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Inflammatory Infiltration (inflammatory + infiltration)
Kinds of Inflammatory Infiltration Selected AbstractsNeurokinin-1 receptor activation induces reactive oxygen species and epithelial damage in allergic airway inflammationCLINICAL & EXPERIMENTAL ALLERGY, Issue 12 2007J. Springer Summary Background An induction of reactive oxygen species (ROS) is characteristic for inflammation but the exact pathways have not been identified for allergic airway diseases so far. Objective The aim of this study was to characterize the role of the tachykinin NK-1 receptor on ROS production during allergen challenge and subsequent inflammation and remodelling. Methods Precision-cut lung slices of ovalbumin (OVA)-sensitized mice were cultivated and ROS-generation in response to OVA challenge (10 ,g/mL) was examined by the 2,,7,-dichloroflourescein-diacetate method. Long-term ROS effects on epithelial proliferation were investigated by 5-bromo-2,-deoxyuridine incorporation (72 h). In vivo, the results were validated in OVA-sensitized animals which were treated intra-nasally with either placebo, the tachykinin neurokinin 1 (NK-1) receptor antagonist SR 140333 or the anti-oxidant N -acetylcystein (NAC) before allergen challenge. Inflammatory infiltration and remodelling were assessed 48 h after allergen challenge. Results ROS generation was increased by 3.7-fold, which was inhibited by SR 140333. [Sar9,Met11(O2)]-Substance P (5 nm) caused a tachykinin NK-1 receptor-dependent fourfold increase in ROS generation. Epithelial proliferation was decreased by 68% by incubation with [Sar9,Met11(O2)]-SP over 72 h. In-vivo, treatment with SR 140333 and NAC reduced epithelial damage (91.4% and 76.8% vs. placebo, respectively, P<0.01) and goblet cell hyperplasia (67.4% and 50.1% vs. placebo, respectively, P<0.05), and decreased inflammatory cell influx (65.3% and 45.3% vs. placebo, respectively, P<0.01). Conclusion Allergen challenge induces ROS in a tachykinin NK-1 receptor-dependent manner. Inhibition of the tachykinin NK-1 receptor reduces epithelial damage and subsequent remodelling in vivo. Therefore, patients may possibly benefit from treatment regime that includes radical scavengers or tachykinin NK-1 receptor antagonists. [source] Circumferential mural bands in the small intestine causing simple obstructive colic: a case seriesEQUINE VETERINARY JOURNAL, Issue 4 2006J. F. PEREZ OLMOS Summary Reasons for performing study: Circumferential mural band (CMB) in the small intestine is an emerging condition in Ireland. The clinical presentation is a simple obstruction of the small intestine of unknown aetiology. Hypothesis: Horses affected with CMB in the small intestine have a good prognosis following surgical decompression into the caecum. Methods: A retrospective study was carried out and 28 cases identified from 559 colic surgeries performed over a 5.5 year period. An exploratory celiotomy was performed in every case. A simple obstruction at the mid or distal jejunum was identified caused by a CMB, which was multiple in some cases. All of the horses except 2 had undergone a regular anthelmintic programme. Results: Manual decompression of the small intestine into the caecum resulted in resolution of the simple jejunal obstruction. A constricted segment of small intestine was resected in one case, as the degree of constriction was severe. A full thickness biopsy was taken from another case. Histopathology was performed on both samples. All horses recovered from surgery and were discharged from the hospital 7,32 days post operatively. Short-term complications were observed. Survival rate was 100% at long-term follow-up. Histopathology showed inflammatory infiltration in the submucosa, muscularis and serosa with eosinophils predominating. Parasites were not detected. Conclusion and potential relevance: Small intestine circumferential mural bands have a good prognosis after surgical decompression of the small intestine into the caecum. [source] Oxidative damage is increased in human liver tissue adjacent to hepatocellular carcinomaHEPATOLOGY, Issue 6 2004Christoph Jüngst Accumulation of genetic alterations in hepatocarcinogenesis is closely associated with chronic inflammatory liver disease. 8-oxo-2,-deoxyguanosine (8-oxo-dG), the major promutagenic DNA adduct caused by reactive oxygen species (ROS), leads to G:C , T:A transversions. These lesions can be enzymatically repaired mainly by human MutT homolog 1 (hMTH1), human 8-oxo-guanine DNA glycosylase (hOGG1) and human MutY homolog (hMYH). The aim of this study was to evaluate the extent of oxidative damage and its dependence on the cellular antioxidative capacity and the expression of specific DNA repair enzymes in tumor (tu) and corresponding adjacent nontumor (ntu) liver tissue of 23 patients with histologically confirmed hepatocellular carcinoma. 