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Results for “Cellular inflammation”

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At least 271 records · Page 15Linked to original sources

PubMed1986

Histological changes in temporomandibular joints from elderly individuals. An autopsy study.

Our aim was to study microscopically the disc position and structural tissue changes such as disc perforation of the temporomandibular joint (TMJ). An autopsy material comprising the right and left TMJ from 21 individuals with a mean age of 75 years was studied. Anterior disc position was found in 11 joints from 8 individuals. Discs in anterior position were most often of even thickness or convex, whereas most discs in normal position were concave. Perforation was found in the central dense part of the disc in one joint and in the posterior disc attachment of five joints. The latter five discs were in anterior position. Of the five joints with anterior disc position and perforation of the posterior attachment, four joints showed marked structural changes also in the condyle and temporal component. Such changes were found only in one of six joints with anterior disc position but without perforation. No signs of cellular inflammation were observed in any of the joints. Fibrous ankylosis was found in four joints from three individuals. Joints with anterior disc position comprised more than one fourth of the examined joints. In some of these joints there were no structural changes; in other of these joints disc perforation was combined with convex disc form and marked structural changes of the condyle and temporal component.

Aged↗

PubMed1996

Exudative and absorptive permeability in different phases of an experimental colitis condition.

BACKGROUND: Increased intestinal 'permeability' in inflammatory bowel disease and in animal models of this disease has been reported. This study asks if permeability changes are bidirectional and parallel cellular inflammation. METHODS: In rats acute inflammatory cell infiltration (ICI) was induced in an excluded bowel loop by instillation of 4% acetic acid. Plasma exudation was investigated by intravenous infusion of 125I-albumin and determination of radioactivity in loop perfusates. Absorption was measured by placing 51Cr-ethylenediaminetetraacetic acid in the loop and counting total radioactivity appearing in urine over 24 h. RESULTS: Acute ICI was induced with acetic acid on day 4 but, as judged by ICI and histology, recovered by day 14. Acetic acid treatment resulted in increased absorption on day 4, which return to control levels by day 14. Acetic acid treatment resulted in increased plasma exudation on day 4, which remained increased on day 14. CONCLUSION: Absorption and exudation changes are not necessarily bidirectional, and ICI may not be required for significant and sustained plasma exudation to take place. We suggest that the exudative response reflects a 'functional inflammation' that may occur and be important also in the absence of the traditional indices of bowel inflammation.

Acetic Acid↗

PubMed1992

Inflammatory leukocytes associated with increased immunosuppression by glioblastoma.

In order to determine the in vivo immune response in glioblastoma, monoclonal and polyclonal antibodies specific for inflammatory leukocytes and immunoregulatory products were utilized to stain tissue from four surgical specimens. The more activated the inflammatory cells, the more activated the tumors appeared to be. In the tumor with the largest infiltration (Case 3), inflammatory cells were stained for interferon-gamma, interleukin-2, interleukin-1 beta, lymphotoxin, tumor necrosis factor-alpha, and transforming growth factor-beta. The tumor cells also expressed interleukin-1 beta, interleukin-6, transforming growth factor-beta, tumor necrosis factor-alpha, and prostaglandin E. In contrast, in the tumor with the least inflammatory response (Case 1), the tumor cells did not express any cytokines. Expression of cytokines by glioma cells was modest in the two cases with modest inflammatory responses. Cellular inflammation, primarily consisting of T cells and macrophages with few or no B cells or natural killer cells, was two- to 15-fold greater outside the tumor than within. In contrast to leukocytes outside the tumor, which were activated and expressing class II major histocompatibility antigens, leukocytes within the tumor parenchyma or at the tumor's edge were negative for these antigens. In the four specimens studied here, the tumor cells themselves were also negative for class II major histocompatibility antigens. These findings, although preliminary, suggest that inflammatory cells within gliomas are inactivated and that glioma cells may increase the expression of immunosuppressive cytokines in response to an increased lymphocyte infiltrate. This observation, if corroborated by more extensive studies, may help to explain the failure of immune treatments in glioblastoma multiforme.

Adult↗

PubMed1989

Herpes simplex virus-specific antibodies present in tears during herpes keratitis.

