SEARCH · PubMed Health

Results for “Inflammatory”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

PubMed2002

Inflammatory myofibroblastic tumor (inflammatory pseudotumor) of the maxillary sinus mimicking malignancy: a case report of an unusual location (is that a true neoplasm?).

The inflammatory myofibroblastic tumor (IMT) is a space-occupying lesion of unknown etiology and a distinctive but controversial lesion. This type of tumor is recently considered neoplastic rather than inflammatory. It is usually occurring during childhood, composed of fascicles of bland myofibroblastic cells admixed with a prominent inflammatory infiltrate consisting of lymphocytes, plasma cells, and eosinophils. IMT of the maxilla is very rare. The diagnosis of IMT can be made on the basis of histopathology and immunohistochemistry. Herein, we presented a patient who had IMT of the maxillary sinus that was initially misinterpreted as a malignant neoplasm upon clinical and radiographic examinations. We discussed the diagnostic and therapeutic procedures and may consider it a true neoplasm.

Combined Modality Therapy↗

PubMed2001

Effect of beta-blockers on circulating levels of inflammatory and anti-inflammatory cytokines in patients with dilated cardiomyopathy.

OBJECTIVES: This study was designed to evaluate the beneficial effect of beta-blockers on circulating cytokine levels in patients with dilated cardiomyopathy (DCM). BACKGROUND: Elevated circulating levels of inflammatory cytokines have been reported in patients with DCM. However, alterations of the levels of inflammatory and anti-inflammatory cytokines in association with beta-blocker therapy are unknown. METHODS: We studied 32 patients with idiopathic DCM who had been treated with digitalis, diuretics and angiotensin-converting enzyme inhibitors. In addition to this combination therapy, beta-blockers were started in all patients. Serum levels of interleukin (IL)-10, tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptors (sTNF-R1 and R2) were measured at baseline and 12 weeks after the initiation of beta-blocker therapy. We also measured plasma levels of neurohumoral factors, as well as left ventricular (LV) size and function. Ten age-matched subjects with no cardiac disease served as the control group. RESULTS: Baseline levels of IL-10, TNF-alpha and sTNF-R2 were significantly higher in patients with DCM than in control subjects (p < 0.05). There was a significant positive correlation between IL-10 and TNF-alpha levels (r = 0.545, p = 0.029). The TNF-alpha/IL-10 ratio correlated well with plasma epinephrine levels (r = 0.677, p = 0.025), and the level of sTNF-R2 was closely related to LV size. Serum levels of IL-10, TNF-alpha and sTNF-R2 were significantly decreased during beta-blocker therapy (p < 0.005). CONCLUSIONS: Our findings indicate that beta-blockers have an important immunoregulatory role in modifying the dysregulated cytokine network in DCM. This effect of beta-blockers may be partly responsible for the efficacy of therapeutic drugs for heart failure.

Adrenergic beta-Antagonists↗

PubMed2000

ICAM-1 and alpha3beta1 expression by bronchial epithelial cells and their in vitro modulation by inflammatory and anti-inflammatory mediators.

BACKGROUND: Adhesion molecules are involved in inflammatory and repair processes of the bronchial epithelium. ICAM-1 is mainly involved in inflammatory reactions, whereas integrins, such as alpha3beta1, are mainly involved in repair processes. METHODS: Using bronchial biopsies from 10 asthmatics and eight controls, we first evaluated by immunohistochemistry expression of alpha3beta1 and ICAM-1 in intact and damaged epithelium. Then, using the human pulmonary epithelial cell line WI-26 VA, we studied, by flow-cytometry, the modulation of ICAM-1 and alpha3beta1 expression, and, by ELISA, the release of fibronectin by proinflammatory cytokines, such as IL-5, and anti-inflammatory cytokines, such as IL-4, TGF-beta, and EGF. RESULTS: alpha3beta1 expression was slightly higher in asthma than in controls, as well as in damaged epithelium than in undamaged epithelium. ICAM-1 expression was higher in asthma than in controls, and similarly distributed in intact or damaged epithelium. In vitro, alpha3beta1 was significantly increased by TGF-beta, EGF, and IL-4, and significantly decreased by IL-5. Fibronectin release was significantly increased by TGF-beta and IL-4, unchanged by EGF, and slightly but significantly decreased by IL-5. ICAM-1 expression was significantly decreased by TGF-beta and IL-4, unchanged by EGF, and significantly increased by IL-5. CONCLUSIONS: These differences in adhesion molecule expression and fibronectin release may be important in epithelial cell inflammation and repair.