8-oxo-dG levels, as detected by high-pressure liquid chromatography with electrochemical detection, were significantly (P = .003) elevated in ntu tissue (median, 129 fmol/,g DNA) as compared to tu tissue (median, 52 fmol/,g DNA), and were closely associated with inflammatory infiltration. In ntu tissue, the hepatic iron concentration and malondialdehyde levels were significantly (P = .001) higher as compared to tu tissue. Glutathione content, glutathione peroxidase activity and manganese superoxide dismutase messenger RNA (mRNA) expression did not show statistical differences between ntu and tu tissue. Real-time reverse transcription polymerase chain reaction revealed in tu tissue significantly (P = .014) higher hMTH1 mRNA expression compared to ntu tissue. In contrast, hMYH mRNA expression was significantly (P < .05) higher in ntu tissue. No difference in hOGG1 mRNA expression was seen between tu and ntu. In conclusion, these data suggest that ROS generated by chronic inflammation contribute to human hepatocarcinogenesis. The role of DNA repair enzymes appears to be of reactive rather than causative manner. (HEPATOLOGY 2004;39:1663,1672.) [source] Major histocompatibility complex (MHC) class II but not MHC class I molecules are required for efficient control of Strongyloides venezuelensis infection in miceIMMUNOLOGY, Issue 1pt2 2009Rosāngela M. Rodrigues Summary Strongyloides stercoralis is an intestinal nematode capable of chronic, persistent infection and hyperinfection of the host; this can lead to dissemination, mainly in immunosuppressive states, in which the infection can become severe and result in the death of the host. In this study, we investigated the immune response against Strongyloides venezuelensis infection in major histocompatibility complex (MHC) class I or class II deficient mice. We found that MHC II,/, animals were more susceptible to S. venezuelensis infection as a result of the presence of an elevated number of eggs in the faeces and a delay in the elimination of adult worms compared with wild-type (WT) and MHC I,/, mice. Histopathological analysis revealed that MHC II,/, mice had a mild inflammatory infiltration in the small intestine with a reduction in tissue eosinophilia. These mice also presented a significantly lower frequency of eosinophils and mononuclear cells in the blood, together with reduced T helper type 2 (Th2) cytokines in small intestine homogenates and sera compared with WT and MHC I,/, animals. Additionally, levels of parasite-specific immunoglobulin M (IgM), IgA, IgE, total IgG and IgG1 were also significantly reduced in the sera of MHC II,/, infected mice, while a non-significant increase in the level of IgG2a was found in comparison to WT or MHC I,/, infected mice. Together, these data demonstrate that expression of MHC class II but not class I molecules is required to induce a predominantly Th2 response and to achieve efficient control of S. venezuelensis infection in mice. [source] Histological evaluation of the osteoinduction capability of human dentineINTERNATIONAL ENDODONTIC JOURNAL, Issue 11 2006M. E. L. Machado Abstract Aim, To assess whether human dentine has the potential to promote the development of calcified tissues when implanted in the muscle tissue of mice. Methodology, Root canals in extracted human teeth were instrumented to produce dentine fragments. The dentine fragments produced were divided into two. In group 1, fragments were demineralized and sterilized. In group 2, the fragments were not submitted to any additional treatment. The dentine fragments were then implanted in the muscle of mice. In group 3, the muscles were implanted with rehydrated lyophilized human bone powder. Animals were killed following test periods of 7, 15, 30, 60, 120 and 180 days, the fragments were removed together with adjacent muscle and examined under light microscopy to assess calcification. Results, Areas of calcification were observed in groups 1 and 3 after a period of 180 days. In group 2, the surrounding tissues displayed only chronic inflammatory infiltration. Conclusions, On the basis of the experimental model adopted in this study, fibroblast-rich connective tissue formed in groups 1 and 3, which could reflect an osteoinductive process. Further studies are suggested to identify which dentinal factors are capable of inducing the formation of a calcified matrix. [source] Bullous variant of Sweet's syndromeINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 11 2005Susanne