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PubMed2001

The role of inflammation in the anaemia of end-stage renal disease.

Chronic inflammation is a common feature of end-stage renal disease (ESRD) that is gaining increasing attention as a major cause of morbidity and mortality. It is well established that ESRD per se carries a heightened risk of inflammatory disorders and other co-morbid conditions, but it should also be pointed out that dialysis treatment per se can bring additional risk factors for inflammation, such as impure dialysate or bio-incompatible membranes. Inflammation has recently been associated with atherosclerosis and malnutrition in ESRD, and this link has led to the development of the malnutrition, inflammation, atherosclerosis (MIA) hypothesis. This describes a syndrome whereby raised levels of pro-inflammatory cytokines (such as IL-1, IL-6 and TNF-alpha) are a common link between malnutrition, inflammation and atherosclerosis. Also, anaemia appears to be an important element linking elevated cytokine levels with poor patient outcomes. Several mechanisms for cytokine-induced anaemia have been proposed, including intestinal bleeding, impaired iron metabolism and suppression of bone marrow erythropoiesis and erythropoietin production. These effects suggest that pro-inflammatory cytokines may also be an important cause of lack of response to recombinant human erythropoietin (rh-Epo) therapy. In the light of this putative role of pro-inflammatory cytokines, anti-cytokine agents may prove useful to optimize efficacy of rh-Epo in anaemic chronic renal failure patients. Other potential therapeutic strategies include minimizing exposure to causes of inflammation from various co-morbid conditions, such as persistent infections and chronic heart failure.

Anemia↗
PubMed2026

Examining the Relationship Between Physical Neglect, Inflammation and Anterior Cingulate Activation During Facial Emotion Recognition in Patients With Schizophrenia and Healthy Controls: A Functional Magnetic Resonance Imaging Study.

Physical neglect is associated with poorer cognitive functioning in patients with schizophrenia, including deficits in facial emotion recognition. Recent research by our group showed the relationship between physical neglect and facial emotion recognition is mediated by inflammation. While this mediation effect was observed at the level of behaviour, examining the relationship between physical neglect, inflammation and neural activation during facial emotion recognition would help confirm brain regions impacted and support behavioural findings, but these relationships are unclear. Two hundred twelve participants (52 patients with schizophrenia and 160 healthy controls) underwent functional magnetic resonance imaging while performing an established facial emotion recognition task and a subset completed the Childhood Trauma Questionnaire and provided blood samples outside of the scanner. Inflammation was measured using a latent variable that combined basal plasma levels of interleukin-6, tumour necrosis factor-alpha and C-reactive protein. The relationships between physical neglect, inflammation and neural activation were examined using multiple regression. Neither physical neglect nor inflammation predicted altered neural response during facial emotion recognition at p&#x2009;<&#x2009;0.05, family-wise error corrected for multiple comparisons within an anterior cingulate region of interest, across the whole brain, in the whole sample or separately in patients or controls. Future research should examine relationships between physical neglect, inflammation and brain activation in larger samples, which may have sensitivity to detect smaller effects, and use tasks that require active recognition of emotions, in addition to passive viewing of faces, which might be associated with additional neural responses.

Humans↗
PubMed2005

Markers of inflammation are negatively correlated with serum leptin in rheumatoid arthritis.

BACKGROUND: Leptin regulates food intake and modulates immunity and inflammation. A positive feedback mechanism has been described between tumour necrosis factor (TNF) and leptin, and it has been suggested that leptin potentiates inflammation in patients with rheumatoid arthritis (RA). OBJECTIVE: To assess whether inflammation correlates with leptin concentrations in patients with RA, and whether anti-TNF treatment modulates leptin concentrations in these patients. METHODS: Leptin, IL6 and CRP were measured (at baseline and after 2 weeks of treatment) in the blood of 31 patients with RA starting either anti-TNF treatment or placebo, and in 18 healthy controls. RESULTS: In patients with RA, plasma leptin concentrations at baseline correlated inversely with the degree of inflammation as assessed by C reactive protein (CRP; r(s)(2) = 0.21, p<0.01) or interleukin (IL) 6 concentrations (r(s)(2) = 0.22, p<0.008). Mean (SD) leptin concentrations did not differ between patients with RA and controls (6.0 (4.6) v 4.2 (2.8) ng/ml in men; 15.1 (7.9) v 13.4 (5.2) ng/ml in women). Short course anti-TNF treatment for 2 weeks did not modify leptin concentrations, despite significant reduction of CRP and IL6. CONCLUSION: A significant inverse correlation between inflammation and leptin concentrations was found in patients with active RA, although plasma leptin concentrations did not significantly differ from those in healthy controls. This suggests that active chronic inflammation may lower plasma leptin concentrations. Two weeks' treatment with anti-TNF did not change plasma leptin concentrations and longer treatment may be needed to see an effect on leptin.

