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At least 145 records · Page 8Linked to original sources
PubMed1988

Characteristics of ingress and life span of neutrophils at a site of acute inflammation, determined with the Sephadex model in rats.

Neutrophils labelled in vivo with 3H-thymidine accumulate in subcutaneously injected Sephadex, which causes an acute inflammation. Cells die and disintegrate within the Sephadex implants, leaving behind labelled nuclear fragments representing the number of dead cells. The total of immigrated cells and their life span can be calculated from the number of intact cells along with disintegrated cells found in a Sephadex implant. Intensive neutrophil ingress starts after 5 h, and after 6.5 h reaches a maximum of 52 x 10(6) cells per hour. After 11 h, a total of 137 x 10(6) cells has entered a Sephadex implant. The life span varies during the course of the experiment. The shortest life span of 20 min was measured during the period of intensive neutrophil ingress 5.5 h after onset of inflammation. Cellular death and disintegration is evidently due to self-destruction of the cells by peroxidation.

Animals↗
PubMed1982

[Clinical value of bronchoalveolar lavage in progressive systemic scleroderma (author's transl)].

As an enlargement of conventional diagnostic methods the cell spectrum of bronchoscopically obtained bronchoalveolar lavage was investigated in 10 patients with progressive systemic scleroderma. Two cases showed marked lymphocytosis, one increased numbers of granulocytes, two patients had marginally increased percentages of inflammatory cells. Four of these patients were in a progressive active phase of scleroderma with humoral inflammation signs and round cell infiltrates of the skin. In contrast, the lavage cell picture of the other five patients was unremarkable. One of these had advanced pulmonary fibrosis, however without signs of progression. The results show that the lavage cell pattern reflects the acute phase with cellular inflammation of lung parenchyma disease such as occurs in progressive systemic scleroderma. Staging of pulmonary organ manifestation in progressive systemic scleroderma can be markedly improved by low-risk bronchoalveolar lavage.

Adult↗
PubMed1990

Defective generalized extracellular matrix in the neoplasm bearing host: decreased inflammation, immunity and resistance.

Neoplasms have extensive qualitative and quantitative changes in their extracellular matrix. Lytic factors from neoplasms breakdown extracellular matrix of the areas adjacent to the neoplasms and fibroblasts in these areas produce increased extracellular matrix. Some of the extracellular matrix fractions are normally present in serum. Multiple fractions derived from extracellular matrix are present in the serum of tumor patients. Tumor patients often have decreased early cellular inflammation and immunity. These reactions depend on a normal extracellular matrix. A number of known facts about the tumor bearing host can be explained by the concept that the host's generalized extracellular matrix is altered by circulating fractions of extracellular matrix. These could be qualitative or quantitative defects as well as an abundance of depolymerized fractions. The beneficial effects of cytokines, streptococcal infections and pyridoxine deficiency on tumors can be explained by this concept.

Animals↗
PubMed1989

Cellular response to inflammation at the limbus.

The role in ocular (limbal) inflammation of the rich vascular and lymphatic supply is discussed in detail. The distribution of lymphocytes, mast cells, Langerhans cells, macrophages and other cellular elements are discussed as well as their individual and collective response to inflammation whether due to infectious or non-infectious disease states. Among the non-infectious causes of limbal cellular inflammation are the four types of hypersensitivity response.

Conjunctivitis↗
PubMed1996

Correlation between Banff classification, acute renal rejection scores and reversal of rejection.