Voelter-Mahlknecht MD A 69-year-old woman presented to our clinic as an emergency with erythematous, well-circumscribed plaques, which were partly vesicular, on her extremities and in her armpits, and additionally hemorrhagic blisters on both her palms and her fingers (Fig. 1a), which had developed 2 days after the first appearance of the skin lesions. The rapid onset of the lesions (within a few hours) and the pain associated with them were extremely troublesome to the patient. On admission she complained of fever, tiredness and being easily fatigued. Because of a urinary tract infection 1 month prior to admission, trospiumchloride was given. On clinical examination, body temperature was found to be above 38 °C and infraclavicular lymph nodes were enlarged but not tender. Figure 1. (a) Bullae on the patient's right hand. (b) Multiple partly confluent vesicles with neutrophilic granulocytes intraepidermally and a dense interstitial perivascular infiltration of neutrophilic granulocytes and lymphomononuclear cells (H&E, ×200) Normal or negative laboratory tests included blood counts, liver and kidney parameters, electrolytes and infection screen. Laboratory examination demonstrated minor leukocytosis and absolute neutrophilia (white blood cell count 10 440 cells/µL, neutrophils 8030 cells/µL). X-ray screening, abdominal ultrasound and laboratory investigations were all normal. There was no response to antibiotics when erythromycine was given. However, there was a good response to systemic corticosteroids. The patient was treated with a low dosage of prednisolone, beginning at 50 mg/day, which was then tapered off. Skin lesions resolved within 7 days. Histology from a lesion on the patient's left forearm showed a dense interstitial inflammatory infiltration consisting predominantly of neutrophilic granulocytes from the subepidermal layer to the middle of the reticular dermis. Inflammatory cells penetrated into both blood vessels and vessel walls; vasculitis was not prominent. In the lower dermis, perivascular infiltrations of lymphomononuclear cells were found. In addition, intraepidermally multiple partly confluent vesicles, with inclusions of neutrophilic granulocytes, were found, confirming the diagnosis of this rare variant of an acute febrile neutrophilic dermatosis (Fig. 1b). [source] Cutaneous sarcoid-like granulomas with alveolar hemorrhage and c-ANCA PR-3INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 9 2004Natividade Rocha MD A 28-year-old woman, employed as a leather factory worker, noted asymptomatic, well-delimited plaques on both knees, 6 years ago. The plaques were violaceous with a smooth surface. One appeared over a post-traumatic scar from childhood (Fig. 1). Two years later, she began to complain of symptoms suggestive of polyarthritis, first of the small joints of the hands (proximal interphalanges) and then of the larger joints (wrists, elbows, and knees). She was diagnosed with rheumatoid arthritis and began treatment with nonsteroidal anti-inflammatory drugs for 1 month without any change. Deflazacort, 12 mg/day, and hydroxychloroquine, 400 mg/day, were administered for 3 months, with improvement of her articular complaints, but not her skin lesions. Figure 1. Well-delimited, violaceous plaques with a smooth surface on the knees, one over an old post-traumatic scar One year later, she complained of dysphonia, which remitted spontaneously after some weeks. After one additional year, she noted papules, with similar characteristics to the plaques, on the elbows, and two well-delimited orange-to-brown plaques on the forehead (Fig. 2). Figure 2. Orange,brown plaques symmetrically placed on the forehead During the fifth year of the disease, she was referred for the first time to a dermatologist, who biopsied one of the knee lesions. The histologic result was compatible with "sarcoid granuloma." At that time, she presented with skin lesions as her only complaint. Sarcoidosis was suspected based on a chest X-ray, which revealed hilar lymphadenopathy and diffuse accentuation of the interstitium. In November 2000, she suddenly developed fever (40 °C), cough with hemoptysis, dysphonia, and subcutaneous nodules on the palmar surface of the fingers of both hands that were painless, well-delimited, 5 mm in diameter, and firm (Fig. 3). She reported a weight loss of 12 kg in the previous 3 months. Pulmonary condensation was found on auscultation, and she had palpable hepatomegaly. Peripheral lymphadenopathy was not present. Figure 3. Painless, well-delimited, firm subcutaneous nodules on the palmar surface of the fingers Laboratory investigations revealed normochromic, normocytic anemia (hemoglobin, 7.7 