Adalimumab↗
PubMed2002

Inflammation and atherosclerosis.

Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.

Aged↗
PubMed2002

Mechanisms and markers of airway inflammation in cystic fibrosis.

Airway inflammation is now recognized as a major factor in the pathogenesis of lung disease in cystic fibrosis (CF). Its most characteristic feature is a marked and persistent influx into the airways of neutrophils, which damage the lung by releasing noxious mediators, such as reactive oxygen species and proteolytic enzymes. Recent studies suggest that inflammation occurs very early and may even happen in the absence of infection. Furthermore, links between CF transmembrane conductance regulator dysfunction and both infection and inflammation are postulated; dysregulation of cytokine production and abnormal epithelial host defences have been regarded as causes of sustained inflammation. Bronchoalveolar lavage and the evaluation of neutrophils and inflammatory mediators provide the most accurate picture of airway inflammation. Routine bronchoscopy with bronchoalveolar lavage, however, is unpleasant for the patient and usually is of no immediate benefit to the management of individual cases. Therefore, surrogate markers collected by noninvasive procedures would be of great assistance in the follow-up of cystic fibrosis patients. Several markers have been evaluated in the sputum, serum and urine of cystic fibrosis patients and related to the degree of airway inflammation. Long-term studies are needed to confirm their potential clinical utility and specificity, and to determine which can be used clinically to monitor disease outcome and efficacy of treatment.

Animals↗
PubMed2005

Macrophages in inflammation.

The inflammatory process is usually tightly regulated, involving both signals that initiate and maintain inflammation and signals that shut the process down. An imbalance between the two signals leaves inflammation unchecked, resulting in cellular and tissue damage. Macrophages are a major component of the mononuclear phagocyte system that consists of closely related cells of bone marrow origin, including blood monocytes, and tissue macrophages. From the blood, monocytes migrate into various tissues and transform macrophages. In inflammation, macrophages have three major function; antigen presentation, phagocytosis, and immunomodulation through production of various cytokines and growth factors. Macrophages play a critical role in the initiation, maintenance, and resolution of inflammation. They are activated and deactivated in the inflammatory process. Activation signals include cytokines (interferon gamma, granulocyte-monocyte colony stimulating factor, and tumor necrosis factor alpha), bacterial lipopolysaccharide, extracellular matrix proteins, and other chemical mediators. Inhibition of inflammation by removal or deactivation of mediators and inflammatory effector cells permits the host to repair damages tissues. Activated macrophages are deactivated by anti-inflammatory cytokines (interleukin 10 and transforming growth factor beta) and cytokine antagonists that are mainly produced by macrophages. Macrophages participate in the autoregulatory loop in the inflammatory process. Because macrophages produce a wide range of biologically active molecules participated in both beneficial and detrimental outcomes in inflammation, therapeutic interventions targeted macrophages and their products may open new avenues for controlling inflammatory diseases.

Animals↗
PubMed1988

Suppression of monosodium urate crystal-induced acute inflammation by diets enriched with gamma-linolenic acid and eicosapentaenoic acid.

A subcutaneous air pouch formed in Sprague-Dawley rats was used to study the effect of diets enriched in gamma-linolenic acid (GLA) (in plant seed oil) and eicosapentaenoic acid (EPA) (in fish oil) on acute inflammation induced by monosodium urate crystals. The GLA-enriched diet suppressed significantly the cellular phase of inflammation (polymorphonuclear leukocyte accumulation, crystal phagocytosis, and lysosomal enzyme activity), but it had little effect on the fluid phase (exudate volume and protein concentration). In contrast, the EPA-enriched diet suppressed the fluid phase but not the cellular phase of inflammation. The findings indicate that the fluid and cellular phases of acute inflammation can be controlled independently. A combined diet of fish oil and plant seed oil (EPA-enriched and GLA-enriched) reduced both the cellular and fluid phases of inflammation. Thus, dietary provision of alternative substrates for oxidative metabolism (other than arachidonic acid) modifies monosodium urate crystal-induced acute inflammation.

