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PubMed2004

Heme oxygenase attenuates allergen-induced airway inflammation and hyperreactivity in guinea pigs.

Heme oxygenase (HO), the heme-degrading enzyme, has shown anti-inflammatory effects in several models of pulmonary diseases. HO is induced in airways during asthma; however, its functional role is unclear. Therefore, we evaluated the role of HO on airway inflammation [evaluated by bronchoalveolar lavage (BAL) cellularity and BAL levels of eotaxin, PGE(2), and proteins], mucus secretion (evaluated by analysis of MUC5AC gene expression and periodic acid-Schiff staining), oxidative stress (evaluated by quantification of 4-hydroxynonenal adducts and carbonylated protein levels in lung homogenates), and airway responsiveness to histamine in ovalbumin (OVA)-sensitized and multiple aerosol OVA or saline-challenged guinea pigs (6 challenges, once daily, OVA group and control group, respectively). Airway inflammation, mucus secretion, oxidative stress, and responsiveness were significantly increased in the OVA group compared with the control group. HO upregulation by repeated administrations of hemin (50 mg/kg i.p.) significantly decreased airway responsiveness in control animals and airway inflammation, mucus secretion, oxidative stress, and responsiveness in OVA animals. These effects were reversed by the concomitant administration of the HO inhibitor tin protoporphyrin-IX (50 micromol/kg i.p.). Repeated administrations of tin protoporphyrin-IX alone significantly increased airway responsiveness in control animals but did not modify airway inflammation, mucus secretion, oxidative stress, and responsiveness in OVA animals. These results suggest that upregulation of the HO pathway has a significant protective effect against airway inflammation, mucus hypersecretion, oxidative stress, and hyperresponsiveness in a model of allergic asthma in guinea pigs.

Allergens↗
PubMed1995

Acute inflammation is the harbinger of glomerulosclerosis in anti-glomerular basement membrane nephritis.

The degree of glomerular inflammation and injury during immune-mediated glomerulonephritis is felt to be critical to the eventual development of glomerulosclerosis, although the relative contributions of acute and chronic inflammation are uncertain. By grading the initial dose of antibody in accelerated anti-glomerular basement membrane nephritis, we observed that only animals with the most substantial acute inflammation (in terms of neutrophil influx and acute proteinuria) developed sustained proteinuria followed by an increase in serum creatinine and evidence of severe glomerulosclerosis. Chronic inflammation (i.e., glomerular macrophage influx and evidence of glomerular cell proliferation), in contrast, was evident without the development of glomerulosclerosis. Decreasing the degree of acute inflammation during severe nephritis by complement depletion diminished both the initial and sustained proteinuria and the influx of neutrophils, prevented the terminal increase in serum creatinine, and attenuated the evolution of glomerulosclerosis. Complement depletion, however, did not affect peak proteinuria, macrophage influx, or glomerular cell proliferation. Regression analysis of the entire data set demonstrated that acute (day 1) proteinuria was predictive of the eventual histopathological index, more so than chronic (day 7) proteinuria. To recapitulate, glomerulosclerosis following antiglomerular basement membrane nephritis appears to be substantially dependent on the degree of acute inflammatory injury.

Animals↗
PubMed1981

Pulmonary hypertension induced by repeated pulmonary inflammation in the rat.

The effect of repeated lung inflammation on the pulmonary vascular bed was studied in rats. Nonbacterial lung inflammation was induced by repeated carrageenan instillations into the lungs. Three days after the single carrageenan injection, the mean pulmonary arterial blood pressure was only slightly raised [16.3 +/- 0.6 (mean +/- SE) Torr in controls and 19.5 +/- 0.5 Torr in rats with lung inflammation, P less than 0.001]. A substantial pulmonary hypertension was found in rats 3 days after the sixth lung inflammation (24.6 +/- 1 Torr). In this group, arterial hypoxemia, hypercapnia, and right-heart hypertrophy were found. In the 14th day of recovery after the last injection of carrageenan, the mean pulmonary artery blood pressure decreased (18.5 +/- 0.9 Torr) but remained higher than in the control group. There was no difference in cardiac output measured by dye-dilution technique between the experimental and control groups. After repeated inflammation, the media of distal pulmonary vessels thickened and the number of pulmonary arterioles with distinct media increased.