The Banff classification of acute rejection is based on histologic grades and scores for borderline changes, glomerular, vascular, interstitial and tubular lesions. We reviewed 56 episodes of acute rejection occurring in 44 kidney allograft recipients (30 cadaveric and 14 living donor transplants), comparing Banff classification to degree of reversibility of rejection. Rejection reversal was defined as complete if serum creatinine returned < or = 25% of baseline, partial if creatinine was > 25% to < 75% of baseline, and irreversible if creatinine was > or = 75% of baseline or graft loss occurred. Eight biopsies were classified as borderline (SUM score 1.6 +/- 0.5), 14 grade I (SUM score 3.3 +/- 0.4), 19 grade II (SUM score 4.2 +/- 0.3), and 15 grade III (SUM score 8.5 +/- 0.4). SUM distinguished borderline and grade III rejections, but not grades I and II. Clinically, grade and SUM score correlated with rejection reversal. Complete reversal of rejection occurred in 93% of patients with grade I rejection, while 47% of patients with grade III had irreversible rejection. The mean SUM for complete reversal was 3.9 +/- 0.34 and was different from SUM of partial (6.0 +/- 0.86) and irreversible (8.5 +/- 0.93), P < 0.006. Meanwhile, vascular scores were similar for rejections with complete (0.9 +/- 0.2) or partial (1.0 +/- 0.4) reversal, but significantly higher in those with irreversible rejection (3.0 +/- 0.4, P < 0.000). Likewise, mean scores for tubulitis and interstitial inflammation were significantly higher for irreversible rejection. Resolution of rejection by steroids was correlated to low vascular score (steroid sensitive 0.65 +/- 0.25 vs. steroid resistant 1.42 +/- 0.18, P < 0.01), and low SUM score (steroid sensitive 3.7 +/- 0.5 vs. steroid resistant 5.22 +/- 0.43, P < 0.04). Neither scores for tubulitis nor interstitial cellular inflammation were predictive of steroid sensitivity. These data demonstrate that Banff scoring has clinical relevance in predicting rejection reversal and has implications to first-line therapy of rejection episodes.

Adolescent↗
PubMed2004

Gene expression profiling in mouse lung following polymeric hexamethylene diisocyanate exposure.

Isocyanates are a common cause of occupational lung disease. Hexamethylene diisocyanate (HDI), a component of polyurethane spray paints, can induce respiratory symptoms, inflammation, lung function impairment, and isocyanate asthma. The predominant form of HDI in polyurethane paints is a nonvolatile polyisocyanate known as HDI biuret trimer (HDI-BT). Exposure of mice to aerosolized HDI-BT results in pathological effects, including pulmonary edema, lung inflammation, cellular proliferation, and fibrotic lesions, which occur with distinct time courses following exposure. To identify genes that mediate lung pathology in the distinct temporal phases after exposure, gene expression profiles in HDI-BT-exposed C57BL/6J mouse lungs were analyzed. RNase protection assay (RPA) of genes involved in apoptosis, cell survival, and inflammation revealed increased expression of IkappaBalpha, Fas, Bcl-X(L), TNFalpha, KC, MIP-2, IL-6, and GM-CSF following HDI-BT exposure. Microarray analysis of approximately 10000 genes was performed on lung RNA collected from mice 6, 18, and 90 h after HDI-BT exposure and from unexposed mice. Classes of genes whose expression was increased 6 h after exposure included those involved in stress responses (particularly oxidative stress and thiol redox balance), growth arrest, apoptosis, signal transduction, and inflammation. Types of genes whose expression was increased at 18 h included proteinases, anti-proteinases, cytoskeletal molecules, and inflammatory mediators. Transcripts increased at 90 h included extracellular matrix components, transcription factors, inflammatory mediators, and cell cycle regulators. This characterization of the gene expression profile in lungs exposed to HDI-BT will provide a basis for investigating injury and repair pathways that are operative during isocyanate-induced lung disease.

Administration, Inhalation↗
PubMed2004

Molecular therapeutic targets in inflammation: cyclooxygenase and NF-kappaB.

