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PubMed1983

[The cell populations of the lower lung and their response to stress. Interrelations between cells and secretions of inflammation mediators in the distal air spaces].

Broncho-alveolar cells (BAC) act as defence means in the lower respiratory tract and acinus; equally they determine the evolution of inflammatory phenomena, whatsoever its cause. Alveolar macrophages (AM) play an important role in the regulation of the immune response and presentation of antigen to lymphocytes. In the alveolar microclimate AM exert a suppressor effect. AM can be equally considered as true inflammatory cells, either through their own mediators or through the skewed pattern of cellular recruitment. Among these cells polymorphonuclear cells and eosinophils, present in small numbers in broncho-alveolar lavage (BAL) may be encountered in a number of pathological conditions. Finally, free mast cells probably play an important role in the induction of the inflammatory reaction in the distal air spaces.

Animals↗
PubMed1992

Continuum model of fibroblast-driven wound contraction: inflammation-mediation.

We propose a mathematical model to aid the understanding of how events in wound healing are orchestrated to result in wound contraction. Ultimately, a validated model could provide a predictive means for enhancing or mitigating contraction as is appropriate for managing a particular wound. The complex nature of wound healing and the lack of a modeling framework which can account for both the relevant cell biology and biomechanics are major reasons for the absence of models to date. Here we adapt a model originally proposed by Murray and co-workers to show how cell traction forces can result in spatial patterns of cell aggregates since it offers a framework for understanding how traction exerted by wound fibroblasts drives wound contraction. Since it is a continuum model based on conservation laws which reflect assumed cell and tissue properties, it is readily extended to account for emerging understanding of the cell biology of wound healing and its relationship to inflammation. We consider various sets of assumed properties, based on current knowledge, within a base model of dermal wound healing and compare predictions of the rate and extent of wound contraction to published experimental results.

Extracellular Matrix↗
PubMed1996

Differential expression of interleukin-10 mRNA in Wallerian degeneration and immune-mediated inflammation of the rat peripheral nervous system.

Interleukin-10 (IL-10) is a potent immunosuppressant cytokine which downregulates MHC class II antigen expression and inflammatory cytokine production. In this study we localized mRNA for IL-10 in the rat peripheral nervous system (PNS) by nonradioactive in situ hybridization using a digoxygenin-labeled riboprobe specific for rat IL-10. IL-10 mRNA was expressed by some Schwann cells (SCs) in the normal sciatic nerve. During Wallerian degeneration, SCs strongly expressed IL-10 mRNA between days 2 and 4 after transection. By day 14 only occasional cells were positive for IL-10 mRNA. The vast majority of ED1-positive macrophages were IL-10 negative after axotomy. Contrastingly, infiltrating macrophages expressed IL-10 mRNA conincident with beginning clinical recovery in experimental autoimmune neuritis (EAN), the rat model of human Guillain-Barré syndrome. Our data suggest that SCs provide a constitutive immunosuppressant system in the PNS. In EAN additional macrophage-derived IL-10 may be important for the resolution of the T cell-mediated immune response.

Animals↗
PubMed2002

T cells expressing the gammadelta receptor are essential for Th2-mediated inflammation in patients with acute exacerbation of asthma.

OBJECTIVE: T lymphocytes have a central regulatory role in the pathogenesis of asthma. The objective of this study was to characterize immunologically the activation stage of asthma and the functional profile of lymphocytes from induced sputum, with particular emphasis on gammadelta T cells. METHODS: Induced sputum was collected from 10 patients with acute exacerbation of asthma, and from healthy controls. The expression of activation markers on freshly isolated induced sputum lymphocytes and T-cell subsets was analyzed by double immunofluorescent staining and flow cytometry. Fas ligand (FasL) was determined by reverse transcriptase-polymerase chain reaction analysis. The phenotype of gammadelta T-cell subpopulations was tested by A13 and BB3 monoclonal antibodies. In this context, the functional profile of gammadelta T cells was tested in a chromium releasing test. RESULTS: A significantly decreased proportion of alphabeta T cells and an increased proportion of gammadelta T cells, CD56+ cells and CD8+ gammadelta T cells were found in asthma patients compared with healthy controls. In asthmatic patients, there is a significantly increased proportion of T cells expressing CD69 and CD25 antigen. After stimulation of gammadelta T cells, an increased expression of intracellular tumour necrosis factor-alpha, interleukin (IL)-4 and IL10 cytokines were found at higher levels than controls. Interferon-gamma was observed at similar levels in asthma patients and healthy controls. Freshly isolated T-cell receptor (TCR) gammadelta+ cells exhibited an increased percentage of FasL in our patient group. FasL mRNA was detected in TCR gammadelta+ cells before and after IL2 stimulation. TCR gammadelta+ cells were cytotoxic against the K562 cell line. This natural killer activity was mediated by the A13-positive subpopulation. CONCLUSION: The presence of cytokines producing gammadelta cells in induced sputum of asthmatic patients is consistent with regulatory activities. These cells display also cytotoxic function.