Animals↗
PubMed1989

Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections.

Neuropeptides such as substance P are implicated in inflammation mediated by sensory nerves (neurogenic inflammation), but the roles in disease of these peptides and the peptidases that degrade them are not understood. It is well established that inflammation is a prominent feature of several airway diseases, including viral infections, asthma, bronchitis, and cystic fibrosis. These diseases are characterized by cough, airway edema, and abnormal secretory and bronchoconstrictor responses, all of which can be elicited by substance P. The effects of substance P and other peptides that may be involved in inflammation are decreased by endogenous neutral endopeptidase (NEP; also called enkephalinase, EC 3.4.24.11), which is a peptidase that degrades substance P and other peptides. In the present study, we report that rats with histories of infections caused by common respiratory tract pathogens (parainfluenza virus type 1, rat corona-virus, and Mycoplasma pulmonis) not only have greater susceptibility to neurogenic inflammatory responses than do pathogen-free rats but also have a lower activity of NEP in the trachea. This reduction in NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentrations of substance P to reach tachykinin receptors in the trachea. Thus decreased NEP activity may exacerbate some of the pathological responses in animals with respiratory tract infections.

Animals↗
PubMed2003

Connective molecular pathways of experimental bladder inflammation.

Inflammation is an inherent response of the organism that permits its survival despite constant environmental challenges. The process normally leads to recovery from injury and to healing. However, if targeted destruction and assisted repair are not properly phased, chronic inflammation can result in persistent tissue damage. To better understand the inflammatory process, we recently introduced a profiling methodology to identify common genes involved in bladder inflammation. The method represents a complementation to the classic quantification of inflammation and provides information regarding the early, intermediate, and late events in gene regulation. However, gene profiling fails to describe the molecular pathways and their interconnections involved in the particular inflammatory response. The present work introduces a new statistical technique for inferring functional interconnections between inflammatory pathways underlying classic models of bladder inflammation and permits the modeling of the inflammatory network. This new statistical method is based on variants of cluster analysis, Boolean networking, differential equations, Bayesian networking, and partial correlation. By applying partial correlation analysis, we developed mosaics of gene expression that permitted a global visualization of common and unique pathways elicited by different stimuli. The significance of these processes was tested from both biological and statistical viewpoints. We propose that connective mosaic may represent the necessary simplification step to visualize cDNA array results.

Animals↗
PubMed2005

Asbestos-induced lung inflammation and epithelial cell proliferation are altered in myeloperoxidase-null mice.

Asbestos fibers are carcinogens causing oxidative stress and inflammation, but the sources and ramifications of oxidant production by asbestos are poorly understood. Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung deposition of asbestos fibers. In comparison with sham mice, asbestos-exposed myeloperoxidase-null (MPO-/-) and normal (MPO+/+) mice exhibited comparable increases in polymorphonuclear leukocytes, predominately neutrophils, in BALF after 9 days of asbestos inhalation. Differential cell counts on BALF revealed decreased proportions of macrophages and increased lymphocytes in all mice exposed to asbestos, but numbers were decreased overall in asbestos-exposed myeloperoxidase-null versus normal mice. Asbestos-associated lung inflammation in myeloperoxidase-null mice was reduced (P < or = 0.05) in comparison with normal asbestos-exposed mice at 9 days. Decreased lung inflammation in asbestos-exposed myeloperoxidase-null mice at 9 days was accompanied by increases (P < or = 0.05) in Ki-67- and cyclin D1-positive immunoreactive cells, markers of cell cycle reentry, in the distal bronchiolar epithelium. Asbestos-induced epithelial cell proliferation in myeloperoxidase-null mice at 30 days was comparable to that found at 9 days. In contrast, inflammation and epithelial cell proliferation in asbestos-exposed normal mice increased over time. These results support the hypothesis that myeloperoxidase status modulates early asbestos-induced oxidative stress, epithelial cell proliferation, and inflammation.

Animals↗
PubMed1999

Time course of pharmacological modulation of peak eosinophilic airway inflammation after mite challenge in guinea pigs: a therapeutic approach.