Inflammation is the host response to infection and injury. Inflammatory cells respond to foreign substances and inflammatory stimulus by producing bioactive mediators such as prostanoids, cytokines and chemokines. These mediators have complex, pleiotropic effects and interact with many cell types to amplify the inflammatory response. Dysregulation of these processes can lead to acute and chronic inflammatory diseases and pharmacological intervention is necessary to attenuate cellular inflammation pathways. Cyclooxygenase-2, the key inducible enzyme responsible for producing prostanoids, and the nuclear factor-kappa B (NF-kappaB) activation pathway, which regulates the transcription of inflammatory genes, represent attractive targets for developing anti-inflammatory therapeutics, as both pathways are activated by diverse inflammatory stimuli. This article reviews recent advances in anti-inflammatory drug development in both of these areas. Selective inhibitors of inflammation including cyclooxygenase inhibitors, antibodies against inflammatory cytokines, cytokine receptor antagonist, antibodies against adhesion molecules and therapeutics directed against the NF-kappaB activation pathway will be discussed.

Anti-Inflammatory Agents↗
PubMed2004

Polarized fibronectin secretion induced by adenosine regulates bacterial-epithelial interaction in human intestinal epithelial cells.

Fibronectin (FN) is a multifunctional protein that plays important roles in many biological processes including cell adhesion and migration, wound healing and inflammation. Cellular FNs are produced by a wide variety of cell types including epithelial cells, which secrete them and often organize them into extensive extracellular matrices at their basal surface. However, regulation of FN synthesis and the polarity of FN secretion by intestinal epithelial cells have not been investigated. In the present study we investigated the role of adenosine, whose levels are up-regulated during inflammation, in modulating FN synthesis, the polarity of FN secretion and the downstream effects of the secreted FN. Polarized monolayers of T84 cells were used as an intestinal epithelial model. Adenosine added to either the apical or basolateral aspect of the cells led to a time- and dose-dependent accumulation of FN in the culture supernatants, polarized to the apical compartment and reached maximal levels 24 h after apical or basolateral addition of adenosine. Confocal microscopy confirmed that FN localized to the apical domain of model intestinal epithelial cells stimulated with apical or basolateral adenosine. The induction of FN was significantly down-regulated in response to the adenosine receptor antagonist alloxazine and was inhibited by cycloheximide. Moreover, adenosine increased FN promoter activity (3.5-fold compared with unstimulated controls) indicating that FN induction is, in part, transcriptionally regulated. Interestingly, we demonstrated that adenosine, as well as apical FN, significantly enhanced the adherence and invasion of Salmonella typhimurium into cultured epithelial cells. In summary, we have shown for the first time that FN, a classic extracellular matrix protein, is secreted into the apical compartment of epithelial cells in response to adenosine. FN may be a critical host factor that modulates adherence and invasion of bacteria, thus playing a key role in mucosal immune responses during inflammation.

Adenosine↗
PubMed2001

Adenovirus-mediated gene transfer of human inducible nitric oxide synthase in porcine vein grafts inhibits intimal hyperplasia.

OBJECTIVE: The aim of this study is to determine whether adenoviral inducible nitric oxide synthase (iNOS) gene transfer could inhibit intimal hyperplasia (IH) in porcine internal jugular veins interposed into the carotid artery circulation. METHODS: Porcine internal jugular veins were transduced passively with 1 x 10(11) particles of an adenoviral vector carrying either the human iNOS (AdiNOS) or beta-galactosidase (AdlacZ) cDNA for 30 minutes and then interposed into the carotid artery circulation. Segments of each vein graft were maintained in an ex vivo organ culture to measure nitrite accumulation, a marker of nitric oxide synthesis. The grafts were analyzed immunohistochemically for the presence of neutrophils, macrophages, and leukocytes by staining for myeloperoxidase, ED1, and CD45, respectively, at 3 (n = 4) and 7 (n = 4) days. Morphometric analyses and cellular proliferation (Ki67 staining) were assessed at 3 (n = 4), 7 (n = 4), and 21 days (n = 8). RESULTS: AdlacZ-treated vein grafts demonstrated high levels of beta-galactosidase expression at 3 days with a gradual decline thereafter. Nitrite production from AdiNOS-treated vein grafts was approximately fivefold greater than AdlacZ-treated grafts (P =.00001). AdiNOS or AdlacZ treatment was associated with minimal graft inflammation. Cellular proliferation rates were significantly reduced in AdiNOS-treated grafts as compared with controls at both 3 (41%, P =.000004) and 7 days (32%, P =.0001) after bypass. This early antiproliferative effect was most pronounced at the distal anastomosis (65%, P =.0005). The iNOS gene transfer reduced the intimal/medial area ratio in vein grafts at 7 (36%, P =.009) and 21 days (30%, P =.007) versus controls. This inhibition of IH was again more prominent in the distal segments of the grafts (P =.01). CONCLUSION: Adenovirus-mediated iNOS gene transfer to porcine internal jugular vein grafts effectively reduced cellular proliferation and IH. Although iNOS gene transfer reduced IH throughout the entire vein graft, the most pronounced effect was measured at the distal anastomosis. These results suggest potential for iNOS-based genetic modification of vein grafts to prolong graft patency.

