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PubMed2004

Ischaemia-reperfusion injury and regional inflammatory responses in abdominal aortic aneurysm repair.

OBJECTIVES: The inflammatory response to abdominal aortic aneurysm repair is likely to result in response to an ischaemia-reperfusion injury (IRI) to the lower-limbs and gastrointestinal tract. This paper reviews the pathogenesis of the inflammatory response to abdominal aortic aneurysm repair, with specific reference to the levels of evidence in the current literature regarding the potential origin of the inflammatory response. DESIGN: Review article. METHODS: The current literature (1966 to August 2003) was reviewed specifically for all articles employing techniques of regional blood sampling from the venous drainage of the lower limbs or gastrointestinal tract during abdominal aortic aneurysm repair. RESULTS: Ten relevant studies were identified. These demonstrated that regional blood sampling techniques could be easily performed, and provided useful information regarding the potential sites of origin of the inflammatory response. CONCLUSIONS: Regional blood sampling techniques provide useful information regarding the potential sites of origin of the inflammatory response. Current evidence suggests that both the lower limbs and gastrointestinal tract are clearly important in their roles, however more work is now required to compare directly the roles and contributions of the lower limbs and gastrointestinal tract to the inflammatory response during abdominal aortic aneurysm repair.

Aortic Aneurysm, Abdominal↗
PubMed1996

Gender influences the magnitude of the inflammatory response within embolic cerebral infarcts in young rats.

BACKGROUND AND PURPOSE: The inflammatory response within cerebral infarcts may have an influence on tissue damage. Since old animals with an impaired immune response have decreased inflammation after experimental cerebral infarction, we postulated that female animals with an increased immune response will have an increased inflammatory response after cerebral infarction. METHODS: Embolic cerebral infarcts were produced by photochemical irradiation of the right carotid artery in 12 female Fischer rats. The inflammatory response within 4-day-old infarcts was quantitated by histology with the use of computer-assisted image analysis and compared with that in 12 male rats from a previous series. RESULTS: Severe infarcts had the most pronounced inflammatory response. Female rats had an increased inflammatory response in infarcts of all severity, which was statistically significant in severe cerebral infarcts even after adjustment for infarct size. Severe infarcts in males were significantly larger than those in females. CONCLUSIONS: Gender influences the outcome of embolic cerebral infarcts after photochemical damage to the carotid artery, both in terms of the magnitude of the inflammatory response and infarct size. There are numerous gender-related differences in neurochemicals, cytokine production, and drug metabolism that may influence tissue damage after stroke and responsiveness to therapeutic intervention. The preponderance of male animals in stroke research may produce results not applicable to female stroke patients. The use of female animals will be required to provide adequate models for the study of stroke in women.

Animals↗
PubMed1981

Quantification, dynamics, and mechanisms of pulmonary inflammatory response around schistosomula of Schistosoma mansoni.

The inflammatory response around schistosomula injected into the lungs of uninfected mice and mice infected with Schistosoma mansoni was quantified. In uninfected mice, the inflammatory response started at 1 hour and peaked at 6 days, whereas in the infected mice, the inflammatory response was accelerated and peaked at 24 hours. This latter inflammatory reaction was 1.5 times greater than the 6-day reaction found in uninfected controls. Neutrophils and mononuclear cells were seen around schistosomula impacted into the pulmonary microvasculature by 1 hour; later, however, eosinophils constituted the predominant cell. This augmented inflammatory response was detected in mice infected with S mansoni first at 4 weeks after injection and peaked at 12 weeks. The augmented response correlated with acquired resistance as assayed by the recovery of the organisms from the lungs 4 days after challenge. Augmented inflammatory reaction and increased protection was induced by subcutaneous sensitization with dead schistosomula or eggs but not by cercariae or adult worms. Adoptive transfer of serum but not lymphoid cells from 12-15 week-infected mice resulted in augmented inflammation and enhanced resistance in recipient normal animals. The serum activity was absorbed by both schistosomula and eggs and was shown to reside in the fraction containing IgG1.

Animals↗
PubMed2003

Pulmonary adenoma susceptibility 1 (Pas1) locus affects inflammatory response.