BACKGROUND: It is well known that eosinophilic airway inflammation develops after allergen challenge in sensitized humans and animals. However, the detailed time course of suppression of early eosinophilic airway inflammation by pharmacological agents given just after challenge has not been discussed. Therefore, we aimed to evaluate the time course relationship of the suppression of peak eosinophilia by anti-cytokines and pharmacological agents given several hours after the aerosol challenge by a therapeutic approach. METHODS: We used crude mite extract as an allergen to create a sensitization and inhalation challenge, and performed bronchoalveolar lavages (BAL) after the inhalation challenge to observe the degree of eosinophilic airway inflammation in guinea pigs. Various anti-cytokines (anti-IL-3 and anti-IL-5) and pharmacological agents (dexamethasone, theophylline, and roxithromycin) were given within several hours after the acute aeorosol challenge to evaluate the suppressive effect on peak eosinophilia in BAL fluid, which occurred 24 h after the challenge. RESULTS: Our results show that anti-IL-5 and dexamethasone, given within 4 and 8 h after the inhalation challenge, respectively, inhibit the acute allergen-induced peak eosinophilia in BAL fluid. However, anti-IL-3, theophylline, and roxithromycin had no effect on peak eosinophilic airway inflammation after challenge. CONCLUSION: These observations suggest that several hours are needed to complete the process of cytokine-induced recruitment of eosinophils from the blood to the airways after acute allergen challenge. This may be the optimal time to administer anti-cytokines and dexamethasone to attenuate the subsequent eosinophilic airway inflammation after acute allergen-induced asthmatic attacks.

Aerosols↗
PubMedDate not supplied

Postoperative inflammation after cataract surgery in patients with rheumatoid arthritis.

The purpose of the present study was to assess the influence of preoperative activity of rheumatoid arthritis (RA) on early postoperative anterior chamber inflammation after phacoemulsification and intraocular lens implantation. Twenty-three eyes in 18 patients were included in our study. On the first postoperative day, anterior chamber inflammation was observed in 11 eyes (47.8%). Five days after surgery, we found postoperative inflammation only in 1 eye (4.3%). Keratic precipitates were observed in 1 eye (4.3%) on the second postoperative day. We found no correlation between the extent of anterior chamber inflammation and the preoperative activity of RA. Postoperative anterior chamber inflammation was also not associated with the medical management of RA.

Aged↗
PubMed2000

Relationship of surface epithelium concentrations of IL-1 alpha and IL-1 beta to clinical inflammation during experimental gingivitis.

Experimental evidence has clearly demonstrated that IL-1 cytokine levels increase in experimental gingivitis (EG) models in response to plaque accumulation following the cessation of oral hygiene. These changes in cytokine production are reported to occur prior to visible signs of clinical inflammation, and as such may represent early markers of gingival inflammation. This clinical study used a novel dermal sampling tape as a method to collect cytokines from gingival epithelium, as opposed to the more commonly sampled gingival crevicular fluid. The primary objective of the study was to examine the relationship between changes in cytokine levels and clinical inflammation. Ten subjects participated in a 14-day EG model, where 5 days following a dental prophylaxis subjects refrained from all oral hygiene measures for 14-days. Clinical measures including the Löe-Silness Gingival Index (GI), a bleeding index derived from the GI, and the inflammation index (II) were made at baseline prior to the initiation of the EG period and following 14 days of EG. Dermal tape samples were collected from the right posterior buccal quadrant of each subject at both baseline and day 14. The tapes were extracted and the extracts analyzed for both IL-1 alpha and IL-1 beta by ELISA. Results of this study indicate that over a 14-day EG period statistically significant (p < 0.05) increases in GI, gingival bleeding, II, and IL-1 alpha were observed (tested by matched-pairs t test and Wilcoxon signed ranks test). A directional increase in IL-1 beta was also observed. Linear regression analyses demonstrated a strong positive correlation between the number of gingival bleeding sites from the region of gingiva sampled with Sebutape and IL-1 alpha (r = 0.93), as well as IL-1 beta (r = 0.90). In addition, linear regression analyses also demonstrated a strong positive correlation between the mean II score from the region of gingiva sampled with Sebutape and IL-1 alpha (r = 0.93), as well as IL-1 beta (r = 0.86). Similar correlations were observed for whole mouth scores of the number of gingival bleeding sites and mean II with respect to IL-1 alpha and IL-1 beta levels. Collectively, these data confirm the utility of the dermal tape for sampling epithelium cytokine levels from the gingiva and demonstrate a strong positive correlation between IL-1 alpha and IL-1 beta concentrations and gingival inflammation.

