Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “inflammatory response”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed2004

Immature anti-inflammatory response in neonates.

The inflammatory response plays a major role in the induction of several neonatal diseases. We hypothesize that an imbalance between the pro- and anti-inflammatory response is crucial for the previously shown enhanced production of proinflammatory cytokines in term and preterm infants during infection. To test this hypothesis, we compared the capacity to produce the main anti-inflammatory cytokines IL-10 and TGF-beta in term infants, preterm infants and adults at different levels of synthesis by quantitative real time reverse-transcribed PCR, flow cytometry, as well as enzyme-linked immunoassay. Term and preterm infants showed a profoundly diminished IL-10 mRNA-expression and IL-10 production after stimulation. In addition, the amount of TGF-beta-positive lymphocytes was significantly less in neonates than adults. Furthermore, there was a considerably lower inhibition of production of IL-1alpha, IL-6, IL-8 and TNF-alpha by the use of recombinant IL-10 in term and preterm infants compared with adults. These results demonstrate not only a diminished anti-inflammatory capacity but also a reduced response to anti-inflammatory stimuli in term and preterm infants. From these data we conclude that neonates display an immature compensatory anti-inflammatory response syndrome (CARS) which may predispose preterm infants to harmful effects of proinflammatory cytokines resulting in severe organ sequelae during infection.

Adult↗
PubMed1995

Antibodies to intercellular adhesion molecule-1 ameliorate the inflammatory response in acetic acid-induced inflammatory bowel disease.

The transendothelial migration of leukocytes in many inflammatory responses is now believed to be dependent on the interaction of leukocyte and endothelial cell-derived adhesion molecules. To examine the role of intercellular adhesion molecule-1 (ICAM-1) in the development of inflammation in a rat model of colitis, we investigated the effects of antibodies to rat ICAM-1 given 24 hrs after inflammation was induced by acetic acid. Antibodies to rat ICAM-1 substantially ameliorated the inflammatory response as indicated by a reduction in gross inflammatory characteristics, tissue/body weight ratio, myeloperoxidase activity and superoxide levels. The results demonstrate that ICAM-1 plays an important role in the development of inflammatory bowel disease in rats. The use of antibodies to ICAM-1 to inhibit the adherence of leukocytes to endothelium, may be of potential therapeutic value in the treatment of inflammatory bowel disease in man.

Acetates↗
PubMed1991

Avian inflammatory response: mediation by macrophages.

The inflammatory response is one of the best defined components of nonspecific immunity in birds. Introduction of an immunogen into the skin or peritoneal cavity results in a characteristic series of local and systemic responses. Initially, locally produced chemotactic substances cause heterophils and monocytes to emigrate from the blood through postcapillary venules to the site of immunogen. Monocytes and heterophils phagocytize the immunogen and monocytes can initiate specific immunity mediated by lymphocytes. Monocytes release a variety of hormone-like substances (monokines) that act locally to coordinate the localized inflammatory response and facilitate lymphocyte responses. These same monokines can gain entrance into the circulation and act systemically to orchestrate the acute phase response. Monokine activities characterized to date are similar to mammalian interleukin-1, interleukin-2, tumor necrosis factor, and granulocyte-stimulating factor. The inflammatory response is active in the embryo midway through incubation and is probably instrumental in protection of the embryo. Inappropriate or overexuberant inflammatory responses can lead to a variety of pathologies in the chicken, demonstrating the importance of precise regulation of the inflammatory response.

Animals↗
PubMed1996

Molecular determinants of acute inflammatory responses to biomaterials.

The frequent inflammatory responses to implanted medical devices are puzzling in view of the inert and nontoxic nature of most biomaterials. Because implant surfaces spontaneously adsorb host proteins, this proteinaceous film is probably important in the subsequent attraction of phagocytes. In fact, earlier we found that acute inflammatory responses to experimental polyethylene terephthalate implants in mice require the precedent adsorption of one particular host protein, fibrinogen. The present investigations were aimed at defining the molecular determinants of fibrinogen-mediated acute inflammatory responses to implanted biomaterials. We find: (a) plasmin degradation of purified fibrinogen into defined domains reveals that the proinflammatory activity resides within the D fragment, which contains neither the fibrin cross-linking sites nor RGD sequences; (b) the major (and, perhaps, exclusive) proinflammatory sequence appears to be fibrinogen gamma 190-202, previously shown to interact with CD11b/CD18 (Mac-1). The chemically synthesized peptide, cross-linked to albumin (which itself does not promote inflammatory responses), mimics the proinflammatory effect of adsorbed native fibrinogen; and (c) this sequence probably promotes inflammatory responses through interactions with Mac-1 because phagocyte accumulation on experimental implants is almost completely abrogated by administration of recombinant neutrophil inhibitory factor (which blocks CD11b-fibrin(ogen) interaction). We conclude that improved knowledge of such surface-protein-phagocyte interactions may permit the future development of more biocompatible implantable materials.