We examined the specificity and levels of antibodies present in rabbit tears after induced infection of the rabbit cornea. Two strains of herpes simplex virus-1 (HSV) with different patterns of ocular disease were used: RE which produces stromal disease, and F which produces epithelial disease. We found that (i) IgG, IgA, and IgM antibodies were produced, (ii) the number of specific HSV antigens recognized by these antibodies was no significantly different, and (iii) postinfection (PI) timing and concentration of antibodies varied according to the disease pattern of the virus strain. The animals infected with strain F produced high levels of IgG antibodies early PI which remained constant, while IgA and IgM antibodies also increased early PI but declined after Day 16 PI. Animals infected with strain RE showed low levels of IgA and IgM antibodies which remained low. IgG antibodies increased early PI but declined at Day 16 PI. These differences in times of appearance and in amounts of antibodies in tears may be related to the clinical course of the disease. It has been shown that stromal disease has an immunopathologic basis. Inflammation, cellular infiltration of lymphocytes, and plasma cells are seen in the stroma of RE-infected animals, but these are not present in the stroma of F-infected animals. Infectious virus was not isolated from corneal explants taken from animals during the quiescent stage of the disease. The difference in pathogenicity cannot be explained in terms of specificity of tear antibodies. Even though the disease patterns were different, the number and types of HSV polypeptides recognized by both sets of tears was similar. Consequently, we believe that the immunopathology seen in the stromal disease may be due to the anatomical site of HSV antigens, rather than to differences in specificity of tear antibodies.

Animals↗

PubMed2001

Antigen-independent Th2 cell differentiation by stimulation of CD28: regulation via IL-4 gene expression and mitogen-activated protein kinase activation.

To delineate the molecular mechanisms regulating Th2 cell differentiation, CD28-mediated generation of Th2 effectors was analyzed. In the absence of TCR ligation CD28 stimulation induced Th2 differentiation of memory but not of naive CD4(+) T cells, whereas costimulation via CD28 and the TCR enhanced Th2 differentiation from naive T cells but suppressed it from memory T cells. Stimulation of T cells via the CD28 pathway, therefore, provided critical signals facilitating Th2 cell differentiation. By comparing the responses to CD28 stimulation in memory and naive T cells and by using specific inhibitors, signaling pathways were defined that contributed to Th2 differentiation. CD28-induced Th2 differentiation required IL-4 stimulation and the activation of the mitogen-activated protein kinases p38 and extracellular signal-regulated kinases 1/2. CD28 engagement directly initiated IL-4 gene transcription in memory T cells and induced activation of phosphatidylinositol 3-kinase, p38, and c-Jun NH(2)-terminal kinase/stress-activated protein kinase pathways. Extracellular signal-regulated kinase phosphorylation that was necessary for Th2 differentiation, however, required stimulation by IL-2. These results indicate that optimal TCR-independent generation of Th2 effectors requires coordinate signaling via the CD28 and IL-2 pathways. TCR-independent generation of Th2 effectors might provide a mechanism to control Th1-dominated cellular inflammation.

Adult↗

PubMed1999

Biological activities of scyphostatin, a neutral sphingomyelinase inhibitor from a discomycete, Trichopeziza mollissima.

Scyphostatin is a specific inhibitor for mammalian neutral magnesium-dependent sphingomyelinase with a fifty percent inhibition concentration (IC50) value of 1.0 microM. When used to inhibit lysosomal acid sphingomyelinase, an approximately 50-fold greater concentration is required. In human peripheral monocytes, the compound inhibits bacterial lipopolysaccharide (LPS)-induced prostaglandin E2 production and LPS-induced interleukin-1beta production with IC50 values of 0.8 microM and 0.1 microM, respectively. In rat, p.o. administration of the compound has also been shown to inhibit carrageenin-induced paw edema. Thus, it is hoped that utility of scyphostatin as a pharmacological tool will contribute to our understanding of the role of ceramide in the cellular inflammation process.

Amides↗

PubMed1999

Biphasic response to gut manipulation and temporal correlation of cellular infiltrates and muscle dysfunction in rat.