Two outbred mouse lines, phenotypically selected for differential subcutaneous (s.c.) acute inflammatory response (AIR), were analysed for urethane-induced lung inflammatory response and susceptibility to lung tumorigenesis. AIR(min) mice, which show a low response to s.c. acute inflammation, developed a persistent subacute lung inflammatory response and a 40-fold higher lung tumor multiplicity than did AIR(max) mice, which are selected for high response to s.c. acute inflammation and showed a transient lung inflammatory response. A highly significant linkage disequilibrium pattern was observed in AIR(max) and AIR(min) mice at marker alleles located within a 452-kb pulmonary adenoma susceptibility 1 (Pas1) locus region, thus defining the location of gene candidacy for inflammatory response and for the biological effects of Pas1 in this region. AIR(min) and AIR(max) mice segregated by descent the Pas1(s) and Pas1(r) alleles, respectively, providing evidence for the involvement of the Pas1 locus in the inflammatory response. The 452-kb region contains Kras2 and four additional genes, including the lymphoid-restricted membrane protein (Lrmp) gene, whose Pro-->Leu nonconservative variation was linked with inflammatory response and Pas1 allelotype. These results provide a model to explore the mechanism underlying inherited predisposition to lung cancer in the context of a link to inflammation.

Adenoma↗
PubMed1999

Vesnarinone and amrinone reduce the systemic inflammatory response syndrome.

OBJECTIVE: The systemic inflammatory response is an important cause of organ dysfunction. The present study tested the hypothesis that 2 clinically used agents, amrinone and vesnarinone, would decrease inflammation and cardiac dysfunction in a relevant model of systemic inflammatory response activation. METHODS: Rabbits received intravenous endotoxin, alone or in conjunction with amrinone or vesnarinone. Systemic effects were assessed by death, fever, behavior, and acidosis. Measures of inflammatory signaling were (1) plasma tumor necrosis factor-alpha and interleukin-1 beta production, (2) lung tissue myeloperoxidase activity, and (3) myocardial inducible nitric oxide synthase activity. Indices of systolic and diastolic myocardial function were measured in Langendorff-perfused hearts. RESULTS: Vesnarinone, in particular, reduced mortality rates (19% vs 61% for lipopolysaccharide alone, P =.01) and acidosis in lipopolysaccharide-treated rabbits. Both agents markedly reduced systemic tumor necrosis factor and interleukin-1 concentrations, lipopolysaccharide-mediated effects on myocardial systolic and diastolic function and on myocardial inducible nitric oxide synthase activity. Vesnarinone, but not amrinone, (1) decreased fever and lethargy, consistent with decreased central nervous system effects of endotoxin, and (2) decreased lung leukocyte infiltration. CONCLUSIONS: Vesnarinone and amrinone, which are used clinically for their inotropic and vasodilating properties, may be useful to limit inflammatory activation and consequent organ dysfunction. Structure-activity and/or pharmacokinetic between the compounds may be important, particularly in preventing inflammatory signaling within certain tissues.

Adjuvants, Immunologic↗
PubMedDate not supplied

Inflammatory responses to carrageenan injection in LEW/N and F344/N rats: LEW/N rats show sex- and age-dependent changes in inflammatory reactions.

We studied the inflammatory responses of LEW/N and F344/N inbred rat strains after peripheral injection of carrageenan. The inflammatory responses were assessed in terms of volume, relative and total white blood cell counts of the exudates. Moreover, in both strains, blood CD4, CD8, CD25, naive CD4 (CD4/CD45RC) cell and B (CD45R) cell counts and plasma corticosterone levels, constituents of systemic inflammatory responses to carrageenan were evaluated. In general, LEW/N rats are highly responsive to challenge with carrageenan, whereas F344 rats are not. The strong local inflammatory responses to carrageenan are primarily exhibited by female LEW/N rats. The intensity of local inflammatory responses of LEW/N rats changes with the rat age, the highest exhibited by LEW/N rats up to 3 months of age, thereafter the carrageenan-induced inflammatory responses decline. Our results indicate that peripheral injection of carrageenan induces strong systemic immune component. After carrageenan injection, increases in CD8 and naive CD4 blood lymphocytes are seen. Although the carrageenan challenge does not change CD4 blood lymphocytes in both LEW/N and F344/N rat strains, LEW/N rats exhibit higher levels of CD4 cells than F344/N rats. Additionally, LEW/N rats demonstrated lower levels of B cells and higher naive CD4 lymphocytes. Carrageenan challenges induce significant increases in plasma corticosterone response in F344/N rats, as well as increases in LEW/N rats 1 h after injection. Our data stress the importance of rat age and gender in experiments studying inflammatory responses.