Acute Disease↗
PubMed2006

The systemic inflammatory response syndrome.

The systemic inflammatory response syndrome (SIRS) is the body's response to an infectious or noninfectious insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components. This review outlines the pathophysiology of SIRS and highlights potential targets for future therapeutic intervention in patients with this complex entity.

Biomarkers↗
PubMed2000

A regulatory role for interleukin 4 in differential inflammatory responses in the lung following infection of mice primed with Th1- or Th2-inducing pertussis vaccines.

Protection against infectious pathogens at mucosal surfaces is dependent on local antibody responses, production of inflammatory mediators, and recruitment of immune effector cells to the site of infection. Since Th1 and Th2 cells produce cytokines with pro- and anti-inflammatory activities, immunization with vaccines that induce these T-cell subtypes may regulate the subsequent inflammatory response to infection. We have demonstrated that immunization of mice with pertussis whole-cell or acellular vaccines (Pw or Pa) selectively induces Th1 and Th2 cells, respectively. In this study we have used a murine respiratory-infection model to demonstrate that priming with a Th1- or Th2-inducing pertussis vaccine can influence the local inflammatory response and immune effector cells in the lung following aerosol challenge with Bordetella pertussis. Analysis of bronchoalveolar lavage (BAL) fluid taken during the course of B. pertussis infection of naïve mice or mice immunized with Pw revealed an early influx of neutrophils and local production of interleukin 1beta (IL-1beta) in the lungs. In contrast, neutrophil infiltration and IL-1beta production were not observed following challenge of mice immunized with the Th2-inducing Pa. Conversely, during infection local production of IL-6 and IL-1ra was significantly greater in mice immunized with Pa than in those immunized with Pw. Studies of knockout mice revealed neutrophil and lymphocyte infiltration in the lungs following B. pertussis infection of IL-4-defective (IL-4(-/-)) mice but not in wild-type mice immunized with Pa. Furthermore, the levels of IL-1beta, IL-6, and IL-1ra in Pa-immunized IL-4(-/-) mice were comparable to those in mice immunized with Pw. These results demonstrate distinct influences of Th1- and Th2-inducing vaccines on the protective inflammatory responses in the lungs following challenge with B. pertussis and implicate IL-4 as an important regulator of inflammatory-cell recruitment.

Animals↗
PubMedDate not supplied

Aortic aneurysm repair is associated with a lower inflammatory response compared with surgery for inflammatory bowel disease.

BACKGROUND: Since the plasma cytokine profile reflects the body's inflammatory response to injury, this study was designed to prospectively observe the plasma cytokine levels in response to the degree of different sorts of abdominal surgical trauma. METHODS: Plasma levels of TNF-alpha, type I TNF receptor (p55), type II TNF receptor (p75), IL-6, IL-8, IL-10, phospholipase A(2) (PLA(2)), and haptoglobin were measured peri-operatively in patients undergoing bowel resection for inflammatory bowel disease or diverticulitis (IBD) (n = 9), elective repair of abdominal aortic aneurysm (AAA) (n = 9), or laparoscopic cholecystectomy (lap chole) (n = 9). RESULTS: The IBD patients showed a significant (p < 0.05) post-operative elevation in plasma IL-6, p55, p75, and PLA(2) levels, but no significant change in TNF-alpha, IL-8, IL-10 or haptoglobin levels. The AAA patients had a significant post-operative rise in IL-10 levels and a significant decrease in plasma haptoglobin levels, but no significant change of TNF-alpha, IL-6, IL-8, p55, p75, or PLA(2) concentrations. The lap chole patients demonstrated no significant change in any of these parameters. CONCLUSION: These data show that IL-6, IL-10, p55, and p75 are markers to measure the degree of inflammatory stress associated with abdominal operative procedures and demonstrate the relative lack of a cytokine response to laparoscopic cholecystectomy.

Adult↗
PubMed2003

Polymorphisms in Toll-like receptor 4 and the systemic inflammatory response syndrome.