BACKGROUND: Surgical manipulation of the intestine results in the massive movement of leukocytes into the intestinal muscularis at 24 hours. This is associated with muscle inhibition. The aim of this study was to temporally associate leukocyte extravasation with ileus after surgical manipulation. METHODS: Rats underwent a simple manipulation of the small bowel and were killed at various times (0, 0.25, 0.5, 1, 3, 6, 12, and 24 hours) postoperatively. Jejunal circular-muscle contractile activity was assessed in a standard organ bath. Both extravasating and resident leukocytes were immunohistochemically stained in muscularis whole mounts. RESULTS: Contractile activity was significantly reduced immediately after surgery, but rapidly returned to control levels at 3 hours. After recovery, muscle function decreased at 12 and 24 hours (41% and 81%, respectively). The resident muscularis macrophage network demonstrated cellular activation 1 hour postoperatively. The number of leukocytes increased over time (neutrophils, 67.5-fold; monocytes, 98.2-fold; and mast cells, 47-fold at 24 hours). CONCLUSIONS: The functional results demonstrate a biphasic response in the suppression of muscle activity after surgical manipulation. Regression analysis (r2 = 0.998) of the temporal development of leukocyte infiltration and the protracted phase of muscle inhibition provides evidence for a correlation between cellular inflammation and postoperative dysmotility.

Animals↗

PubMedDate not supplied

Proinflammatory cytokines in cervicogenic headache.

Interleukin-1 beta (IL-1 beta) and Tumour Necrosis Factor-alpha (TNF-alpha) exert their multifunctional biological effect by promoting and increasing the molecular events of cellular inflammation. The aim of this study was to find out whether the cytokine pattern of cervicogenic headache (CH) patients tends, like that seen in cluster headache, towards an inflammatory status. Fifteen CH patients, diagnosed according to the 1998 CHISG criteria, were analysed for serum IL-beta (ELISA) and TNF-alpha (bioassay and ELISA) both during the natural course of a painful attack and during a phase of mechanically worsened pain. The control groups consisted of 15 migraine without aura (MWA) patients and 15 historically healthy subjects. The MWA patients were studied both during (MWA-IN) and outside (MWA-OUT) a migraine attack. Higher levels of both IL-1 beta and TNF-alpha were detected in the sera of CH patients than in that of MWA-IN and MWA-OUT and C subjects. A difference also emerged in CH between spontaneous and mechanically worsened pain phases. We conclude that the degree of cytokine production may depend on the different pathophysiological mechanisms at work in MWA and CH.

Adult↗

PubMed1997

The Histopathology of Angiographic Chronic Total Coronary Artery Occlusions Ñ Changes in Neovascular Pattern and Intimal Plaque Composition Associated with Progressive Occlusion Duration.

The current study describes the histopathology of angiographic chronic total occlusions including residual lumen patency, intimal plaque composition, patterns of neovascular channel formation, intimal plaque calcification, and cellular inflammation, analyzed according to occlusion duration and intimal plaque type (fibrocalcific vs. lipid laden vs. mixed). Histologic findings are related to previously described clinical and angiographic predictors of successful chronic total occlusion revascularization.

Journal Article↗

PubMedDate not supplied

Proinflammatory pathways in cervicogenic headache.

Cervicogenic headache (CEH) is a relatively common form of headache arising from the neck structures. The pathophysiology probably results from various local pain-producing factors such as intervertebral dysfunction, with a no less important role played by the frequent coexistence of a history of head traumas. This report represents a series of pathophysiological studies in CEH patients and the results achieved by pharmacological treatment of the disease. Interleukin-1 beta (IL-1 beta) and Tumour Necrosis Factor alpha (TNF-alpha) exert their multifunctional biological effects by promoting and increasing the molecular events of cellular inflammation. We found that the cytokine pattern of CEH patients is--similar to cluster headache--biased towards an inflammatory status. Higher levels of both IL-1 beta and TNF-alpha were detected in the sera of CEH patients than the levels in patients with migraine without aura and in healthy subjects. There were also differences between the spontaneous and mechanically worsened pain phases of CEH. Nitric oxide (NO) synthase is also activated in cervicogenic headache. No change in NO metabolites levels has been observed after NO donor administration. This behaviour is clearly different from that observed in migraine and tension headache patients. We conclude that the high degree of cytokine and NO production in CH may depend on the differing pathophysiological mechanisms at work in CEH than in other forms of headache.

Cytokines↗

PubMed1997

[Fracture healing of the face. General principals].

To obtain good and uncomplicated primary fracture healing, anatomical repositioning, direct bone apposition and stable fixation are mandatory. The course of primary fracture healing starts with acute inflammation (cellular and vascular), stabilization (formation of new bone), and remodeling. Besides good fixation, local factors such as age and type of fracture will influence the healing. If good reposition, apposition or adequate stabilization of the bony fragments are not achieved, the bone healing will be secondary. In secondary healing fracture repair and stabilization occurs through the formation of callus.