Acute Disease↗
PubMed2001

Pentoxifylline prevents autoimmune mediated inflammation in low dose streptozotocin induced diabetes.

Xanthine derivative, pentoxifylline (PTX), has been recently shown to exert a protective effects in certain animal models of autoimmunity, including diabetes in NOD mice. In the present study, the immunomodulatory potential of PTX was investigated in autoimmune diabetes induced by multiple low doses of streptozotocin (MLD-SZ) in genetically susceptible CBA/H mice (tested with 40 mg SZ/kg b.w. for 5 days) and DA rats (tested with 20 mg/kg b.w. for 5 days). In both species, 2-3 weeks following the MLD-SZ treatment, sustained hyperglycemia developed, as an outcome of inflammatory reaction with endothelial cell activation and accumulation of mononuclear cells. Although there was no evidence of typical insulitis in early disease development (day 10), in both rats and mice, macrophages, CD4+ and CD8+ cells were present in the islets of Langerhans as diffuse mononuclear infiltrates with the expression of IFN-gamma, and inducible NO synthase (iNOS). Administration of PTX (200 mg/kg/day for 10 days) in combination with MLD-SZ reduced insulitis and the production of mediators tested, and prevented the development of hyperglycemia. These results suggest that beneficial effects of PTX involve down-regulation of local proinflammatory cytokine-mediated NO synthase pathway. They also demonstrate that in addition to ameliorating spontaneous autoimmunity in NOD mice, PTX may be effective in downregulating an inflammatory autoimmune process triggered in susceptible host by an external agents, such as streptozotocin.

Animals↗
PubMedDate not supplied

[Breath condensate--a medium obtained by a noninvasive method for the detection of inflammation mediators of the lung].

Collection of exhaled condensate (freezing of expired air under conditions of spontaneous breathing) is a non-invasive method permitting the collection of material originating from the lung and the lower respiratory tract so that it can be used for diagnostic examinations. In order to be able to evaluate the diagnostic evidence of exhaled condensate samples in cases of respiratory disease of the calf, leukotriene B4 (LTB4) in bovine exhaled condensate was determined. The influence of the breathing pattern and body temperature on the quantity of condensate to be collected was tested in a total of 49 exhaled condensate samples. It became obvious that the exhaled condensate quantity obtained per time unit is dependent on the ventilation volume per time unit (minute volume). In exhaled condensate samples from 35 clinically healthy calves, LTB4 concentrations of less than 250 pg/mL exhaled condensate were detected. A total of 14 exhaled condensate samples from 7 calves was analyzed before and after experimental respiratory infection with Pasteurella multocida D. In parallel to the analysis of LTB4 in exhaled condensate, the lung function of the calves was examined by means of impulse oscilloresistometry. The increase of LTB4 in the exhaled condensate post infection correlated significantly (p < or = 0.05) with decreases of respiratory reactance. The determination of LTB4 concentrations in exhaled condensate seems to be suitable, in principle, for the detection of inflammations in the respiratory system of the calf. Further studies are needed for the evaluation of the diagnostic validity of the method.

Animals↗
PubMed2003

Role of microglia in inflammation-mediated neurodegenerative diseases: mechanisms and strategies for therapeutic intervention.

Evidence from postmortem analysis implicates the involvement of microglia in the neurodegenerative process of several degenerative neurological diseases, including Alzheimer's disease and Parkinson's disease. It remains to be determined, however, whether microglial activation plays a role in the initiation stage of disease progression or occurs merely as a response to neuronal death. Activated microglia secrete a variety of proinflammatory and neurotoxic factors that are believed to induce and/or exacerbate neurodegeneration. In this article, we summarize recent advances on the study of the role of microglia based on findings from animal and cell culture models in the pathogenesis of neurodegenerative diseases, with particular emphasis on Parkinson's disease. In addition, we also discuss novel approaches to potential therapeutic strategies.

Animals↗
PubMed2002

Inflammation-mediated damage in progressing lacunar infarctions: a potential therapeutic target.