Animals↗
PubMed2004

Oral administration of food antigen induces T cell mediated intestinal inflammation: a model using TCR-transgenic mice.

To investigate the mechanisms inducing food-sensitive intestinal inflammation, we focused on the OVA23-3 mouse, a transgenic mouse strain expressing a T cell receptor that recognizes ovalbumin (OVA). Mice administered an egg-white (EW) diet containing OVA showed a trend of loose feces and significant weight loss. Histology of the jejunum showed severe inflammation with villous atrophy. Thus, we studied the role of T cells and intestinal microflora in the development of the inflammation. Severe villous disruption was observed in sections of the jejunum from OVA23-3 mice and RAG-2 gene-deficient OVA23-3 mice fed with EW-diet. Further, a larger number of T cells was found in the lamina propria of the jejunum of EW-diet fed OVA23-3 mice, RAG-2 gene-deficient mice and germfree OVA23-3 mice compared with those of control-diet fed mice. However, severe inflammation was not detected in the jejunum of germfree OVA23-3 mice. CD4+ T cells from the MLN of EW-diet fed OVA23-3 mice showed a Th2 cytokine secretion profile. These observations have thus clarified that antigen-specific Th2 cells play important roles in the development of intestinal inflammation. Although the presence of indigenous bacteria was not essential for the inflammation, T cells could mediate a more severe inflammatory response in their presence.

Animals↗
PubMed2006

Polyethylenimine-based antisense oligodeoxynucleotides of IL-4 suppress the production of IL-4 in a murine model of airway inflammation.

BACKGROUND: Interleukin-4 (IL-4) plays a crucial role as an inflammatory mediator in allergic asthma via inducing Th2 inflammation and IgE synthesis. To develop an effective therapeutic agent which specifically inhibits production of IL-4, antisense oligodeoxynucleotides (AS-ODNs) against murine IL-4 mRNA were generated and complexed with polyethylenimine (PEI) to improve intracellular delivery. METHODS: AS-ODNs were generated against the translation initiation region of murine IL-4 mRNA, and complexed with linear PEI. In vitro efficacy of AS-ODNs/PEI complexes was tested by measuring IL-4 production in the D10.G4.1 cell line, and cytotoxicity was tested by XTT assay. Physicochemical properties of polyplexes were examined using atomic force microscopy (AFM) and DNase I protection assay. In vivo effects of IL-4 AS-ODNs/PEI complexes were tested in a murine model of airway inflammation. IL-4 concentrations in the bronchoalveolar lavage (BAL) fluid and circulating IgE levels were measured by ELISA, and histological analysis of lung tissues was performed. RESULTS: IL-4 AS-ODNs/PEI complexes were spheres with an average diameter of 98 nm and resistant to DNase I-mediated degradation. IL-4 AS-ODNs/PEI complexes showed up to 35% inhibition of IL-4 production in D10.G4.1 cells without causing any toxicity, while naked ODNs gave less than 1% reduction. Furthermore, IL-4 AS-ODNs/PEI complexes were effective in suppressing secretion of IL-4 (up to 30% reduction) in the BAL fluid in an ovalbumin-sensitized murine model of airway inflammation. Circulating IgE levels were decreased, and airway inflammation was alleviated by treatment with IL-4 AS-ODNs polyplexes. CONCLUSIONS: These data demonstrate that complexation of IL-4 AS-ODNs with PEI provides a potential therapeutic tool in controlling inflammation associated with allergic asthma, and further presents an opportunity to the development of clinical therapy based on combination of multiple AS-ODNs of cytokines and/or signaling effectors involved in Th2 inflammation and eosinophilia.

Animals↗
PubMed2005

Lower airway inflammation in infants with cystic fibrosis detected by newborn screening.