Adolescent↗

PubMed2001

Immunohistochemical analysis of CD1a-labeled Langerhans cells in human dental periapical inflammatory lesions--correlation with inflammatory cells and epithelial cells.

OBJECTIVE: Distribution and density of CD1a-labeled Langerhans cells (LCs) were examined in human dental periapical inflammatory lesions, and compared with inflammatory cell infiltration or epithelial cell proliferation. MATERIALS AND METHODS: Eighty three periapical lesions (26 apical granulomas (AGs), 8 epitheliated granulomas (EGs), 34 radicular cysts (RCs), 15 residual radicular cysts (RRCs)) were collected. As control, specimens of periodontal ligaments including Malassez epithelial rests were curetted from 21 teeth. LC densities were measured and various degrees of inflammatory cell infiltration were examined immunohistochemically. Labeling indices for the cellular proliferation markers Ki-67 antigen and DNA topoisomerase II alpha were calculated in the epithelial components. RESULTS: LCs were found in all periapical lesions but not in Malassez epithelial rests. LCs were more abundant in epithelial components than in subepithelial layers. Intraepithelial LCs were more frequent in RCs than in RRCs, whereas subepithelial LCs were less frequent in RRCs than in AGs and EGs. T lymphocytes consistently outnumbered macrophages, plasma cells and B lymphocytes. The range of the CD4/CD8-positive cell ratio differed according to the lesions. Increased LC density was associated with the severity of CD3-positive cell infiltration. Ki-67- and Topo II-LI showed various degrees of epithelial immunoreactivity. There was a significant correlation between LC density and proliferative potential of the epithelium in periapical lesions. CONCLUSION: These findings suggested that LCs appeared to be associated with T lymphocyte infiltration and proliferative potential of the epithelial tissue in periapical lesions.

Adult↗

PubMed1988

Resolution of the two components of macrophage inflammatory protein 1, and cloning and characterization of one of those components, macrophage inflammatory protein 1 beta.

A number of macrophage-derived mediators have been implicated in the vascular changes of inflammation. We recently reported the isolation of a novel monokine, macrophage inflammatory protein 1 (MIP-1), which causes local inflammatory responses in vivo, and induces superoxide production by neutrophils in vitro. Purified native MIP-1 comprises two peptides with very similar physical characteristics. We report here the resolution of MIP-1 into component peptides by SDS-hydroxylapatite chromatography, and compare the NH2-terminal sequences of the two peptides, now referred to as MIP-1 alpha and MIP-1 beta. A synthetic oligonucleotide probe pool corresponding to the NH2-terminal amino acid sequence of MIP-1 beta was used to isolate a cDNA clone containing its coding sequence. The sequence codes for a 109 amino acid-long polypeptide, of which 69 amino acids correspond to the mature product. Comparison of this MIP-1 beta cDNA with our previously cloned MIP-1 alpha sequence reveals that the MIP-1 peptides, members of a growing family of potential inflammatory mediators, are distinct but highly homologous (58.9% sequence identity) products of different genes.

Animals↗

PubMed1993

Zinc distribution in blood components, inflammatory status, and clinical indexes of disease activity during zinc supplementation in inflammatory rheumatic diseases.

The effects of zinc supplementation on zinc status and on clinical and biological indicators of inflammation were investigated in 18 patients with chronic inflammatory rheumatic diseases and in 9 healthy control subjects. Patients with mild and recent onset disease were assigned to a 60-d trial to receive either 45 mg Zn (as gluconate)/d or a placebo, while control subjects received the zinc supplement. Baseline mean plasma zinc of the patients was low whereas mononuclear cell zinc content was elevated, suggesting a redistribution of the element related to the inflammatory process rather than to a zinc-deficient state. Zinc supplementation increased plasma zinc to a similar extent in patients and in control subjects, which suggested no impairment of zinc intestinal absorption as a result of the inflammatory process. On the contrary, erythrocyte and leukocyte zinc concentrations were not modified in the two groups examined. No beneficial effect of zinc treatment could be demonstrated on either clinical or inflammation indexes.