BACKGROUND AND PURPOSE: The mechanisms underlying neurological deterioration in patients with lacunar infarction are not completely understood. In this study, we sought to investigate the role of proinflammatory molecules in the early worsening and outcome of acute lacunar stroke. METHODS: We performed a secondary analysis of 113 consecutive patients with lacunar infarction included within the first 24 hours of the onset of symptoms in a previous study aimed at investigating clinical and biochemical factors of early neurological deterioration (END). END was defined as a fall of > or =1 points in the motor items of Canadian Stroke Scale between inclusion and 48 hours. Poor outcome at 3 months was considered death or Barthel Index <85. Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule-1 (ICAM-1) were determined by enzyme-linked immunoabsorbent assay in blood samples obtained on admission. RESULTS: END was recorded in 27 patients (23.9%); poor outcome was noted in 26 (23%). Median (quartiles) concentrations in plasma of TNF-alpha [16.5 pg/mL (13.7 and 21.2 pg/mL) versus 7.5 pg/mL (6.2 and 9.0 pg/mL)], IL-6 [28.8 pg/mL (22.5 and 35.7 pg/mL) versus 11.5 pg/mL (8.5 and 16.2 pg/mL)], and ICAM-1 [285 pg/mL (219 and 315 pg/mL) versus 158 pg/mL (137 and 187 pg/mL)] were significantly higher in patients who had END than in those with nonprogressing strokes (P< 0.001). Significant differences were also observed between patients with poor and good outcome at 3 months. Logistic regression analysis after adjustment for potential confounders showed that TNF-alpha >14 pg/mL and ICAM-1 >208 pg/mL were independently associated with both END (OR, 511; 95% CI, 17 to 4937; P<0.001; and OR, 315; 95% CI, 17 to 5748; P< 0.001, respectively) and poor outcome at 3 months (OR, 3.0; 95% CI, 1.0 to 8.5; P=0.042; and OR, 4.2; 95% CI, 1.3 to 13.6; P<0.015, respectively). CONCLUSIONS: High concentrations of inflammatory markers in blood are associated with END and poor functional outcome in lacunar infarctions. These findings suggest that inflammation contributes to brain injury in lacunar stroke.

Aged↗
PubMed1991

Further cytological observation on 'activation' by superimposed antigen of inflammation-mediated macrophages.

Compact cell aggregates were induced by an injection of a superimposed antigen, sheep erythrocytes (SRBC) into PSK (a protein-bound polysaccharide)-'prepared' mouse footpad. Major cell types in the cell aggregate were macrophages which rapidly digested superimposed SRBC but not PSK substances which were retained over seven days within their phagosomes. Macrophages without PSK like substances-containing phagosomes occurred invariably outside the cell aggregate. The macrophages in the cell aggregate were interlocked via their cytoplasmic projections. Ruthenium red, a specific dye for extracellular proteoglycans, clearly revealed their surface coats and also closely contacted zones of adjoining macrophages. The surface coats were not uniform in distribution and became sporadically thickened deposits at invaginations of the plasma membrane. Ladder-like structures among adjacent cytoplasmic projections also showed a strong affinity to the dye. It is suggested that a primary function of these structures is the maintenance of close contact of aggregating macrophages. Another observation was that binucleate macrophages occurred in the cell aggregates. Careful inspection on sections of well-preserved tissues concludes that such cells were not formed by a cell fusion between mononucleate macrophages in the cell aggregates. Formation of such a binucleate cell from the macrophage in the aggregates is also discussed.

Animals↗
PubMed2005

Inflammation-mediated dysfunction and apoptosis in pancreatic islet transplantation: implications for intrahepatic grafts.

Recent advances in clinical protocols have improved the outcomes of pancreatic islet transplantation (PIT), yet PIT recipients typically require pancreatic islet grafts derived from multiple donors to achieve insulin independence. This along with experimental models of syngeneic PIT, showing that up to 60% of pancreatic islet tissue undergoes apoptosis within the first several days post-transplantation, strongly suggest the involvement of nonalloantigen-specific, inflammatory events in partial destruction of the graft following PIT. Interleukin-1beta appears to be among the most important inflammatory mediators, causing pancreatic islet dysfunction and apoptosis through the up-regulation of inducible nitric oxide (NO) synthase and cyclooxygenase-2. Kupffer cells secrete many molecules, including cytokines, NO, and free radicals, which are known to be directly toxic to the pancreatic islets, and depletion or inhibition of Kupffer cells improves outcomes following experimental PIT. Immediately after transplantation, the pancreatic islets are perfused only by portal vein blood until the process of angiogenesis restores arterial blood flow some 7-10 days later. This delayed vascularization may have implications for the expression of leukocyte adhesion molecules, the effects of free radicals, and the role of ischemia-reperfusion injury. Finally, in the immediate post-transplant period, hepatocytes may contribute to pancreatic islet injury through the production of NO. This paper reviews literature regarding the inflammatory events that follow PIT as well as the pathogenesis of diabetes and the pathophysiology of hepatic ischemia-reperfusion and their relation to the survival and function of intrahepatic pancreatic islet grafts.