Bone Remodeling↗

PubMed1992

Inflammatory cells and mediator release during ragweed challenge: correlation between histamine content in nasal secretions and appearance of inflammatory cells.

The early and late phase responses in the nasal tissues exhibit release of inflammatory mediators and a mixed cellular influx in separate nasal challenges. To explore this phenomenon further, histamine concentration was determined along with characterization of cell influx during dose-dependent ragweed challenges. Ten subjects with allergic rhinitis underwent two unilateral nasal lavages using incremental 3-fold concentrations of short ragweed. Low doses of ragweed (0.016 to 0.114 units Amb a I) rarely induced cell influx (1/18 challenges), whereas moderate doses (0.432 to 1.3 units Amb a I) caused cell influxes in 7/18 and high doses (3.39 to 11.7 units Amb a I) resulted in cell influxes in 8/17. The eluent contained greater than 50% neutrophils in seven challenges; greater than 50% eosinophils in three; and a mixed pattern in six. There was a significant association between the dose of antigen and the level of histamine. Challenges with an eosinophilic influx tended to be associated with higher concentrations of histamine than neutrophilic influxes. Similar to the immediate skin response, the early allergic response in the nose demonstrated a cell influx with release of histamine. Nasal cellular inflammation therefore can occur within minutes of allergen exposure.

Adult↗

PubMed1990

Pathophysiologic effect of interleukin-1b in the rabbit retina.

Interleukin-1 is a potent immunomodulator and has been shown to initiate many aspects of the inflammatory response. To determine the effects of IL-1b in the central nervous system (CNS), the rabbit retina was used, adjacent to which factors can be injected with minimal trauma and both pathologic and physiologic effects can be monitored. Intravitreal injection of 300 units of IL-1b induced an alteration in the visual evoked potentials (VEP) that was associated with marked intravascular red blood cell accumulations, hemorrhage, and cellular inflammation of the epiretinal vessels. Analysis of these events showed slowing and occasional hyper-excitability of the compound action potential of the optic tract and of the cortical VEP that correlate with the maximum inflammatory response. Histologic studies show the following: no apparent response occurs within the first 1.5 hours after intraocular challenge; and between 3 and 6 hours after injection an extensive intravascular red blood cell accumulation and progressive hemorrhage is accompanied by an increase in the number of mononuclear (MN) cells and the appearance of polymorphonuclear (PMN) cells. Polymorphonuclear cells continue to increase with time to give a single wave of inflammation that peaks 24 hours after injection, while the number of MN cells steadily increases. These events are associated with changes in the permeability of the blood-brain barrier and correlate with the electrophysiologic dysfunctions. Forty-one hours after injection, MN inflammation, reactive gliosis, and residual PMN inflammation are evident. Neutralization with specific antibody inhibited the responses through 6 hours after injection. It is concluded that the rabbit retina provides a valuable model for the in vivo analysis of CNS inflammation.

Animals↗

PubMed1990

Toxic effects for lambs of cytotoxic necrotising factor from Escherichia coli.

The lethal effect, clinical signs and lesions caused by the intravenous inoculation into six lambs (seven to 10 days old) of a partly purified preparation of cytotoxic necrotising factor (CNF) from Escherichia coli, strain BM2-1, were investigated. Two control preparations were also tested in two lambs each: (i) the same as above but heated for one hour at 60 degrees C, a treatment which inactivates CNF and preserves residual endotoxic activity; and (ii) purified material from a CNF-defective mutant of BM2-1. Whereas none of the lambs in either of the control groups died or showed significant clinical signs or lesions, all the lambs inoculated with partly purified CNF developed severe clinical signs starting six hours after inoculation which consisted mainly of neurological signs and mucoid diarrhoea. The most striking lesions were oedema and haemorrhages in the central nervous system, and foci of coagulation necrosis in the myocardium. Mucus hypersecretion in the gastrointestinal tract was not associated with cellular inflammation.

Animals↗

PubMed1989

Increased vesicular transport and decreased mitochondrial content in blood-brain barrier endothelial cells during experimental autoimmune encephalomyelitis.