Controversy exists over whether the lower airway inflammation that characterizes cystic fibrosis (CF) is initiated primarily by the genetic defect. To determine if inflammation precedes infection, we examined bronchoalveolar lavage (BAL) fluid cytology, cytokines (interleukin (IL)-1beta, IL-4, IL-5, IL-6, IL-8, IL-10, and tumor necrosis factor-alpha), and free neutrophil elastase activity from 70 CF (aged 1.5-71 months) children detected by newborn screening and 19 (aged 2.0-48 months) controls with chronic stridor. CF subjects were selected and categorized as pristine (13 aged </= 6 months, lacking prior respiratory symptoms and exposure to antibiotics, and without respiratory pathogens on BAL), infected (42 with viruses or >/= 10(5) colony-forming units/ml of pathogenic bacteria in BAL), and uninfected (15 aged > 6 months, asymptomatic, not taking antibiotics at bronchoscopy, and free of pathogens in their BAL). To further resolve if inflammation develops without infection, inflammatory mediators in paired annual BAL samples from 38 CF subjects were measured, and results were grouped according to whether BAL showed persistence (n = 6), acquisition (n = 8), clearance (n = 13), or absence (n = 11) of infection. While pristine, uninfected, and control subjects had similar BAL profiles, infected patients showed elevated inflammatory indices, including increased IL-10 (P < 0.001). Pristine subjects had the fewest signs of inflammation. Analysis of BAL pairs found differences between the four infection groups for changes in neutrophil percentages, IL-8 (P < 0.001), and free neutrophil elastase (P = 0.009). Infection was associated with elevated inflammatory mediators in BAL fluid. In contrast, minimal or reduced signs of inflammation accompanied absence of eradication of infection from BAL fluid. We conclude that in CF, infection initiates and sustains airway inflammation.

Bronchoalveolar Lavage Fluid↗
PubMed2007

Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis.

BACKGROUND: Chronic inflammation is postulated to contribute to prostate carcinogenesis. We developed a mouse model of chronic prostatitis to test whether infection-induced chronic inflammation would incite reactive changes in prostatic epithelium. METHODS: Prostate tissues harvested from either phosphate-buffered saline (PBS) or E. coli-infected mice were evaluated for histological changes and immunostained for markers of oxidative stress and epithelial cell proliferation. RESULTS: As compared to PBS-treated controls, mice infected with E. coli bacteria for 5 days showed foci of uniformly acute inflammation in the glandular lumen and a persistent inflammation at 12 weeks post-inoculation in the stroma. Prostatic glands showing varying degrees of atypical hyperplasia and dysplasia had stronger staining for oxidative DNA damage and increased epithelial cell proliferation than normal prostatic glands. CONCLUSIONS: These data demonstrate that chronic inflammation induces reactive hyperplasia associated with oxidative stress injury and support the proposed linkage among inflammation, oxidative DNA damage, and prostate carcinogenesis.

Animals↗
PubMed1997

Serum ferritin iron, a new test, measures human body iron stores unconfounded by inflammation.

Serum ferritin protein is an acute phase reactant. We hypothesized that serum ferritin protein generated in response to an inflammatory process would have much less iron (Fe) in it than would "normal" ferritin protein, and therefore measuring serum ferritin iron would assess human body iron status unconfounded by inflammation. BASIC METHODS: We measured serum ferritin iron in 140 clinical samples obtained from the serum banks of Bronx VA Medical Center Hematology and Nutrition Laboratory (Bronx, NY), the CDC Nutritional Biochemistry serum sample bank (Atlanta, GA), and the sample bank from patients with thalassemia and iron overload treated at New York Hospital (New York, NY). Each was analyzed for three conventional criteria of iron status: serum iron, percentage of transferrin saturation and ferritin protein. In addition, tests for inflammation were also performed: C-reactive protein, WBC and transaminases. Seventy-seven patients' sera from 140 screened met each of three consistent criteria for stages of iron status. Serum ferritin was immobilized by immunoprecipitation with rabbit antihuman polyclonal antibody bound to agarose and separated from other iron-containing proteins, digested with 0.2 ml of 3N nitric acid and analyzed for iron content by atomic absorption spectroscopy. RESULTS: Serum ferritin iron ranged in normal controls from 10 ng to 35 ng Fe/ml. The patients with iron deficiency (4/4) and those in negative iron balance (5/6) had values < or = 10 ng. Positive iron balance (8/9) and iron overload (22/22) values were > 35 ng/ml, in contrast to 11/19 with inflammation. Seventeen of twenty-two with overload had values > 100 ng/ml while only 1/19 with inflammation had such a value. Ferritin iron in ferritin protein was > 15% by weight in 14/22 with iron overload but in 0/19 with inflammation. IMPLICATIONS OF THE WORK: Serum ferritin iron is a simple, direct measure of iron stores that we propose, in conjunction with measuring serum ferritin protein, as a minimally invasive screening procedure for accurately assessing the whole range of human body iron status, unconfounded by inflammation.

Blood Chemical Analysis↗
PubMed2001

Important roles for L-selectin and ICAM-1 in the development of allergic airway inflammation in asthma.