Adenoviridae↗
PubMed2006

Differential requirements for soluble and transmembrane tumor necrosis factor in the immunological control of primary and secondary Listeria monocytogenes infection.

The relative contributions of transmembrane tumor necrosis factor (memTNF) and soluble tumor necrosis factor (solTNF) in innate and adaptive immunity are poorly defined. We examined the capacities of wild-type (WT) mice, TNF-/- mice, and memTNF mice, which express only transmembrane TNF, to control primary and secondary Listeria monocytogenes infections. Soluble TNF was not required for induction or maintenance of protective immunity against a low-dose (200-CFU) Listeria infection. In contrast to TNF-/- mice, both WT and memTNF mice cleared the bacilli within 10 days and were fully protected against rechallenge with a lethal infective dose. Furthermore, T cells transferred from immune mice, but not from naïve, WT, and memTNF mice, protected TNF-/- recipients against an otherwise lethal infection. By contrast, infection with a higher dose of Listeria (2,000 CFU) clearly demonstrated that solTNF is required to coordinate an optimal protective inflammatory response. memTNF mice were more susceptible to a high-dose infection, and they exhibited delayed bacterial clearance, increased inflammation, and necrosis in the liver that resulted in 55% mortality. The dysregulated inflammation was accompanied by prolonged elevated expression of mRNAs for several chemokines as well as the macrophage effector molecules inducible nitric oxide synthase and LRG-47 in the livers of memTNF mice but not in the livers of WT mice. These data demonstrated that memTNF is sufficient for establishing protective immunity against a primary low-dose Listeria infection but that solTNF is required for optimal control of cellular inflammation and resistance to a primary high-dose infection. By contrast, memTNF alone is sufficient for resolution of a secondary, high-dose infection and for the transfer of protective immunity with memory T cells.

Animals↗
PubMedDate not supplied

Vasography - Clinical and experimental investigations.

In order to examine the effect of contrast mediums of different concentration and composition upon the vas, experiments in 90 rats were done. In comparison to three control groups of 10 animals each (surgery only, vas ligation only, saline injection) six contrast mediums caused a varying degree of damage to the vas deferens. The latter included irritation of the epithelium, inflammation, cellular infiltration, fibrosis of the wall, septum-formation and fenestration within the vas and actual obliteration. According to these experiments only hydrophilic contrast mediums of low concentration should be used in humans for vasography.

Animals↗
PubMed1995

Tissue factor antigen levels in various biological fluids.