Mechanisms involved in the loss of blood-brain barrier function in Lewis rats with experimental autoimmune encephalomyelitis (EAE) were examined using horseradish peroxidase (HRP) as a tracer. In animals injected with HRP before fixation, tracer was observed in two intracytoplasmic compartments: multivesicular bodies (presumably secondary lysosomes) and transcytotic vesicles. Quantitative morphometry of electron micrographs of capillary endothelial cells demonstrated a 5.2-fold increase in these vesicles. This increase in vesicular transport was associated with a decrease in mitochondrial content from 13.7% of the endothelial cytoplasmic area in the normal rat to 4.2% in EAE rats at the height of clinical disease. These alterations correlated with the clinical course of EAE. In animals infused with tracer after fixation, tracer was restricted to areas of cellular inflammation. Immunogold staining of endogenous albumin demonstrated the presence of albumin in cytoplasmic vesicles and in channel-like tubular structures adjacent to endothelial cell junctions. These results indicate that there is a role for vesicles in transendothelial cell transport and edema formation in animals with EAE.

Animals↗

PubMed1988

Immune responses to Mycoplasma bovis vaccination and experimental infection in the bovine mammary gland.

This study characterized the immune responses in four vaccinated and four control cows in response to vaccination and experimental intramammary inoculation with Mycoplasma bovis. Specific antibody responses occurred in serum and milk in response to vaccination and experimental infection. Lymphocytes from peripheral blood, but not from the mammary gland of vaccinated cows had increased responsiveness to mitogens. No lymphocytes tested were responsive to M. bovis antigen. Both vaccination and experimental infection resulted in skin test reactivity. These results imply that vaccination results in immune responses which may alter the course of experimental M. bovis mastitis, but may contribute to cellular inflammation.

Animals↗

PubMed1986

The pathology of pulmonary cryptococcal infections in the acquired immunodeficiency syndrome.

Specimens from premortem pulmonary cytology, transbronchial biopsy, and autopsy were studied in 11 patients with acquired immunodeficiency syndrome who developed pulmonary cryptococcal disease. Nine of 11 patients had culture-proved cryptococcal meningitis. Extremely low T-cell helper/suppressor ratios (mean, 0.12) were observed in seven of 11 patients. In six of eight patients, transbronchial biopsy specimens showed a characteristic interstitial pattern with yeasts in the alveolar septae, minimal cellular inflammation, and no well-formed granulomas. On cytologic examination, organisms were present in seven (100%) of seven cell blocks and five (83%) of six smears prepared from the bronchoalveolar lavage, and in five (63%) of eight bronchial brushings. Small, poorly encapsulated yeast forms were sometimes present, requiring mucicarmine and acid mucopolysaccharide stains for confirmation of the diagnosis of pulmonary cryptococcosis. Overall, bronchoscopy yielded a diagnosis in seven of eight patients. At autopsy, two of five patients demonstrated an interstitial pattern of infection in all lobes of the lung with marked pleural thickening and giant-cell formation; two other patients showed mixed interstitial and intra-alveolar cryptococcal infiltrates. Nodal and disseminated infection were present in four patients. In patients with acquired immunodeficiency syndrome who have cryptococcal meningitis, pulmonary cryptococcal disease is common and must be distinguished from other opportunistic infections.

Acquired Immunodeficiency Syndrome↗

PubMed1979

Degenerative vascular disease and myocardial infarction in mice with lupus-like syndrome.

The pathogenesis of the degenerative vascular disease and myocardial infarction that develop in mice with lupus-like disease was studied by immunofluorescence, light microscopy, and electron microscopy. Medium and small coronary arteries and arterioles of both infarcted and noninfarcted hearts had focal degenerative lesions consisting of deposits of periodic-acid--Schiff (PAS)-positive or eosinophilic material in the intima and to a lesser extent in the media, degenerative changes in the media without accompanying cellular inflammation, and occasional proliferation or swelling of intimal cells. These lesions often narrowed and, together with platelet aggregation, occasionally occluded the vascular lumens. Granular deposits of mouse immunoglobulin, C3, and occasionally gp70 were present in the walls of medium and small arteries, arterioles, and venules of both infarcted and noninfarcted myocardium. Dense deposits of foreign material were found by electron microscopy in areas corresponding to the immune deposits. These findings are consistent with the interpretation that these noninflammatory vascular lesions are caused by local deposition of antigen--antibody complexes. The immune-complex--mediated injury appears to lead to thrombotic and/or obliterative vascular changes that contribute to decrease of the coronary blood flow and to the development of myocardial infarction.

Animals↗