The systemic inflammatory response syndrome (SIRS) is a major cause of morbidity and mortality, and is thought to be due to an over-amplification of an inflammatory response. The Toll-like receptor 4 ( TLR4 ) Asp-299-->Gly polymorphism has been shown to reduce lipopolysaccharide responsiveness. We examined whether this TLR4 polymorphism is associated with severity of SIRS. A trend was found between the minor allele and mortality in SIRS (odds ratio of 4.3; P =0.076), suggesting a role for TLR4 signalling in the severity of SIRS.

APACHE↗
PubMed1997

The inflammatory response to cardiopulmonary bypass.

The inflammatory response to cardiopulmonary bypass is the product of a complex interplay of humoral and cellular components. Contact activation cascades, the complement system, and cytokines comprise the humoral elements and interact in such a way as to propagate their own cascades and to activate the cellular elements. Neutrophils and endothelial cells are the cellular components and become involved after their "activation" by the humoral mediators. Neutrophil-endothelial cell adherence is the initial step of the cellular inflammatory response and is promoted by the expression of specific adhesion molecules on the surfaces of both of these cells leading to the emigration of neutrophils into the extravascular space where they release toxins that damage surrounding tissues. The resulting organ dysfunction produces the clinical picture referred to as the "postperfusion syndrome." Strategies to attenuate this response include the administration of corticosteroids, aprotinin, and anticytokine monoclonal antibodies, as well as various modifications of the bypass circuit. The existence of multiple pathways to trigger this inflammatory response hampers efforts at its attenuation and leaves much investigation to be done as the quest to understand the body's inflammatory response to cardiopulmonary bypass continues.

Adrenal Cortex Hormones↗
PubMed1997

A comparison of mucosal inflammatory responses to Giardia muris in resistant B10 and susceptible BALB/c mice.

In the first three weeks of primary Giardia muris infections B10 mice clear infection more rapidly than BALB/c mice. There is evidence that interferon-gamma contributes to the relative resistance of B10 mice. The nature of the functional contribution of interferon-gamma is unclear and does not relate to the secretory or serum antibody response. Mucosal inflammatory events in these strains have been studied. Apart from a small rise in both strains of goblet cell and mucosal mast cell numbers, associated with release of mast cell protease-1 in serum, no inflammatory infiltrate was observed at the time trophozoites were cleared from the intestinal lumen. Inhibition of mast cell products (5-hydroxytryptamine and histamine) by cyproheptadine enhanced the intensity of infection in both strains. The relative resistance of B10 mice could not be explained in terms of the mucosal inflammatory response.

Animals↗
PubMed2006

Emerging roles for ectodomain shedding in the regulation of inflammatory responses.

The multistep model of leukocyte recruitment to sites of inflammation has helped elucidate specific molecular cues for each of the individual steps. However, it is less clear how cells transition between the different steps and how the complex interactions are coordinately regulated. Once a leukocyte sticks to the endothelium, it only takes a few minutes to reach the subendothelial basement membrane, so the transitions and regulatory mechanisms must be rapid. We put forward the hypothesis that proteolytic shedding of cell surface proteins provides a mechanism to aid in the rapid transition of cells and coordinate the complex, multistep process of leukocyte recruitment in response to inflammatory stimuli. Support for this hypothesis is provided from analyses of disease states and from studies with protease inhibitors and genetically engineered mutations that prevent "ectodomain shedding" of cell surface proteins and consequently perturb the inflammatory response.

ADAM Proteins↗
PubMedDate not supplied

[Systemic inflammatory response in pediatric cardiac surgery].

Systemic Inflammatory Response (SIR) constitutes generalized, non-specific response to tissue injury of whatever etiology, and is a rapid, highly amplified, controlled humeral and cellular response. Cardiopulmonary Bypass (CPB) is necessary in many cardiac surgery as in adults as children. Also we know the undesirable effects of SIR. The pediatric surgical team to treat of management very well if exist the threat of undesirable outcome after CPB. There are several key components of the inflammatory response to cardiac surgery involve the complement, immune and endothelial systems. Cytokines may exert either proinflammatory or antiinflammatory effects. Cytokines are essential for immunologic and physiologic homeostasis, are normally subject to thight homeostatic control, and are produced in response to a variety of physiologic and pathologic stimuli. An uncontrolled inflammatory response appears to play a significant role in the morbidity or mortality observed in patients undergoing CPB. The inflammatory response contributes to the pathogenesis of acute pulmonary, cardiovascular, neurologic, splanchnic, hematologic, and immune system dysfunction following cardiac surgery. The development of strategies to control the inflammatory response following cardiac surgery is currently the focus of considerable research efforts. Diverse techniques, including maintenance of hemodynamic stability, minimization of exposure to CPB circuitry, and pharmacologic and immunomodulatory agents have been studied. Also hemofiltration, leukodepletion, the use of serine protease inhibitors and corticosteroids. Molecular biology is revolutionizing medicine and the ability to assess the impact of genetic variability on disease characterization and perioperative outcome. Recent evidence suggests that the degree and severity of surgical-induced inflammation may be significantly influenced by genotype.