Tissue factor (TF), a transmembrane surface protein, is known to initiate thrombogenesis through plasmatic and cellular activation processes. Besides complexing with factor VII, eventually leading to fibrin generation via the extrinsic pathway, TF can also activate factor IX, resulting in the intrinsic activation of coagulation. Other functions of TF are currently unknown, although various cells are believed to have TF receptors. Many of the post-surgical and post-interventional thrombotic events are due to the release of TF. Increased levels of TF are associated with several pathologic conditions such as cancer, sepsis and inflammation. Cellular necrosis also results in an increase of TF as the cells in the traumatized area lyse and release endogenous cell surface-bound TF. An ELISA method (American Diagnostica, Greenwich, CT) has been developed to assay TF antigen levels in various biological fluids. This ELISA employs a murine monoclonal antibody raised against native human TF for antigen capture. In this study, cerebrospinal fluid, peritoneal fluid, pleural effusion and urine from patients were assayed for their TF content using this ELISA method. Normal individual serum and plasma were also assayed as controls against which the levels of TF in the patients' body fluids could be compared. The amount of TF antigen in normal human plasma and serum was 165 +/- 139 pg/ml and 165 +/- 110 pg/ml, respectively. Concentrations of TF antigen in other fluids were: cerebrospinal fluid 868 +/- 721 pg/ml, peritoneal fluid 124 +/- 247 pg/ml, pleural effusion 385 +/- 569 pg/ml, synovial fluid 97 +/- 23 pg/ml, seminal plasma 11,485 +/- 875 pg/ml and urine 86 +/- 57 pg/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

A platelet-activating factor antagonist reduces corneal allograft inflammation and neovascularization.

We assessed the role of platelet-activating factor (PAF) in corneal allograft rejection and evaluated the effects of a PAF antagonist on corneal inflammation, cellular infiltration, vascularization, and edema. Rabbits with vascularized corneas served as recipients of allogeneic cornea grafts. Rabbits with normal corneas underwent autografts as controls. All of the allografts developed the progression of signs characteristic of rejection. Nevertheless, treatment with the PAF antagonist BN52021 significantly inhibited corneal allograft vascularization for up to 10 days after transplantation and reduced the number of eosinophils in the allografts at 28 days after transplantation. In contrast, saline-treated allografts exhibited florid vascularization and intense inflammatory infiltrates. Control autografts survived without developing significant inflammation or vascularization. The retardation of allograft eosinophilia and graft vascularization by the PAF antagonist was most likely the result of suppression of PAF-mediated reactions in the cornea. These results indicate that PAF may play a role in corneal inflammation and vascularization after corneal transplantation, and that PAF antagonists may be clinically useful in delaying some of the pathophysiologic consequences of corneal graft rejection.

Animals↗
PubMed1979

[The influence of hypnotics on the development of morphological and biochemical wound reaction (author's transl)].

The influence of hypnotics (barbital and carbromal) on the development of the early wound reactions in mechanically injured skin of guinea pigs was investigated: 1) The cellular reactions in incised wounds were retarded after moderate intoxication by hypnotics (300 mg/kg barbital; 3 g/kg carbromal). The histomorphological changes in wounds were inhibited by carbromal twice as much as by barbital. The hitherto published investigations had not shown any retardation of the early cellular inflammation by weakening influences such as loss of blood or alcohol without symptoms of shock (Berg et al., 1977) or local disturbances by acids and bases (Kampmann et al., 1978). 2). A moderate delay of the activity of structure bound enzymes was found in barbital intoxication, a stronger restriction under the influence of carbromal. 3) After barbital intoxication significant elevation of histamine or serotonin in wounds was not seen. Under the influence of carbromal there was also no increase of histamine but an increase of serotonin. Thus, although the cellular reactions seem to be the most reliable indicator among the methods for the determinations of wound age under devitalizing influences, their value is reduced in cases of intoxications by hypnotics needing treatment. Possible pathophysiological connections of the alterations of morphological and biochemical wound reaction with shock are discussed.

Animals↗
PubMed1986

Prazosin treatment suppresses increased vascular permeability in both acute and passively transferred experimental autoimmune encephalomyelitis in the Lewis rat.