Airway inflammation and airway hyperresponsiveness (AHR) are fundamental features of asthma. Migration of inflammatory cells from the circulation into the lungs is dependent upon adhesion molecule interactions. The cell surface adhesion molecules L-selectin and intercellular adhesion molecule (ICAM)-1 have been demonstrated to mediate leukocyte rolling on inflamed pulmonary endothelium, and ICAM-1 has also been shown to mediate capillary sequestration in inflamed lung. However, their roles in the development of airway inflammation and AHR in asthma have not been directly examined. We have characterised the roles of L-selectin and ICAM-1 in the recruitment of inflammatory cells to the lung and in the development of airway hyperresponsiveness using an ovalbumin (OVA)-induced allergic airway disease model of asthma and adhesion molecule-deficient mice. OVA-sensitized/challenged ICAM-1-deficient mice have dramatically reduced inflammatory influx into the airway/lung and a corresponding attenuation of AHR as compared to wild-type controls. OVA-sensitized/challenged L-selectin-deficient mice demonstrate significantly reduced numbers of CD3(+)lymphocytes and increased numbers of B220(+)lymphocytes in BAL as compared to wild-type mice (P< 0.05). However, other parameters of airway/lung inflammation in OVA-sensitized/challenged L-selectin-deficient mice were equivalent to wild-type control mice. Remarkably, despite a fulminant inflammatory response in the airway/lung, AHR was completely abrogated in OVA-sensitized/challenged L-selectin-deficient mice. These findings suggest a crucial role for ICAM-1 in the development of airway inflammation and AHR in asthma. In contrast, L-selectin plays a more selective role in the development of airway hyperresponsiveness but not allergic inflammation in this animal model of asthma. Thus, L-selectin and ICAM-1 represent potential targets for novel asthma therapies specifically aimed at controlling airway inflammation and/or airway hyperresponsiveness.

Airway Resistance↗
PubMed1980

Characteristics and effect of antiinflammatory drugs on adriamycin-induced inflammation in the mouse paw.

A subplantar injection of 5--100 micrograms adriamycin in the mouse hind paw produced a biphasic inflammatory response. The first phase peaked at 2 h while the second, more severe phase peaked at four to five days. The magnitude of inflammation was dose related. Administration of [EH]adriamycin revealed that 78% of the drug was lost from the paw within one day. The loss of the remaining drug followed a biphasic decay curve. The first-phase half-life was 1.2 days, and the second-phase half-life was 16.0 days. Vascular permeability, as measured by the leakage of intravenously administered [125I]albumin, was increased between day 4 and day 8. Pathologically, the paw had mild edema and hemorrhage by 4 h after adriamycin injection. The most severe pathological response was seen at 5 days with diffuse inflammation characterized by edema of the dermis, cellular debris, and mononuclear inflammatory cells. By 10 days the inflammatory response was still present but the edema was milder. The antihistamine diphenhydramine, an H1-blocker, inhibited the first phase of inflammation at the highest dose tested but had no effect on the second phase of inflammation. The antihistamine metiamide, an H2-blocker; the antiserotonin drug, p-chlorophenylalanine; and the antiinflammatory drugs, aspirin, hydrocortisone, and ibuprofen failed to antagonize adriamycin-induced inflammation at 2 h or 5 days after adriamycin injection. Indomethacin reduced the inflammation after 5 days but only at toxic dose levels.

Animals↗
PubMed1993

Alteration in rat apolipoprotein C-III gene expression and lipoprotein composition during inflammation.

A cloned rat apolipoprotein (apo) C-III cDNA was used as a hybridization probe to measure apo C-III mRNA levels in rats after induction of inflammation. Hepatic apo C-III mRNA levels decrease to a minimum value of 46% of normal 72 h after the induction of inflammation. The changes observed are very similar to the changes in mRNA levels of rat apo A-IV, while the hepatic mRNA levels for apo A-I and apo C-I during inflammation remain relatively constant. Alterations in apo C-III gene expression during inflammation were associated with changes in lipoprotein particle size and composition. A decrease of approximately twofold in the amount of apo C-III-containing HDL particles was found in rats 24 h after the induction of inflammation. The average size of apo C-III-containing HDL particles in rats during inflammation is significantly larger than that of the control group. A decrease in the concentration of apo A-I-containing HDL particles was also observed in these rats. The results indicate altered apolipoprotein gene expression associated with alterations in the size and composition of HDL particles.