Age Factors↗
PubMed1998

Neutrophil signaling alteration: an adverse inflammatory response after burn shock.

The inflammatory response syndrome in shock-like states might frequently be accompanied by an oxidative cell/tissue damage in one or more organ-systems in the body. The inflammatory response related hyperactivation of neutrophils can contribute to oxidative cell/tissue damage. Studies discussed in this review examined the role of cell signaling pathways in the hyperactivation of neutrophils in an early stage of burn injury shock. The studies were carried out in peripheral blood neutrophils isolated from rats with a 25% body surface area scald burn. Neutrophil cell signaling responses were evaluated by measuring cytosolic [Ca2+] and protein kinase C activity, and were correlated with neutrophil superoxide production. The cytosolic [Ca2+] and protein kinase C responses were highly upregulated along with enhanced superoxide production in the early phase of burn injury. The treatment of burn-injured rats with the calcium antagonist diltiazem abrogated enhanced Ca2+ and protein kinase C signaling and superoxide generation. The signaling upregulation in neutrophils could result from potentiation of actions of burn-injury induced chemotactic mediators on the leukocytes. The neutrophil signaling upregulation leading to increased superoxide generation could thus be responsible for the oxidative cell/tissue damage. The organ-system dysfunction/failure accompanying burn shock may be initiated with the oxidative cell/tissue damage.

Animals↗
PubMed1988

Receptor-mediated effects of glucocorticoids on inflammation: enhancement of the inflammatory response with a glucocorticoid antagonist.

Glucocorticoids suppress the inflammatory response by altering leukocyte traffic and function, cytokine secretion and action, and phospholipid metabolism. We employed the glucocorticoid receptor antagonist RU 486, to examine whether glucocorticoids suppress the inflammatory response through a receptor-mediated mechanism and whether basal glucocorticoid secretion exerts antiinflammatory effects in the resting (non-stress) state. To test these hypotheses we evaluated the effects of increasing doses of dexamethasone, RU 486, or dexamethasone plus RU 486 on the exudate volume and concentrations of leukocytes, prostaglandin E2, (PGE2) and leukotriene B4 (LTB4) in intact rats that received subcutaneous carrageenin. Exudate volume, leukocyte concentration and LTB4 and PGE2 levels were all suppressed by dexamethasone in a dose-dependent fashion (P less than 0.005). RU 486 was able to antagonize fully the suppressive effects of dexamethasone on the inflammatory response (P less than 0.001) and to cause increases of exudate volume and leukocyte, PGE2 and LTB4 concentrations when given alone (P less than 0.05). These increases ranged between 30 and 100% above the basal inflammatory response. We conclude that glucocorticoids most likely suppress the inflammatory response by a glucocorticoid receptor-mediated mechanism and under basal conditions exert tonic antiinflammatory effects.

Alprostadil↗
PubMed2006

Effects of single dose of dexamethasone on patients with systemic inflammatory response.

CONTEXT AND OBJECTIVE: Systemic inflammatory response syndrome (SIRS) is a very common condition among critically ill patients. SIRS, sepsis, septic shock and multiple organ dysfunction syndrome (MODS) can lead to death. Our aim was to investigate the efficacy of a single dose of dexamethasone for blocking the progression of systemic inflammatory response syndrome. DESIGN AND SETTING: Prospective, randomized, double-blind, single-center study in a postoperative intensive care unit (Surgical Support Unit) at Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo. METHODS: The study involved 29 patients with SIRS. All eligible patients were prospectively randomized to receive either a single dose of 0.2 mg/kg of dexamethasone or placebo, after SIRS was diagnosed. The patients were monitored over a seven-day period using Sequential Organ Failure Assessment score (SOFA). RESULTS: The respiratory system showed an improvement on the first day after dexamethasone was administered, demonstrated by the improved PaO2/FiO2 ratio (p < 0.05). The cardiovascular system of patients requiring vasopressor therapy also improved over the first two days, with a better evolution in the dexamethasone group (p < 0.05). Non-surviving patients presented higher lactate assays than did survivors (p < 0.05) during this period. CONCLUSIONS: Dexamethasone enhanced the effects of vasopressor drugs and evaluation of the respiratory system showed improvements (better PaO2/FiO2 ratio), one day after its administration. Despite these improvements, the single dose of dexamethasone did not block the evolution of SIRS.