Adult↗
PubMed2003

Role of IgE in Th2 cell-mediated allergic airway inflammation.

Recent studies with gene knockout mice have demonstrated that T helper 2 (Th2) cell-derived cytokines, including IL-4, IL-5, and IL-13, play important roles in causing allergic airway inflammation. In addition to Th2 cytokines, IgE-dependent activation of mast cells has been suggested to play a role in allergic airway inflammation. In this review, we will discuss the role of IgE in Th2 cell-mediated allergic airway inflammation. We used IgE transgenic mice, which enabled us to investigate the role of IgE without the influence of activated T cells and other immunoglobulins. Whereas IgE cross-linking by antigens did not induce eosinophil recruitment into the airways or airway hyperreactivity, IgE cross-linking induced CD4+ T cell recruitment into the airways. In addition, when antigen-specific Th2 cells were transferred to IgE transgenic mice, IgE cross-linking significantly enhanced antigen-induced eosinophil recruitment into the airways. These findings suggest that IgE-dependent mast cell activation plays an important role in allergic airway inflammation by recruiting Th2 cells into the site of allergic inflammation.

Animals↗
PubMed2005

Role of inflammation in pancreatic carcinogenesis and the implications for future therapy.

BACKGROUND: The link between inflammation and pancreatic cancer has been observed for a number of gastrointestinal neoplasms. This review examines the role of inflammation in pancreatic carcinogenesis and how it can be utilised to develop new therapies against pancreatic cancer. METHODS: A literature review of Pubmed, Medline and Web of Science databases was undertaken using the key words, pancreatic cancer, inflammation, inducible nitric oxide, interleukins, pro-inflammatory cytokines, cyclooxygenase-2, NF-kappa B, reactive oxygen species, DNA adducts, lipoxygenases, chemoprevention. RESULTS: Epidemiological evidence and molecular studies both in vitro and in vivo all support the hypothesis that inflammation plays an important in the initiation and progression of pancreatic tumours. CONCLUSION: Sustained damage caused by chronic inflammation may precede the onset of frank malignancy by a significant interval. As such, suppression of inflammatory changes and oxidative damage, may help delay or even prevent the inception of pancreatic neoplasia.

Cyclooxygenase 2↗
PubMed2005

Exposure to endotoxins during sensitization prevents further endotoxin-induced exacerbation of airway inflammation in a mouse model of allergic asthma.

BACKGROUND: We have shown previously that lipopolysaccharides (LPS) inhibited airway inflammation in allergen-sensitized and challenged mice when administered during sensitization, while exacerbating the inflammation when given upon challenge. We have here investigated the effect of LPS administered during both sensitization and challenge on airway inflammation, as well as on the profile of the T-helper (Th) response to allergen. METHODS: Mice were sensitized and challenged with ovalbumin (OVA), in the presence or absence of effective doses of LPS, namely 1 mug during sensitization and 1 ng during challenge. Inflammation was assessed by measuring cell counts and cytokine levels in bronchoalveolar lavage fluid (BALF). The profile of the Th response was determined by quantifying OVA-specific IgE and IgG2a in serum and Th1/Th2 cytokines in the culture medium of splenocytes and in BALF. RESULTS: Allergen-induced airway eosinophilia was increased in mice exposed to LPS during challenge only when compared with controls, whereas it was similarly reduced in animals exposed during sensitization only and during both sensitization and challenge. Mice exposed to LPS during sensitization only or during both sensitization and challenge also displayed a decrease in IgE and an increase in IgG2a, suggesting a switch in the immune response toward the Th1 profile. This was confirmed by quantification of Th1/Th2 cytokines in culture medium of splenocytes and in BALF. CONCLUSIONS: Our data demonstrate that exposure to endotoxins during sensitization prevents allergen-induced airway inflammation, as well as its exacerbation triggered by further exposure to endotoxins during challenge, while switching the immune response to allergen from a Th2 to a Th1 profile.