Adult↗

PubMed1995

Are CD4+ Th1 cells pro-inflammatory or anti-inflammatory? The ratio of IL-10 to IFN-gamma or IL-2 determines their function.

Human CD4+ T cells have, like their murine counterparts, been classified on the basis of their cytokine profile. Th1 cells produce IL-2 and IFN-gamma, but little or no IL-4. Th2 cells produce IL-4 but not IFN-gamma or IL-2, and Th0 produce IL-2, IL-4 and IFN-gamma. As IL-2 is the most potent T cell growth factor and IFN-gamma is the strongest activator of macrophages it is not surprising that CD4+ Th1 cells are considered to be pro-inflammatory. However, unlike results in the mouse, where IL-10 is only produced by Th2 cells, human IL-10 is produced by Th0, Th1 and Th2 cells. Hence some human Th1 cells are capable of producing both pro-inflammatory (IL-2, IFN-gamma) and anti-inflammatory (IL-10) cytokines, therefore the function of these cells may not be accurately encapsulated by the 'Th1' terminology. We thus investigated the correlation of cytokine production and function in human CD4+ Th1 clones. Cytokine production (IL-2, IFN-gamma, IL-10) was measured in supernatants by ELISA after stimulation with solid-phase anti-CD3. The capacity of these supernatants to activate or inhibit T cell proliferation or LPS induced TNF-alpha production by monocytes was assessed. The ratio of IL-2/IL-10 or IFN-gamma/IL-10 was of critical importance in determining the function of the supernatants. The inhibitory effects were verified to be due to IL-10, as they were neutralized by anti-IL-10 mAb.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗

PubMed1991

Inflammatory pseudotumor of lymph nodes. Additional observations and evidence for an inflammatory etiology.

Inflammatory pseudotumor of lymph nodes (IPT), a recently described benign cause of lymphadenopathy, was studied in 14 patients using paraffin-section immunohistochemistry. All biopsies showed a proliferation of spindle cells (small blood vessels, histiocytes, and "activated" fibroblasts resembling myofibroblasts) containing a mixture of inflammatory cells without atypia and involving the connective tissue framework (hilum and sinuses) of the lymph node. Ten patients had additional histologic features of IPT originally described (extranodal extension, obliterative vasculitis, and endothelial infiltration), and nine of these had associated fever of unknown origin, which in some was relieved by biopsy alone. Additional features observed focally in some cases but not previously described included lymph node parenchymal infarction, fibrinoid vascular necrosis, karyorrhexis, and involvement of only part of the lymph node. Immunostaining showed the lymphoid infiltrate to be predominantly of T-lineage (except for plasma cells), only a minority of which marked as T-helper cells. Numerous mononuclear cells resembling histiocytes were identified, some of which had a spindled shape but reacted with an antibody (KP1) of myelomonocytic specificity. Large fibroblastic cells expressed alpha-muscle actin but not desmin, similar to myofibroblasts in granulation tissue. The morphologic and immunohistologic features were similar to those in inflammatory pseudotumors of spleens and livers also studied, but the lack of simultaneous lymph node involvement argued against a common etiology. The findings suggest that the mass lesion of IPT is produced in response to localized lymph node inflammation or injury and further exclude hematolymphoid or mesenchymal neoplasia as a cause.

Adolescent↗

PubMed1991

Inflammatory fibrosarcoma of the mesentery and retroperitoneum. A tumor closely simulating inflammatory pseudotumor.

