synovitis score (CSS; e.g., lining cell hyperplasia, presence of diffuse and lymphoid aggregates). Immunohistologic analyses were performed using 7 monoclonal antibodies directed against PMN, macrophages, and T-cell subsets (total of 1,584 preparations). Knee function was assessed after an average follow-up of 28 months by Lysholm score (modified by Klein and Jensen), Insall functional and knee scores, and Lequesne score. Arthroscopic synovectomy led to an overall significant (P between .005 and .05) reduction of the acute inflammatory infiltrates (ASS) by 82.1%, but to a significant reduction of chronic inflammatory infiltrates (CSS) by only 62.5%. Accordingly, the density of PMN was reduced by 81.8%, whereas that of macrophages and different T-cell subsets was only decreased by < or = 61.6%. With respect to the anatomic regions, a significantly (P < or = .05) less marked reduction of inflammatory infiltrates was observed in the upper lateral and central recess, at the medial and lateral capsule, as well as at the femoral insertion of the anterior cruciate ligament. All knee joint scores showed a significant (P < or = .01) improvement over preoperative values at follow-up. Arthroscopic synovectomy effectively reduces acute and chronic inflammatory infiltrates in patients with RA who have refractory synovitis of the knee joint (immediately after synovectomy) and improves knee function (28-month follow-up). However, the reduction of inflammatory infiltrates appears to depend on the anatomic region of the joint. Level III.

The gingival inflammatory infiltrate in cardiac patients treated with calcium antagonists.

To analyse the periodontal inflammatory infiltrates in patients with cardiac disease, some of these patients were treated with calcium antagonists (nifedipine and diltiazem) and some were not, to compare them with a healthy control group, and to evaluate the changes in the inflammatory infiltrate after periodontal treatment. A "healthy group" (HG, n=12), a "cardiac group" (CG, n=12) without treatment with calcium antagonists, a "nifedipine group" (NG, n=18) and a "diltiazem group" (DG, n=13) were analysed. Biopsies were taken from a zone 2-3 mm below the upper part of the interproximal papillae 12-13 and 33-32 before causal periodontal treatment and after 1 year. Using haematoxylin-eosin staining, the plasma cells (P), lymphocytes (L), histiocytes (H) and polymorphonuclear cells (PMN) were counted. T and B lymphocytes were evaluated using the monoclonal antibodies anti-CD20 and anti-CD45RO. Statistical tests used: chi2 for study of the sample composition; ANOVA for comparison between groups; Student t-test and Wilcoxon test for comparison between visits; post-hoc test Bonferroni. When the cells were compared statistically, differences were established for L at the first visit (p<0.00001) and at the last visit (p<0.02), for the B lymphocytes (first visit p<0.0021, last visit p<0.022) and for the T lymphocytes (first visit p<0.0042, last visit p<0.0021). Between the 2 visits, HG showed significant reductions for P (p<0.01), L (p<0.045) and H (p<0.033); and the NG for L (p<0.0001). Lymphocytes showed differences in the NG with respect to the B lymphocytes (p<0.008). Nifedipine affects the inflammatory infiltrate with a greater number of lymphocytes (especially B) and these cells fell significantly in number after periodontal treatment.

What you should know about PR3-ANCA: Evidence for the role of T cells in the pathogenesis of systemic vasculitis

The pathogenesis of systemic vasculitis is complex and is likely to involve many mechanisms. There is a growing body of evidence that T cells may contribute to the pathogenesis of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides. Predominantly, T cells and monocytes are found in inflammatory infiltrates in patients with Wegener's granulomatosis (WG). The production of ANCA appears to be T-cell-dependent. T lymphocytes from the peripheral blood of patients with ANCA-associated vasculitis have been shown to proliferate in response to proteinase 3 (PR3). These and other findings outlined in this review indicate T-cell involvement, although further studies are still needed to elucidate the exact contribution of T cells to the pathogenesis of systemic vasculitis.

Analysis of the IgG subclass distribution and inflammatory infiltrates in patients with anti-Hu-associated paraneoplastic encephalomyelitis.

Using immunohistochemistry, we studied the IgG subclass distribution of the anti-Hu antibody in serum, nervous system, and tumor of patients with anti-Hu-associated paraneoplastic encephalomyelitis/sensory neuropathy (PEM/PSN). The nervous system was also examined for deposits of complement and the distribution and type of inflammatory cells. IgG1 and IgG3 were the predominant isotypes of the anti-Hu IgG in serum, nervous system, and tumor. A few patients also had anti-Hu IgG2, but this isotype was not consistently present in all the regions of the nervous system studied. There was no correlation between neurologic symptoms and specific anti-Hu isotype, nor was there evidence that different anti-Hu isotypes recognized specific brain regions. Although IgG1 and IgG3 can activate complement, only weak complement reactivity was found, and that only in a few areas of the nervous system. This finding, in addition to the absence of natural killer (NK) cells, suggested that complement-mediated toxicity and antibody-dependent cell cytotoxicity mediated by NK cells are not pathogenic in PEM/PSN. Inflammatory infiltrates included CD19+ (B cells) and CD4+ (helper/inducer) cells in the perivascular spaces, and lymphocytes bearing CD8+CD11b- markers (cytotoxic T cells) in the interstitial spaces. Infiltrates of EBM11+ (monocyte/macrophage) cells were identified in the perivascular spaces (macrophage phenotype) and in those interstitial regions (microglial phenotype) with severe pathologic changes. The ability of the IgG1 and IgG3 isotypes to bind Fc receptors may have played a role in the recruitment of these monocyte/macrophage cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Inflammatory reactions in primary osteoarthritis of the hip and total hip prosthesis loosening

In 14 patients [9 with loosened total hip arthroplasty (THA), 5 with primary osteoarthritis], the inflammatory cell infiltrate was characterized in cryostat tissue sections using antibodies against subsets of macrophages and lymphocytes. In all patients the abundance of a mature type macrophage (25F9+) was observed, whereas 27E10+ macrophages, characteristic of acute inflammatory reactions, were not seen in primary osteoarthritis but were found in 4 out of 9 patients with THA loosening. The RM3/1 + macrophage phenotype was seen in some of both sets of patients (osteoarthritis 4/5; THA loosening 4/9). The markers MRP8 and MRP14 typical of immature macrophages, were found in all patients with osteoarthritis and in some (4/9 and 8/9 respectively) of those with THA loosening. IOT4+ T-helper cells were only present in 1/5 5 patients with osteoarthritis and in 2/9 patients with THA loosening. IOT8+ T-suppressor lymphocytes were more frequently present (in 4/5 and 5/9 respectively). The data reveal remarkable differences between the two groups of patients. While the inflammatory infiltrate in patients with osteoarthritis lacks the characteristics of acute inflammation, in patients THA loosening the inflammatory process seems to be determined by periods of acute reactions. The occasional presence particularly of T-helper cells suggests that the inflammatory process is less T-cell but rather macrophage-driven.