Animals↗
PubMed1994

Antioxidant inhibition of skin inflammation induced by reactive oxidants: evaluation of the redox couple dihydrolipoate/lipoate.

Reactive oxygen species play an important role in mediating skin inflammation, and antioxidants may provide protection. We investigated the anti-inflammatory activity of natural antioxidants, such as superoxide dismutase, catalase, trolox (a water-soluble tocopherol analog) and the redox couple dihydrolipoate/lipoate in skin. Furthermore we compared the anti-inflammatory potency of natural R and racemic dihydrolipoate, as well as R and S lipoate. Skin inflammation in hairless mice was induced by intradermal injection of the hydrogen peroxide producing enzyme glucose oxidase (GOD) or by topical application of the prooxidant drug anthralin. Intradermal injection of the antioxidants inhibited skin inflammation caused by GOD (catalase, dihydrolipoate) and anthralin (trolox, superoxide dismutase, dihydrolipoate). There was no statistically significant difference between the anti-inflammatory activity of the natural R and racemic dihydrolipoate. R or S lipoate did not inhibit skin inflammation when injected intradermally. In feeding experiments, however, R lipoate significantly inhibited GOD-mediated skin inflammation, while S lipoate was only marginally protective. We conclude that (1) several natural antioxidants such as catalase, superoxide dismutase and dihydrolipoate have anti-inflammatory properties in dermatitis induced by reactive oxidants, (2) lipoate (oxidized dihydrolipoate) has skin anti-inflammatory activity when administered orally and (3) naturally occurring R lipoate is a more potent anti-inflammatory agent than the non-physiological S lipoate.

Animals↗
PubMed1996

Effects of inflammation on plasma extravasation and mast cell response in normal and denervated rat skin.

The effects of mild inflammation induced by topical chloroform treatment on plasma extravasation and mast cell response were studied in normal innervated and denervated rat skin. In the absence of inflammation, the reduction in plasma protein extravasation in response to noxious heat was 31.2% in denervated skin compared to the innervated skin. In the presence of inflammation, the reduction in this response was 52.5% in denervated skin compared to the innervated skin. During inflammation, mast cells became abundant, highly degranulated and migrated to the lower dermal tissue forming large aggregations. The ultrastructural observations showed a close anatomical relationship between mast cells and vesicle-containing nerve profiles. These results indicate that repeated topical chloroform treatment of the rat skin induces neurogenic vascular inflammation accompanied by an increase in mast cell response.

Animals↗
PubMed1997

Mite-induced allergic airway inflammation in guinea pigs.

BACKGROUND: Mites are the most common aeroallergen in human allergic asthma. However, no animal model of mite-induced allergic airway inflammation has been reported before. In this study, an animal model of mite-induced allergic airway inflammation in guinea pigs was developed. METHODS: Firstly, we found that two intraperitoneal injections of 100 micrograms crude mite extract (CME), but not multiple aerosol inhalations of 10 mg/ml CME, can cause sensitization in guinea pigs. The sensitization to mites was confirmed by the measurement of serum antimite antibody titer and the detection of anaphylactic bronchoconstriction after intravenous injection of CME solution. Then, single or multiple aerosol challenges with different concentrations (8, 4 or 1 mg/ml) of CME in these sensitized animals were performed. The total white cell and differential counts in the bronchoalveolar lavage (BAL) fluids were studied at different time intervals after challenge in different animals, and tracheal pathology was performed to detect the allergic airway inflammation. For comparison with the study in animals treated with CME, a BAL study in animals treated with ovalbumin was also performed. RESULTS: The inhalation challenge of CME aerosol in sensitized animals caused prolonged eosinophilia in BAL fluid which persisted for at least 7 days after single challenge. Neither inhalation challenge at higher concentrations of CME aerosol nor repeated inhalation challenges increased the degree of eosinophilia in BAL fluid compared to a single challenge. Using the same procedures, we also found that the mite model caused more eosinophilia in BAL fluid than did ovalbumin. CONCLUSION: This is the first report of an animal model of mite-induced allergic airway inflammation in guinea pigs which can provide us with a useful model to study airway inflammation of mite-induced asthma in humans.