We report 38 cases of inflammatory fibrosarcoma occurring in 23 females and 15 males, 2 months to 74 years of age (median, 8.5 years; mean, 15 years) with symptoms of abdominal pain (17 cases), anemia (21 cases), fever (14 cases), mass (16 cases), and gastrointestinal obstruction (7 cases). Primary tumor sites included mesentery and retroperitoneum (31 cases), omentum (two cases), mediastinum (two cases), liver (one case), diaphragm (one case), and abdominal wall (one case). Sizes ranged from 2.4 cm to 20 cm (mean, 9.6 cm). Follow-up data in 27 cases revealed local recurrences in 10 patients, with multiple local recurrences in three and histologically proven distant metastases to lung (two cases) and brain (one case). Five patients died from their disease (median, 20 months). All tumors, including metastases, consisted of fibroblasts, myofibroblasts, and plasma cells, with variable degrees of fibrosis and calcification. Immunostains indicate myofibroblastic differentiation; 18 of 20 (90%) stained for actin, 15 of 18 (83%) for vimentin, and 10 of 13 (77%) for keratin (primarily in a submesothelial location). Ultrastructural studies also disclosed myofibroblastic features. The locally aggressive, recurrent nature of these neoplasms, as well as the occurrence of metastases and tumor deaths, indicate that they are potentially malignant neoplasms that we believe are better classified as inflammatory fibrosarcomas, not as cellular inflammatory pseudotumors.

Adolescent↗

PubMedDate not supplied

Pulmonary inflammatory pseudotumor (inflammatory myofibroblastic tumor): CT features with pathologic correlation.

The objective of this study was to assess the CT features of pulmonary inflammatory myofibroblastic tumors with pathologic correlation. The authors retrospectively reviewed CT and pathologic findings of 10 patients with surgically resected inflammatory myofibroblastic tumor of the lung. On CT, five patients showed a polypoid endotracheal (n = 3) or endobronchial nodule in the left main bronchus (n = 2). Two patients showed a central parenchymal mass, and the remaining three patients showed a peripheral pulmonary nodule. All tumors had well defined margins and were round to ovoid; they ranged in diameter from 13 to 52 mm and showed varying degrees of contrast enhancement (range 13-89 H). On histopathologic examination, the two central parenchymal masses involving segmental bronchi were also mainly endobronchial in location. The three peripheral pulmonary nodules also showed a peribronchiolar location, with a bronchial mucosal lining spared in part. The authors conclude that pulmonary inflammatory myofibroblastic tumors are closely related to the airway.

Adolescent↗

PubMed1998

Localization of mRNA for inflammatory cytokines in radicular cyst tissue by in situ hybridization, and induction of inflammatory cytokines by human gingival fibroblasts in response to radicular cyst contents.

The expression of mRNA encoding the inflammatory cytokines interleukin-1alpha (IL-1alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor alpha(TNF-alpha) have been examined in radicular cysts by in situ hybridization. Furthermore, the biological activity of the contents of radicular cysts (RCC) has been assayed by adding extracts of RCC to cultured human gingival fibroblasts (HGFs) and analyzing the culture medium for the release of inflammatory cytokines. In the epithelial layer, keratinocytes expressed all cytokine mRNAs examined at various levels. Basal layer cells expressed mRNA for each cytokine. In the subepithelial granulation tissue of the cysts, fibroblasts and macrophages expressed mRNA for IL-6, IL-8, IL-1beta and TNF-alpha mRNA at varying levels; especially clear expression of TNF-alpha and IL-1beta mRNA was detected on macrophages. The infiltrating lymphoid cells, largely composed of T cells and plasma cells, expressed these cytokine mRNAs, especially those encoding IL-6 and IL-8, at various levels. In vitro analysis indicated dose-dependent release of both IL-6 and IL-8 by HGFs in response to RCC. After heating to 100 degrees C for 10 min, RCC almost completely failed to stimulate IL-6 release from HGFs. Furthermore, anti-IL-1beta antibody (neutralization test) did not prevent the stimulation of IL-6 release by RCC. Significant amounts of IL-6 and IL-8 were detected in RCC in two cases, and a trace amount of IL-1beta was detected in one case. This study demonstrated the wide expression of mRNA encoding inflammatory cytokines in radicular cyst tissues, and RCC itself was capable of stimulating IL-6 and IL-8 production from HGFs.

Antibodies↗

PubMed1990

Clinical disease activity and inflammatory activity in the rectum in relation to mucosal inflammation assessed by colonoscopy. A study of children and adolescents with chronic inflammatory bowel disease.