Animals↗
PubMed1986

Rheumatoid inflammation and joint destruction: cause and effect or parallel phenomena?

Joint damage is a characteristic and important consequence of rheumatoid arthritis; it is usually considered to be a direct result of the inflammatory synovitis. This view implies that by treating actively the synovial inflammation subsequent joint damage will be reduced and the long-term outlook of patients with rheumatoid arthritis thus improved. However, there is relatively little clinical evidence that suppressing inflammation reduces rheumatoid joint damage. An alternative view is that the mechanisms causing inflammation and those leading to joint destruction are parallel processes related only indirectly. Considerable evidence supports such a concept. Clinical studies show radiological progression of the disease occurs despite improvements in measures of joint inflammation and a reduction in the levels of acute phase proteins. Damage can progress in either actively inflamed hot joints or cool swollen joints. Histopathologically the features of rheumatoid synovitis are non-specific, while the radiological pattern of joint damage is very characteristic. There is evidence that lymphocytic infiltration is not a poor prognostic finding, despite it being a typical feature of inflamed joints. Experimental studies also fail to show a close correlation between inflammation and cartilage damage: this is seen in experimental arthritis, coculture in vitro systems, and the air pouch model of cartilage damage. We suggest that attempts to improve the outcome of rheumatoid arthritis should not merely concentrate on controlling inflammation but should also seek to modify the associated connective tissue changes of the disease.

Anti-Inflammatory Agents↗
PubMed1982

Modulation by various locally applied anti-inflammatory and anti-allergic compounds of the immune and non-immune inflammation induced by picryl chloride in mice.

The authors studied the primary irritation and contact delayed hypersensitivity inflammation induced by picryl chloride in mice. The primary irritation reaction was induced by the application of various concentrations of the phlogogenic agent on an ear. Seven days after contact sensitization of the animals on their shaved abdomen, the immune inflammation was also induced on an ear by various doses of picryl chloride. Clear 24 hour-delayed hypersensitivity reactions were induced only by picryl chloride doses that induced a primary oedematous irritation 3 to 6 hours after application. After selection of the 3%-concentration of picryl chloride for challenge on ear, attempts were made to modulate these two types of reaction pharmacologically with various anti-allergic or anti-inflammatory compounds mixed with the inflammation-inducing agent. The inhibition of the non-immune reaction by mepyramine, methysergide, and the two anti-allergic compounds F 1865 and disodium cromoglycate demonstrated the participation of histamine and serotonin in this inflammation. Vasoactive amines seemed also to be involved in the immune reaction, but to a lesser extent. Hydrocortisone reduced the two types of inflammation by the same amount, while desonide had more effect on the delayed hypersensitivity reaction. In addition, both indomethacin and acetylsalicylic acid affected the two reactions equally, whereas phenylbutazone had a greater effect on the primary irritation inflammation.

Administration, Topical↗
PubMed2001

[Effects of carbocisteine on airway inflammation and related events in SO2-exposed rats].

Airway inflammation leads to secretion of abnormal mucous glycoprotein and ciliary injury. To investigate the possible usefulness of carbocisteine against airway inflammation and events related to it, we conducted a study in SO2-exposed rats of the effects of carbocisteine and ambroxol, as an active control drug, on components of mucous glycoprotein (fucose, sialic acid and protein) in bronchoalveolar lavage fluid (BALF); on infiltration and activation of inflammatory cells in BALF; on tracheal and bronchial-ciliary lesions; and on cAMP levels in tracheal and alveolar tissues. Carbocisteine inhibited or improved all SO2-induced changes tested, and dosages of 125 and 250 mg/kg b.i.d. reduced fucose, sialic acid and protein contents, inflammatory cells (as markers of inflammation), free radicals, and elastase activity in BALF, and suppressed the development of ciliary lesions of the tracheal and bronchial mucosa, while ambroxol (10 mg/kg b.i.d.) showed no such effects. In addition, carbocisteine improved cAMP levels in the tracheal and alveolar tissues. These results indicate that carbocisteine is able to prevent the development of inflammation-related respiratory disease in this rat model, and that this remission of airway inflammation may be associated with carbocisteine-induced normalization of cAMP levels in tracheal and alveolar tissues as well as with its mucoregulant and anti-inflammatory effects. In conclusion, carbocisteine has a unique mucoregulant action and inhibits SO2-induced airway inflammation in a manner different from that of ambroxol.

Ambroxol↗