Cardiac Surgical Procedures↗
PubMed2006

Active spice-derived components can inhibit inflammatory responses of adipose tissue in obesity by suppressing inflammatory actions of macrophages and release of monocyte chemoattractant protein-1 from adipocytes.

Inflammation plays a key role in obesity-related pathologies such as cardiovascular disease, type II diabetes, and several types of cancer. Obesity-induced inflammation entails the enhancement of the recruitment of macrophages into adipose tissue and the release of various proinflammatory proteins from fat tissue. Therefore, the modulation of inflammatory responses in obesity may be useful for preventing or ameliorating obesity-related pathologies. Some spice-derived components, which are naturally occurring phytochemicals, elicit antiobesity and antiinflammatory properties. In this study, we investigated whether active spice-derived components can be applied to the suppression of obesity-induced inflammatory responses. Mesenteric adipose tissue was isolated from obese mice fed a high-fat diet and cultured to prepare an adipose tissue-conditioned medium. Raw 264.7 macrophages were treated with the adipose tissue-conditioned medium with or without active spice-derived components (i.e., diallyl disulfide, allyl isothiocyanate, piperine, zingerone and curcumin). Chemotaxis assay was performed to measure the degree of macrophage migration. Macrophage activation was estimated by measuring tumor necrosis factor-alpha (TNF-alpha), nitric oxide, and monocyte chemoattractant protein-1 (MCP-1) concentrations. The active spice-derived components markedly suppressed the migration of macrophages induced by the mesenteric adipose tissue-conditioned medium in a dose-dependent manner. Among the active spice-derived components studied, allyl isothiocyanate, zingerone, and curcumin significantly inhibited the cellular production of proinflammatory mediators such as TNF-alpha and nitric oxide, and significantly inhibited the release of MCP-1 from 3T3-L1 adipocytes. Our findings suggest that the spice-derived components can suppress obesity-induced inflammatory responses by suppressing adipose tissue macrophage accumulation or activation and inhibiting MCP-1 release from adipocytes. These spice-derived components may have a potential to improve chronic inflammatory conditions in obesity.

3T3-L1 Cells↗
PubMed1999

Interferon response heterogeneity: activation of a pro-inflammatory response by interferon alpha and beta. A possible basis for diverse responses to interferon beta in MS.

Interferon gamma (IFN-gamma) stimulates the (pro-inflammatory) type II interferon receptor and is known to exacerbate multiple sclerosis (MS). In contrast, IFN-alpha and IFN-beta are ligands for the (anti-inflammatory) type I interferon receptor and are beneficial in some (but not all) patients with MS. Should IFN-beta elicit a type-II-like pro-inflammatory response, the beneficial effects might be attenuated. These studies were undertaken to test this possibility with the use of quinolinic acid (QUIN) formation as a measure of type II receptor activation. In normal human macrophage cultures, IFN-gamma was the most potent stimulus for QUIN formation. Generally, IFN-beta and IFN-alpha were less potent. However, an unexpected inter-patient variability was observed. In some subjects, IFN-alpha was more potent than IFN-beta. In other subjects, IFN-beta was more potent than IFN-alpha. The present data demonstrate an inter-subject variability for QUIN production following exposure to the interferons. MS patients who demonstrate a pro-inflammatory response to IFN-beta (e.g., increased QUIN) may be less likely to benefit from this therapy.

Adult↗
PubMed2005

The chemokine receptor D6 limits the inflammatory response in vivo.