Animals↗
PubMed1983

Efficacy of membrane filtration, influence on hemostasis, immunoglobulins and inflammation mediators during daily plasma exchanges.

Plasma exchange (PE) by membrane filtration was performed with the following hollow fibers: cellulose-diacetate (Plasmaflo 01, Plasmaflo 02, Asahi, Japan), polypropylene (Plasmaflux, Fresenius, FRG) and polymethylmethacrylate (Plasmax, Toray, Japan). The elimination-coefficient (EC) for certain plasma proteins was calculated. With all hollow fibers no correlation between the EC for about ten plasma proteins with a molecular weight of 54.000 dalton up to 2.400.000 dalton. The mean EC-values for the fibers studied were: 0.32 (Plasmaflo 01), 0.52 (Plasmaflo 02), 0.52 (Plasmaflux) and 0.58 (Plasmax). Membrane filtration performed with the single needle technique using either Plasmaflo 02 or Plasmaflux resulted in a significantly lower efficiency with mean EC-values of 0.33 and 0.32 respectively. After three or four days of PE treatment using three liters of 3% human albumin solution as replacement fluid several alterations in parameters of hemostasis were altered: Antithrombin III levels dropped to 35% of normal value after each plasma exchange but increased to normal range within 24 hours during the observed period of four consecutive PE, Fibrinogen concentration dropped permanently to a preexchange value of 40% of the initial concentration after three plasma exchanges. A 40-50% decrease was also observed for prothrombin, plasminogen and alpha-2-macroglobulin after plasma exchange. A decrease in the platelet count ranging from 5 to 25% after each plasma exchange was observed but returned to the initial level before the next treatment. The concentrations of IgG IgA and IgM decreased to less than 20% of preexchange values and C 3 and C 4 to 20-30: of preexchange values after three plasma exchanges.(ABSTRACT TRUNCATED AT 250 WORDS)

Filtration↗
PubMed2001

Preferential binding of Staphylococcus aureus to skin sites of Th2-mediated inflammation in a murine model.

Staphylococcus aureus is found on over 90% of atopic dermatitis skin lesions and is thought to contribute to skin inflammation via the production of potent exotoxins. In contrast, less than 5% of normal subjects harbor S. aureus. This suggests that an atopic immune response itself may play a role in preferential binding of S. aureus to the skin. To examine this issue more directly, we analyzed the S. aureus binding characteristics of skin in mice undergoing different T helper type 1 cell versus T helper type 2 cell inflammatory responses using a novel in vitro bacterial binding assay. BALB/C female mice were first sensitized to ovalbumin with alum or ovalbumin with complete Freund's adjuvant to induce T helper type 2 or T helper type 1 responses, respectively. Mice were then challenged intradermally with either saline (control) or ovalbumin. Forty-eight hours later, skin specimens were obtained from the challenge sites, and the number of S. aureus binding to each skin section was quantitated. Bacterial binding was found to be significantly greater at skin sites of BALB/C mice that had been ovalbumin/alum sensitized compared with ovalbumin/complete Freund's adjuvant sensitized (p < or = 0.01). When compared to the ovalbumin sensitized/challenged skin of wild type BALB/C mice or interferon-gamma gene knockout mice, interleukin-4, but not interferon-gamma, gene knockout mice had significantly less S. aureus binding at their ovalbumin sensitized/challenged skin sites. Mutant S. aureus strains that lacked either fibronectin- or fibrinogen-binding protein expression showed significantly reduced S. aureus binding compared with the parent wild type strain (p < 0.005). Moreover, preincubation of the wild type bacteria with fibronectin or fibrinogen, but not collagen, resulted in significantly less skin binding of S. aureus (p < 0.01). Incubation of skin with interleukin-4, and less so with interferon-gamma, led to more binding of wild type S. aureus but not of an S. aureus mutant deficient in fibronectin binding protein expression. After interleukin-4 incubation, but not interferon-gamma, epidermal immunoreactivity for fibronectin was observed in murine skin explants. These results show that a T helper type 2 inflammatory environment can promote skin binding by S. aureus and that this binding is mediated by fibronectin and fibrinogen.