Allergens↗
PubMed1992

The role of sensory nerves in catheter-induced urethral inflammation.

We have studied the contribution of the nervous system on experimentally induced urethral inflammation in the rat. Urethral inflammation was produced by inserting latex strips into the urethra. The effects of different experimental procedures were assessed by using a 4-grade inflammation scale based on histological findings. Attenuation of urethral inflammation was produced by administration of capsaicin at birth. A more complete attenuation was produced by infusion of capsaicin prior to application of the latex strip. These data taken together indicate that sensory innervation of the urethral mucosa is involved in the inflammatory reaction and that infusion of the urethra with capsaicin may be tried to prevent catheter-induced urethral inflammation.

Animals↗
PubMed1999

Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries.

-Retrospectively, plaque rupture is often colocalized with inflammation of the cap and shoulder of the atherosclerotic plaque. Local inflammation is therefore considered a potential marker for plaque vulnerability. However, high specificity of inflammation for plaque rupture is a requisite for application of inflammation markers to detect rupture-prone lesions. The objective of the present study was to investigate the prevalence and distribution (local versus general) of inflammatory cells in nonruptured atherosclerotic plaques. The cap and shoulder of the plaque were stained for the presence of macrophages and T lymphocytes in 282 and 262 cross sections obtained from 74 coronary and 50 femoral arteries, respectively. From most cases, 2 atherosclerotic arteries were studied to gain insight into the local and systemic distribution of the inflammatory process. In 45% and 41% of all cross sections, staining for macrophages was observed in the femoral and coronary arteries, respectively. Rupture of the fibrous cap was observed in 2 femoral and 3 coronary artery segments and was always colocalized with inflammatory cells. At least 1 cross section stained positively for CD68 or acid phosphatase in 84% and 71% of all femoral and coronary arteries, respectively. Only 1 femoral and 6 coronary arteries revealed a positive stain for CD68 in all investigated segments. Inflammation of the cap and shoulder of the plaque is a common feature, locally observed, in atherosclerotic femoral and coronary arteries. The high prevalence of local inflammatory responses should be considered if they are used as a diagnostic target to detect vulnerable, rupture-prone lesions.

Acid Phosphatase↗
PubMed2004

Infliximab improves endothelial dysfunction in systemic vasculitis: a model of vascular inflammation.

BACKGROUND: Endothelial vasomotor dysfunction and markers of systemic inflammation are independent determinants of cardiovascular risk. However, the link between clinical inflammation and endothelial dysfunction is unclear. The aim of this study was to use anti-neutrophil cytoplasmic antibody-associated systemic vasculitis (AASV) as a model of systemic inflammation in which to test the hypothesis that inflammation is associated with endothelial dysfunction and can be reversed with anti-tumor necrosis factor-alpha (TNF-alpha) therapy. METHODS AND RESULTS: Fourteen patients with active AASV and 21 age-matched control subjects were studied. Endothelial function was assessed through the use of forearm plethysmography and related to clinical disease activity: Birmingham Vasculitis Activity Score (BVAS) and serum levels of C-reactive protein (CRP), interleukin-6 (IL-6), and TNF-alpha. The effects of anti-TNF-alpha therapy (infliximab), either alone (n=6) or in combination with standard treatment (n=4), on endothelial function were subsequently determined. Patients had a mean BVAS of 11+/-1, and CRP and IL-6 were higher in the AASV group than in control subjects (34.8+/-10.5 versus 1.6+/-0.2 pg/mL, P<0.001; 9.0+/-0.7 versus 6.7+/-0.6 pg/mL, P=0.02). Forearm blood flow response to acetylcholine (ACh) was reduced in the patients compared with control subjects (P=0.002), but sodium nitroprusside (SNP) responses were not (P=0.3). The response to ACh improved with infliximab treatment (P=0.004) in particular, with infliximab alone (P=0.03). CONCLUSIONS: AASV is associated with endothelial dysfunction. Anti-TNF-alpha therapy, alone or in combination with standard treatment, results in clinical remission, reduced inflammation, and improved endothelium-dependent vasomotor responses.

Anti-Inflammatory Agents, Non-Steroidal↗