g/dL), iron deficit, a white blood cell count of 16,000/µL with neutrophilia, an erythrocyte sedimentation rate of 130 mm/h, elevation of liver enzymes, a slight increase in angiotensin-converting enzyme (ACE) level (72 U/L), hypergammaglobulinemia (IgG, 3350 mg/dL), antinuclear antibody (ANA) of 1 : 320, and a slight increase in CD4 and decrease in CD8 lymphocytes with normal cellular morphology in blood. Renal function, urine sediment, urine and serum calcium, complement (C4), dsDNA, antimitochondrial antibody, direct and indirect Coombs test, antineutrophil cytoplasmic antibody (ANCA), tuberculin skin tests, viral markers of hepatitis B, C, and human immunodeficiency virus (HIV), electrocardiogram (ECG), ophthalmic examinations, and culture for infectious agents in blood and sputum were all normal or negative. Computed tomography (CT) scan showed an infiltrate in the upper right pulmonary lobule with a central cavity and bilateral hilar lymphadenopathy (Fig. 4). Homogeneous hepatosplenomegaly was present. The bronchoalveolar lavage (BAL) showed a slight lymphocytic increase predominantly of CD8 cells and hemosiderosis. Stains for infectious agents, including acid-fast bacillus, fungi, Mycoplasma, and Legionella, were negative. Three biopsies from the forehead, elbows, and knees showed well-formed noncaseating epithelioid cell granulomas with giant cells of the Langhans type in the dermis, suggestive of sarcoidosis (Figs 5 and 6). A fourth biopsy from a finger nodule demonstrated inflammatory infiltration of the dermis and necrosis with cellular debris. Vasculitis was not seen (Fig. 7). Figure 4. Computed tomography scan showing an infiltrate in the upper right pulmonary lobule with a central cavity Figure 5. Beneath a flattened epidermis, several sarcoid granulomas composed of epithelioid histiocytes and several multinucleated giant cells of Langhans type can be seen (hematoxylin and eosin, ×10) Figure 6. Less well-formed sarcoid granulomas in a hyperkeratotic area, surrounded by a sparse rim of lymphocytes (hematoxylin and eosin, ×20) Figure 7. Foci of necrosis and fibrinoid degeneration with some neutrophil infiltration and nuclear dusting (hematoxylin and eosin, ×40) The patient was treated with a broad-spectrum empirical antimicrobial (levofloxacin, 500 mg daily intravenously) over 12 days, with prompt improvement in her symptoms and remission of the forehead and finger lesions. Nevertheless, on the first evaluation after hospitalization, the CT scan showed persistence of the pulmonary cavity (Fig. 8). A repeat ANCA determination was positive (cytoplasmic pattern, c-ANCA) at 1 : 640 by indirect immunofluorescence (IIF). Antiproteinase-3 antibody was demonstrated at 78 by enzyme-linked immunosorbent assay (ELISA). Figure 8. Computed tomography scan showing persistence of the pulmonary cavity She underwent an open lung biopsy which revealed intra-alveolar hemorrhage and scanty noncaseating epithelioid cell granulomas of the sarcoidosis type in the peripheral blood vessels without vasculitis. A diagnosis of Wegener's granulomatosis was made and she began prednisolone (1 mg/kg/day) and oral cyclophosphamide (2 mg/kg/day). One year later, she is asymptomatic, the skin lesions have completely remitted, c-ANCA is negative, and the CT scan shows partial regression of the pulmonary cavity. [source] Evidence for a perforin-mediated mechanism controlling cardiac inflammation in Trypanosoma cruzi infectionINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 2 2002ANDREA HENRIQUES-PONS Summary. ,CD8+ T lymphocytes are considered an important cell population involved in the control of parasitaemia and mortality after Trypanosoma cruzi infection. However, despite recent developments in this field, the mechanism whereby this control is exerted is still not completely understood. Here we have used perforin knockout (,/,) mice infected with Y strain T. cruzi in order to evaluate specifically the participation of the perforin-based cytotoxic pathway in the destruction of cardiomyocytes, cellular inflammatory infiltration, and control of parasitaemia and mortality. We observed that although parasitaemia was equivalent in perforin (+/+) and (,/,) groups, survival rate and spontaneous physical performance were significantly lower in the perforin deficient mice. The cardiac inflammatory cell infiltration, mostly composed of CD8+ cells, was more evident in perforin (,/,) mice. Ultrastructural and immunofluorescence analysis, as well as plasma creatine kinase activity, revealed cardiomyocyte damage and necrosis, more evident in perforin (,/,) mice. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assays performed in heart samples revealed similar and modest levels of apoptosis in both perforin (+/+) and (,/,) mice. These results indicate that perforin does not play a pivotal role in the control of parasitaemia and direct lysis of cardiomyocytes, but seems to be an important molecule involved in the control of cardiac inflammation and pathology induced by a highly virulent strain of T. cruzi. [source] Prognostic significance of tumor shape and stromal chronic inflammatory infiltration in squamous cell carcinomas of the oral tongueJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 9 2010Ioulia Chatzistamou J Oral Pathol Med (2010) 39: 667,671 Background:, Squamous cell carcinoma (SCC) of the oral tongue is well known to be an aggressive disease with early metastatic spread in early stage tumors. It is also established that locoregional recurrences are the main causes of treatment failure. Thus, the identification of histopathological factors possessing a predictive value remains important for the management of the disease. The aim of the present study was to define histopathological parameters of the tumor and to compare with the follow-up and status in primary SCCs of the mobile tongue. Methods:, Histopathological parameters such as mitotic index, the presence of vascular emboli or perineural invasion, the thickness of the tumor, the histological grade, the tumor shape as well as chronic stromal inflammatory infiltration were assessed in 52 patients with SCC of the mobile tongue and compared with the follow-up and status in patients treated initially by surgery. Results:, Tumor shape was significantly associated with the presence of perineural invasion. Well-defined shaped tumors displayed almost half the incidence of perineural invasion when compared with ill-defined shaped tumors. In addition, the high density of the chronic inflammatory infiltration of the stroma exhibited significant correlation with the survival of the patients. Finally, the intense chronic inflammatory infiltration of the stroma was associated with well-defined shaped tumors. Conclusion:, Tumor shape and stromal chronic inflammatory infiltration should be considered in the planning of the management of patients with SCC of the mobile tongue. [source] Magnetic resonance imaging and pathological findings in a case of canine idiopathic eosinophilic meningoencephalitisJOURNAL OF SMALL ANIMAL PRACTICE, Issue 8 2007C Salvadori A case of idiopathic eosinophilic meningoencephalitis in a six-month-old male Maremma shepherd dog is reported. The dog was referred with a four month history of progressive weakness and depression with loss of trained habits. Tendency to recumbency, disorientation, visual impairment, bilaterally decreased menace response and hindlimb conscious proprioception deficits were detected. Magnetic resonance imaging showed a diffuse hypointense signal involving the cerebral grey matter with enlargement of the cerebral sulci on T1-weighted and fast fluid-attenuated inversion recovery (FLAIR) sequences consistent with a diffuse necrosis or atrophy of the cortical grey matter. Histological examination revealed severe inflammatory infiltration mainly composed of eosinophils and macrophages in the subarachnoid space and in the superficial layer of the cerebral cortex where parenchymal rarefaction and necrosis of neurones were also evident. No parasites, cysts or fungi were detected, and an immunologically mediated disorder was suspected. Magnetic resonance imaging may represent a useful diagnostic tool to differentiate idiopathic eosinophilic meningoencephalitis from other inflammatory brain diseases of young dogs. [source] CIDP associated with lung cancer: a paraneoplastic disease?JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004R Fazio We describe a 65-year-old smoker male followed for five years for a pure motor demyelinating peripheral neuropathy. The patient had a monthly motor relapse with severe weakness restricting him to a wheelchair, so he needed monthly high dose IVIg. On EMG the MCV were very slowed (30 m/sec) without evidence of conduction blocks while SCV were in the normal range. CSF disclosed a high protein level. Laboratory findings did not reveal any other abnormality except for the presence of monoclonal gammopathy IgMk and high titer anti GD1a serum IgM antibodies (1:5000). In March 2003 he had the most severe relapse with flaccid tetraplegia and respiratory failure so severe that he required ventilatory support. A total body CT scan revealed a nodular lung lesion with diffuse lymphangiitis. Biopsy disclosed a lung adenocarcinoma with a severe infiltration of CD8 cells. Surgical eradication of the tumor caused the last severe relapse. At