The relationship between clinical disease activity, rectal inflammatory activity and mucosal inflammation established at total colonoscopy has been studied in 36 young patients with ulcerative colitis (UC) and 24 with Crohn's colitis (CC). Semiformed stools, diarrhea and frequent bowel movements seem to be better indicators of extensive mucosal inflammation of a moderate or severe degree than blood in faeces. There were, however, several patients with a discrepancy between the degree of clinical disease activity and the extent and degree of mucosal inflammation at endoscopic and histologic assessment. In about one-third of the patients with UC and in about half of the patients with CC, who had mucosal inflammatory activity of a moderate or severe degree, the rectal inflammatory activity was of a lower degree. Total colonoscopy seems to be necessary in order to establish the extent and degree of mucosal inflammation.

Adolescent↗

PubMed1978

Ankylosing spondylitis and inflammatory bowel disease. I. Prevalence of inflammatory bowel disease in patients suffering from ankylosing spondylitis.

To establish the prevalence of inflammatory bowel disease in ankylosing spondylitis (AS), 79 AS patients underwent detailed medical screening, including sigmoidoscopic and roentgenological examination, 48 had gastrointestinal symptoms and the others did not. In 3 patients a diagnosis of Crohn's disease was made which was previously established. In all other patients inflammatory bowel disease could be excluded. The prevalence of inflammatory bowel disease in this series of patients with AS therefore was 3.8%.

Enteritis↗

PubMed1978

Ankylosing spondylitis and inflammatory bowel disease. II. Prevalence of peripheral arthritis, sacroiliitis, and ankylosing spondylitis in patients suffering from inflammatory bowel disease.

To establish the prevalence of peripheral arthritis, radiographic sacroiliitis, and ankylosing spondylitis in patients with inflammatory bowel disease, 58 consecutive patients suffering from ulcerative colitis (UC) and 51 with Crohn's disease (CD) underwent a detailed rheumatological examination. In addition, all patients were screened for the presence of the antigen HLA B27. Peripheral arthritis was found in 14 (8 UC, 6 CD) patients (12.8%); radiographic sacroiliitis was diagnosed in 11 (5 UC, 6 CD) (10.1%), of whom 10 were asymptomatic; and ankylosing spondylitis was diagnosed in 2 UC and 2 CD patients (3.7%). 18.9% of the UC and 3.9% of the CD patients were HLA B27 positive. One of the 11 patients with radiographic sacroiliitis and 2 of the 4 with ankylosing spondylitis had the HLA B27 antigen. Peripheral arthritis, radiographic sacroiliitis, and ankylosing spondylitis are apparently frequent manifestations in patients suffering from inflammatory bowel disease. Asymptomatic radiographic sacroiliitis in these patients appears to differ from idiopathic ankylosing spondylitis, both clinically and genetically. Evaluation of subjective rheumatological complaints, necessary for a confident diagnosis of ankylosing spondylitis, according to the New York criteria is difficult during a flare-up of the inflammatory bowel process, as was shown in 4 CD cases with marked limitation of lumbovertebral function and chest expansion, but no radiological abnormalities of the SI joints.

Adult↗

PubMed1986

Serum osteocalcin in rheumatoid arthritis and other inflammatory arthritides: relation between inflammatory activity and the effect of glucocorticoids and remission inducing drugs.

Osteocalcin, a vitamin K dependent protein synthesised by osteoblasts, was measured in serum by radioimmunoassay in patients with rheumatoid arthritis (n = 36) and seronegative spondyloarthropathies (n = 23). The serum osteocalcin levels were decreased in both patient groups compared with the levels measured in age and sex matched healthy controls. We found no relation between serum osteocalcin and the disease duration or inflammatory activity of the patients who were without drug treatment at the first examination. After administration of glucocorticoids (20 mg prednisolone a day) circulating osteocalcin decreased significantly after one week of treatment. During gradual reduction of the steroid dosage osteocalcin returned to pretreatment values. Treatment with non-steroidal anti-inflammatory drugs (NSAIDs) did not influence circulating osteocalcin. During treatment with chloroquine or penicillamine serum osteocalcin increased significantly, concomitant with a reduction of the acute phase reactants. Controversy persists about the abnormality of bone turnover in rheumatic diseases, but our data suggest that the overall bone turnover is decreased in patients with rheumatoid arthritis and other inflammatory arthritides.