How the inflammatory response is initiated has been well defined but relatively little is known about how such responses are resolved. Here we show that the D6 chemokine receptor is involved in the post-inflammatory clearance of beta-chemokines from cutaneous sites. After induction of inflammation by phorbol esters, wild-type mice showed a transient inflammatory response. However, in D6-deficient mice, an excess concentration of residual chemokines caused a notable inflammatory pathology with similarities to human psoriasis. These results suggest that D6 is involved in the resolution of the cutaneous inflammatory response.

Animals↗
PubMed1997

Role of the 5-lipoxygenase-activating protein (FLAP) in murine acute inflammatory responses.

Leukotrienes are potent inflammatory mediators synthesized from arachidonic acid (AA) predominately by cells of myeloid origin. The synthesis of these lipids is believed to be dependent not only on the expression of the enzyme 5-lipoxygenase (5-LO), which catalyzes the first steps in the synthesis of leukotrienes, but also on expression of a nuclear membrane protein termed the 5-LO-activating protein (FLAP). To study the relationship of these two proteins in mediating the production of leukotrienes in vivo and to determine whether the membrane protein FLAP has additional functions in various inflammatory processes, we have generated a mouse line deficient in this protein. FLAP-deficient mice develop normally and are healthy. However, an array of assays comparing inflammatory reactions in FLAP-deficient mice and in normal controls revealed that FLAP plays a role in a subset of these reactions. Although examination of DTH and IgE-mediated passive anaphylaxis showed no difference between wild-type and FLAP-deficient animals, mice without FLAP possessed a blunted inflammatory response to topical AA and had increased resistance to platelet-activating factor-induced shock compared to controls. Also, edema associated with Zymosan A-induced peritonitis was markedly reduced in animals lacking FLAP. To determine whether these differences relate solely to a deficit in leukotriene production, or whether they reflect an additional role for FLAP in inflammation, we compared the FLAP-deficient mice to 5-LO-deficient animals. Evaluation of mice lacking FLAP and 5-LO indicated that production of leukotrienes during inflammatory responses is dependent upon the availability of FLAP and did not support additional functions for FLAP beyond its role in leukotriene production.

5-Lipoxygenase-Activating Proteins↗
PubMed2001

Evidence for activin A and follistatin involvement in the systemic inflammatory response.

The inflammatory cascade is a multifactorial process regulated by interwoven cytokine and growth factor networks. This review summarizes the emerging evidence that implicate activin A and follistatin in inflammatory processes. Our recent studies have determined that activin A is released early in the cascade of circulatory cytokines during systemic inflammatory episodes, roughly coincident with tumour necrosis factor (TNF)-alpha and before interleukin (IL)-6 and follistatin. The source(s) of this activin A are not yet established, but prime candidates are monocytes/macrophages, other immune cell types or vascular endothelial cells. Clinical data are limited, but activin beta(A) subunit mRNA or activin A protein is elevated in inflammatory bowel diseases and inflammatory arthropathies, and circulating concentrations of follistatin are elevated in patients with sepsis. In more mechanistic approaches, in vitro studies show that activin A can have both pro- and anti-inflammatory actions on key inflammatory mediators such as TNFalpha, IL-1beta and IL-6. Furthermore, there is emerging understanding of how the intracellular signaling pathway for activin A, incorporating Smads, may interact with and be modulated by other key regulatory cytokines and growth factors.

Activins↗
PubMed1985

Streptozotocin diabetes: prolonged inflammatory response with delay in granuloma formation.

Inflammatory responses to carrageenin in streptozotocin-induced diabetic rats proved to be characterized by low values of granuloma tissue (tissue) weight and granuloma pouch fluid (fluid) volume, high values of fluid beta-glucuronidase (beta-Gl) and leucine aminopeptidase (LAP), and furthermore by high values of fluid lipid peroxide (LPO) and lactate dehydrogenase (LDH) and low values of fluid proamidase. These results in such diabetic rats were similar to those in rats injected with high doses of carrageenin except tissue weight and fluid volume. On the basis of measurements of three basic parameters required for coordinated observation of the inflammatory system, namely lysosomal enzymes, LPO, and proamidase (related respectively to the inflammatory response sensu stricto, to tissue damage, and to tissue repair), it can be concluded that the diabetic rats show an inadequately adapted inflammatory response, with decreased granuloma formation and reduced exudation, to noxious agents. This is probably due to a low sensitivity of the inflamed tissue in diabetic rats to noxious stimuli or chemical mediators, leading to a delay in the normal defence reaction of enhanced granuloma formation and exudation, thus resulting in a prolonged inflammatory response with a delay in wound healing.

Amidohydrolases↗