the moment the patient is relapse-free and no more treatment was administered. The clinical course of the motor demyelinating relapsing neuropathy suggests a possible paraneoplastic pathogenesis of the neurological illness also supported by the severe inflammatory infiltration of the tumor. [source] Sudden death caused by chronic Chagas disease in a non-endemic country: Autopsy reportPATHOLOGY INTERNATIONAL, Issue 3 2010Fumiko Satoh Chagas disease is a tropical disease that is prevalent in Latin America. Described herein is an autopsy case of the sudden death of a 48-year-old Brazilian man who had stayed in Japan for 7 years. The man, who had a history of Chagas disease, collapsed unexpectedly at work. Because the cause of death was unknown, forensic autopsy examination was performed. As gross findings, the heart was dilated and rounded with an increase in size and weight. The esophagus and large intestine were dilated moderately, with extensive interstitial inflammatory infiltration in the cardiac muscle, but no apparent parasite nest was observed in various tissues. On post-mortem laboratory examinations, indirect immunofluorescence antibody test indicated the presence of IgG antibody specific to Trypanosoma cruzi in the serum. Subsequent polymerase chain reaction amplification using DNA extracted from blood yielded the specific product derived from T. cruzi genomic DNA. These examinations indicate that the infection had resulted from the Tripanosoma parasite. The cause of death was judged to be chronic cardiomyopathy caused by Chagas disease. It is important for pathologists to know the possible involvement of chronic Chagas disease in sudden unexpected deaths in the current globalized society of Japan. [source] 006 Efficacy of photochemotherapy and UVA-1 therapy in patients with morphea or lichen sclerosusPHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 2 2002K. Ghoreschi Morphea and lichen sclerosus are inflammatory skin diseases of unknown aetiology. Morphea can be subdivided into plaque morphea, linear morphea and disabling or generalized morphea. In most patients morphea leads to superficial or deep sclerosis of the skin. The characteristic features of lichen sclerosus which often affects the genital area are edema of upper dermis, inflammatory infiltration and hyalinisation to the dermis at advanced stages. Patients with morphea or lichen sclerosus suffer especially from scar formation and morphea may lead to severe disfigurement, contractures and reduction of quality of life. Skin sclerosis seems to be the result of vascular damage, T cell activation and altered connective tissue production. Various therapies have been reported for lichen sclerosus and morphea. Whereas the topical use of ultrapotent corticosteroids is well established for genital lichen sclerosus, immunosuppressive agents are normally not successful in resolving extragenital skin sclerosis. In a retrospective study we confirmed the efficacy of phototherapy in more than 50 patients with morphea. Fourty treatments with 30 J/cm2 UVA-1 or PUVA-bath photochemotherapy resulted in a significant improvement, reduced skin thickness, as determined by high frequency ultrasound and reconstitution of functional mobility of the skin and even the underlying fasciae. In lichen sclerosus phototherapy was successful only in some patients. Thus for lichen sclerosus the use of topical corticosteroids is the first choice therapy, while phototherapy using either PUVA-bath or medium dose UVA-1 are the most effective treatments for morphea. [source] T-cell recognition of a prostate specific antigen is not sufficient to induce prostate tissue destructionTHE PROSTATE, Issue 6 2006Jason R. Lees Abstract METHODS The ability of CD8+ T-cells to induce prostate inflammation was examined using a prostate ovalbumin expressing transgenic mouse (POET) and/or adoptive transfer of T-cell receptor (TCR) transgenic T-cells (OT-I) that specifically recognize ovalbumin. Localization of inflammatory cells to prostate tissue was examined following T-cell activation via endogenous prostatic antigen, recombinant type 5 adenovirus carrying the gene coding ovalbumin (Ad5-mOVA), or adoptive transfer of in vitro antigen stimulated OT-I cells. RESULTS Ovalbumin specific OT-I cells were activated by autologous prostate antigen and trafficked to the prostate, but did not induce inflammation unless present in overwhelming numbers (,65% of CD8+ T-cells). Activation of antigen specific CD8+ T-cells in vitro (peptide pulsed antigen presenting cells) or in vivo (Ad5-mOVA) induced transitory prostate inflammation, without induction of prostate pathology, regardless of CD4+ T-cell