Prazosin, an antagonist of the alpha 1-adrenoceptor, has been found to suppress the clinical and histologic expression of experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. This effect appears to be specific for the alpha 1-receptor. To determine the effect of this drug on vascular permeability to serum proteins and inflammatory cells, leakage of serum proteins into the central nervous system (CNS) was measured with [125I]albumin, and quantitation of cellular inflammation was determined by an estimation of total DNA. The results show that in both actively induced and passively transferred models of the disease, treatment with prazosin significantly suppresses leakage of serum proteins into the CNS but does not significantly suppress the increase of DNA. The results of the [125I]albumin studies additionally support the conclusion that the extent of vascular permeability to serum proteins in the spinal cord is a significant correlate of clinical disease. The results of the DNA estimation were at variance with the histologic evidence of cellular infiltration. We conclude that treatment with prazosin has a significant effect on the development of vascular edema in EAE. These results additionally validate a role for the adrenergic receptor in the development of EAE, and support the hypothesis that the primary site of action of prazosin is on the vascular alpha 1-adrenoceptor.

Animals↗
PubMed2002

Detrimental and beneficial effects of injury-induced inflammation and cytokine expression in the nervous system.

Lesions in the nervous system induce rapid activation of glial cells and under certain conditions additional recruitment of granulocytes, T-cells and monocytes/macrophages from the blood stream triggered by upregulation of cell adhesion molecules, chemokines and cytokines. Hematogenous cell infiltration is not restricted to infectious or autoimmune disorders of the nervous system, but also occurs in response to cerebral ischemia and traumatic lesions. Neuroinflammation can cause neuronal damage, but also confers neuroprotection. Granulocytes occlude vessels during reperfusion after transient focal ischemia, while the functional role of T-cells and macrophages in stroke development awaits further clarification. After focal cerebral ischemia neurotoxic mediators released by microglia such as the inducible nitric oxide synthase (leading to NO synthesis) and the cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) are upregulated prior to cellular inflammation in the evolving lesion and functionally contribute to secondary infarct growth as revealed by numerous pharmacological experiments and by use of transgenic animals. On the other hand, cytokine induction remote from ischemic lesions involves NMDA-mediated signalling pathways and confers neuroprotection. After nerve injury T cells can rescue CNS neurons. In the peripheral nervous system neuroinflammation is a prerequisite for successful regeneration that is impeded in the CNS. In conclusion, there is increasing evidence that neuroinflammation represents a double edged sword. The opposing neurotoxic and neuroprotective properties of neuroinflammation during CNS injury provide arich and currently unexplored set of research problems.

Animals↗
PubMed1992

Silica-induced pulmonary inflammation and fibrosis in mice is altered by acute exposure to nitrogen dioxide.

The biologic impact of consecutive exposures to two environmental pollutants was examined in mice exposed to silica crystals (SI) by intratracheal (IT) injection followed by an inhalation exposure to nitrogen dioxide (NO2). C57Bl/6 mice received an IT injection of 2 mg SI or sterile saline (SAL) followed by a 2-h inhalation exposure to NO2 at 20 ppm either within 2 h of or 24 h after SI instillation. During acute inflammation (d 3 postsilica), mice exposed to NO2 at either time showed a dramatic and significant reduction in the number of lavaged alveolar neutrophils (PMN) when compared to silica/air-exposed mice. Animals exposed to NO2 24 h after silica also evidenced significant decreases in levels of lavage albumin and lactate dehydrogenase (LDH) 3 d after silica, as well as significant decreases in hydroxyproline content of the lung 30 and 60 d postsilica injection when compared to silica/air-exposed animals. NO2 administration 24 h after silica appeared to shift the appearance of PMN in the lung from d 3 to d 14, but did not otherwise alter chronic cellular inflammation. These data suggest that the marked neutrophil response and collagen deposition induced by SI can be modulated by NO2 exposure and that the time of oxidant gas exposure after silica administration is critical to this modulation.

Acute Disease↗