Adrenocorticotropic Hormone↗

PubMed1994

Increased serum proMMP-3 in inflammatory arthritides: a potential indicator of synovial inflammatory monokine activity.

OBJECTIVE: To investigate if the increased concentrations of stromelysin (MMP-3) found in the synovial fluid (SF) of patients with various arthritides reflect the concentrations in the circulation. METHODS: Using a double antibody ELISA, we have measured proMMP-3 concentrations in sera from these patient groups and in others with a heightened acute phase response (APR) as a result of multiple organ failure. RESULTS: The median serum concentration of proMMP-3 was increased by up to ninefold in the inflammatory arthritides, but not in osteoarthritis or in patients with a heightened APR resulting from a non-chronic inflammatory condition. CONCLUSION: In chronic inflammatory diseases such as rheumatoid arthritis, serum proMMP-3 may prove to be a more specific indicator of monokine activity than currently available serum markers.

Acute-Phase Reaction↗

PubMed1992

In vitro regulation of pituitary ACTH secretion in inflammatory disease susceptible Lewis (LEW/N) and inflammatory disease resistant Fischer (F344/N) rats.

We have previously shown that susceptibility to inflammatory disease in Lewis (LEW/N) rats is related to their limited hypothalamic-pituitary-adrenal (HPA) axis responses to a variety of inflammatory stimuli, while the relative resistance to inflammatory disease in Fischer (F344/N) rats is related to their potent HPA axis responses to these same stimuli. In vivo studies also showed that LEW/N pituitary ACTH responses to exogenous corticotropin-releasing hormone (CRH) were blunted compared to F344/N. To determine if there is a fundamental difference in pituitary corticotroph function between the two strains, independent of other factors influencing the HPA axis, we compared ACTH responses to a variety of stimuli in LEW/N and F344/N primary pituitary cell cultures. Here we show that in vitro basal ACTH secretion and peak ACTH response to CRH, forskolin and 8-bromo-cAMP are 50% lower in LEW/N than F344/N rats. However, these findings can be explained by other observations: diminished basal ACTH content, POMC mRNA, and a decreased number of corticotrophs, in pituitary cell cultures from LEW/N compared to F344/N rats. In addition, LEW/N corticotrophs were more sensitive to dexamethasone and to corticosterone suppression of CRH-stimulated ACTH secretion compared to F344/N. The data support the possibility of an HPA axis defect in LEW/N rats at the pituitary level which could be secondary to prolonged understimulation by hypothalamic CRH, or could also be partially related to enhanced glucocorticoid feedback inhibition.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMedDate not supplied

Intracerebroventricularly transplanted embryonic neuronal tissue from inflammatory-resistant F344/N rats decreases acoustic startle responses in inflammatory-susceptible LEW/N rats.

Recently, we have shown that intracerebral transplantation of fetal F344/N hypothalamic tissue into LEW/N rats converts the LEW/N inflammatory-susceptible phenotype into an inflammatory-resistant phenotype in LEW/N hosts. Because LEW/N rats also exhibit relatively high acoustic startle responses (ASRs) compared to F344/N rats, in the present study we examined the effects on ASR of transplantation of F344/N hypothalamic tissue into the third ventricle of LEW/N rats. Dissected neuronal tissue from F344/N rats (Day E15-16) was implanted into the third ventricle of LEW/N rats. After 4 wk of postoperative survival, the animals' responses to acoustic startle stimuli were tested. Compared to naive and sham-operated animals, LEW/N rats transplanted with hypothalamic tissue exhibited significant decreases in ASR amplitudes. A similar decrease in ASR amplitude was observed in the group of LEW/N rats transplanted with embryonic striatal tissue. Our results indicate that the third ventricular neuronal grafts may modulate behavioral responses in the LEW/N rats. Although the mechanism of this effect is unknown, these studies suggest that intracerebral neuronal transplantation is a viable method with which to explore mechanisms of behavioral, neuroendocrine, and inflammatory response associations.

Acoustic Stimulation↗