availability. Inflammation also was observed in OT-I,×,POET mice but again, pathological effects were not observed. CONCLUSIONS T lymphocytes specific for a prostate antigen are capable of inducing inflammatory infiltration of prostatic tissue rapidly following activation, but do not produce pathological prostate injury. Prostate 66:578,590, 2006. © 2005 Wiley-Liss, Inc. [source] Inflammatory rheumatic disease and smoking are predictors of aortic inflammation: A controlled study of biopsy specimens obtained at coronary artery surgery,ARTHRITIS & RHEUMATISM, Issue 6 2007Ivana Hollan Objective Several inflammatory rheumatic diseases are associated with accelerated atherosclerosis. Atherosclerosis may result from systemic and/or local vascular inflammation. The aim of this study was to evaluate the occurrence of chronic inflammatory infiltrates in the aortas of patients with and those without inflammatory rheumatic disease who had undergone coronary artery bypass graft (CABG) surgery, and to assess the relationship between the infiltrates and other factors thought to play a role in atherosclerosis, such as smoking. Methods Aortic specimens routinely removed during CABG surgery in 66 consecutive patients with inflammatory rheumatic disease and 51 control patients without inflammatory rheumatic disease were examined by light microscopy for the occurrence, location, and severity of chronic inflammatory infiltrates and atherosclerotic lesions. Results Mononuclear cell infiltrates in the inner adventitia (apart from those localized along the epicardium) were more frequent in the group of patients with inflammatory rheumatic disease (47% versus 20%; P = 0.002, odds ratio [OR] OR 3.6, 95% confidence interval [95% CI] 1.6,8.5), and the extent of these infiltrates was greater. Multivariate analyses revealed that the occurrence of mononuclear cell infiltrates was associated with inflammatory rheumatic disease (OR 2.99, P = 0.020) and current smoking (OR 3.93, P = 0.012), and they were observed in 6 of 7 patients with a history of aortic aneurysm. Inflammatory infiltrates in the media were seen only in patients with inflammatory rheumatic disease. The frequency of atherosclerotic lesions, inflammation within the plaques, and epicardial inflammatory infiltrates in the 2 groups was equal. Conclusion Among aortic samples collected during CABG surgery, those obtained from patients with inflammatory rheumatic disease had more pronounced chronic inflammatory infiltration in the media and inner adventitia than those obtained from control patients. Current smoking was an independent predictor of chronic inner adventitial infiltrates. The infiltrates may represent an inflammatory process that promotes atherosclerosis and formation of aneurysms. [source] 1263: Symptoms and signs of posterior uveitisACTA OPHTHALMOLOGICA, Issue 2010M KHAIRALLAH Purpose Posterior uveitis (PU) is an important anatomic form of uveitis in which the primary site of inflammation is the choroid or retina, with or without subsequent vitreous involvement. Methods Review of symptoms and signs of PU. Results The onset of PU can be sudden or less frequently insidious. Most common ocular symptoms include blurred vision, loss of vision, and floaters. Some patients with PU may have no symptoms, especially if inflammatory process is asymmetric. PU is usually associated with vitritis that can vary from mild to severe. Vitritis should be graded according to standardized grading systems. Other vitreous changes may include vitreous strands, vitreous hemorrhage, vitreous traction, and posterior vitreous detachment. Retinal and/or choroidal inflammation can be focal, multifocal, or more diffuse. It is important to distinguish between active and inactive chorioretinal disease. Retinal vasculitis can occur in the setting of several PU entities. It can involve retinal veins or arteries. It appears as focal, multifocal, or diffuse vascular cuffing or sheathing. Other retinal vasculitic changes include retinal hemorrhages, retinal vascular occlusion, retinal/optic disc neovascularization, and aneurysms. Maculopathy is common patients with PU. It may result from direct inflammatory infiltration, macular edema, serous retinal detachment, retinal ischemia, epiretinal membrane, or macular hole. Optic nerve involvement that can occur in association with PU include optic disc hyperemia/edema, optic neuritis, neuroretinitis, optic disc exudate, and optic disc granuloma. Conclusion Clinical examination is a key step in the diagnostic approach to PU. Clinician should be aware of the array of ocular symptoms of signs and their importance in orienting the differential diagnosis. [source] | ||||||||||||||||||||||