Adhesins, Bacterial↗
PubMed1987

The inflammation mediators interleukin 1 and hepatocyte-stimulating factor are differently regulated in human monocytes.

Human peripheral monocytes can be induced by bacterial lipopolysaccharide to produce the inflammatory mediators interleukin 1 (IL 1) and hepatocyte-stimulating (HS) activity. IL1 and HS activities were separated by gel permeation chromatography. It is also shown that the two monokines are differently regulated. Evidence for this stems from the finding that monocytes cultured for 24 h lose their ability to produce IL1 in response to lipopolysaccharide, while synthesis of HS activity remains essentially unaffected.

Dose-Response Relationship, Drug↗
PubMed2003

Inhibition of cutaneous ultraviolet light B-mediated inflammation and tumor formation with topical celecoxib treatment.

Inflammation, which includes the release of growth factors, proinflammatory cytokines and prostaglandins, the infiltration and activation of inflammatory cells, and the induction of oxidative DNA damage, is known to play a role in cancer development. The combination of damage to the skin resulting from chronic ultraviolet light B (UVB) exposure itself and the inflammatory response it induces is a major source of skin cancer development. Cyclooxygenase-2 (COX-2), an inflammatory enzyme responsible for the production of prostaglandins, is now implicated in the development of epithelial cancers, including squamous cell carcinoma in the skin. Previous work conducted in our laboratory has shown that topical treatment with celecoxib following UVB irradiation inhibits several parameters of acute inflammation, including vascular permeability, the infiltration and activation of neutrophils, and the production of prostaglandin E(2) (PGE(2)). The present studies expanded these observations, demonstrating the ability of topical celecoxib to inhibit acute oxidative damage. In addition, long-term studies illustrate the effectiveness of topical treatment with this drug in reducing chronic inflammation and UVB-induced papilloma/carcinoma formation. This data provides compelling evidence to explore the clinical efficacy of topically applied COX-2 inhibitors for the prevention of human skin cancers.

Administration, Topical↗
PubMed1991

Azathioprine reduces extravasation and neutrophil trafficking in immune complex-mediated inflammation in the rat colon.

Azathioprine (AZ) has been used in the treatment of refractory inflammatory bowel disease. The mechanism by which AZ decrease colonic inflammation is not known. It is alluded that AZ may be effective in the maintenance of remission. We examined whether AZ in non-immunosuppressive doses reduces extravasation and neutrophil trafficking in a rat model of colonic inflammation. Rats were treated with I.P. injection of AZ (1 mg/kg) for 6 weeks. At the end of 2 and 6 weeks rats were injected I.V. immune complex and on the following day the proximal colon was perfused with 2.5% formaldehyde (local irritant 3 ml/hour for 5 mins). Extravasation was measured by Evans' blue technique and neutrophil concentration in the tissue was determined by measuring myeloperoxidase (MPO). AZ did not inhibit extravasation and MPO after 2 weeks of therapy. However, after 6 weeks, AZ reduced extravasation to 20 +/- 2 micrograms/gm compared to untreated animals (51 +/- 6 micrograms/gm tissue) and MPO levels to 0.3 +/- 13 compared to untreated rats (0.8 +/- 0.32 mU/gm). There was a good correlation between extravasation and MPO levels. These results suggest that long-term treatment with AZ may prevent extravasation and cause reduction in neutrophil trafficking. Such an effect may be beneficial for maintaining remission in IBD.

Aminosalicylic Acids↗
PubMed1995

Role of neutrophil-mediated inflammation in aspirin-induced gastric mucosal injury.

The objectives of this study were to determine the roles of neutrophil-endothelial cell interactions and oxygen-derived free radicals in the pathogenesis of aspirin-induced gastric mucosal injury in rats. Oral administration of acidified aspirin (200 mg/kg) resulted in linear hemorrhagic erosions and an increase in myeloperoxidase activity, an index of neutrophil infiltration, in the gastric mucosa. Aspirin-induced gastric damage and the increase in myeloperoxidase activity were significantly inhibited by the injection of anti-CD11a, anti-CD11b, anti-intercellular adhesion molecule-1 monoclonal antibodies, and the combination of superoxide dismutase and catalase, which are scavengers of active oxygen species. These results suggest that neutrophil-endothelial adhesive interactions, which occur via CD11a/ CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule-1, and oxygen-derived free radicals produced by neutrophils are implicated in the production of aspirin-induced gastric mucosal injury.

Animals↗