Adolescent↗
PubMed1999

Effect of ebrotidine on gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide.

UNLABELLED: Helicobacter pylori lipopolysaccharide is a primary virulence factor responsible for eliciting acute mucosal inflammatory responses associated with H. pylori infection. In this study, we applied the animal model of H. pylori lipopolysaccharide-induced acute gastritis to assess the effect of antiulcer agent, ebrotidine, on the gastric mucosal inflammatory responses by analyzing the interplay between the activity of a key apoptotic caspase, caspase-3, epithelial cell apoptosis, and the expression of inducible nitric oxide synthase (NOS-2). METHODS: Rats, pretreated twice daily with ebrotidine at 100 mg/kg, or the vehicle, were subjected to intragastric application of H. pylori lipopolysaccharide at 50 microg/animal, and after 4 additional days on the antiulcer drug or vehicle regimen their mucosal tissue used for histologic assessment, assays of epithelial cells apoptosis, and the measurements of caspase-3 and NOS-2 activities. RESULTS: In the absence of antiulcer agent, H. pylori lipopolysaccharide induced acute reaction characterized by the inflammatory infiltration of the lamina propria, hyperemia, and epithelial hemorrhage. This was accompanied by an 11.2-fold increase in epithelial cell apoptosis, a 6.5-fold induction in mucosal expression of NOS-2, and a 5.4-fold increase in caspase-3 activity. Treatment with H2-receptor antagonist ebrotidine, also known for its gastroprotective effects, produced a 50.9% reduction in the extent of mucosal inflammatory changes elicited by H. pylori lipopolysaccharide and an 82.5% decrease in the epithelial cells apoptosis, while the activity of caspase-3 decreased by 33.7% and that of NOS-2 showed a 72.8% decline. CONCLUSIONS: The findings implicate caspase-3 involvement in gastric mucosal inflammatory responses to H. pylori lipopolysaccharide, and point towards participation of NOS-2 in the amplification of the cell death-signaling cascade. Our study also demonstrate that ebrotidine exerts modulatory effect on the H. pylori-induced mucosal inflammatory responses by interfering with the events propagated by NOS-2 and caspase-3.

Acute Disease↗
PubMed2003

The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X.

In previous publications, we presented the hypothesis that repeated episodes of acute or chronic psychological stress could induce an acute phase response (APR) and subsequently a chronic inflammatory process such as atherosclerosis. In this paper, that hypothesis, namely that such stress can induce an APR and inflammation, has been extended to include a chronic inflammatory process(s), characterized by the presence of certain cytokines and acute phase reactants (APR), which is associated with certain metabolic diseases. The loci of origin of these cytokines, particularly interleukin 6 (IL-6), and their induction, has been considered. Evidence is presented that the liver, the endothelium, and fat cell depots are the primary sources of cytokines, particularly IL-6, and that IL-6 and the acute phase protein (APP), C-reactive protein (CRP), are strongly associated with, and likely play a dominant role in, the development of this inflammatory process which leads to insulin resistance, non-insulin dependent diabetes mellitus type II, and Metabolic syndrome X. The possible role of psychological stress and the major stress-related hormones as etiologic factors in the pathogenesis of these metabolic diseases, as well as atherosclerosis, is discussed. The fact that stress can activate an APR, which is part of the innate immune inflammatory response, is evidence that the inflammatory response is contained within the stress response or that stress can induce an inflammatory response. The evidence that the stress, inflammatory, and immune systems all evolved from a single cell, the phagocyte, is further evidence for their intimate relationship which almost certainly was maintained throughout evolution.

Acute-Phase Reaction↗
PubMed2004

Mathematical models of the acute inflammatory response.

PURPOSE OF REVIEW: Trauma and infection elicit an acute inflammatory response. In certain circumstances the degree of the acute inflammatory response may result in pathologic manifestations, namely, sepsis and multiple organ failure. Despite an extensive series of clinical trials designed to modulate inflammation in sepsis, only one compound, activated protein C, has emerged from more than 250 failed trials. There is a growing recognition that the complexity of the acute inflammatory response precludes the efficient development of therapies for sepsis and multiple organ failure until systems approaches are brought to bear on this problem. RECENT FINDINGS: Work carried out by the authors' groups suggests that mathematical modeling can provide a means by which in vitro and in vivo data can be synthesized into system-level analytic models of the acute inflammatory response. The authors have focused on agent-based modeling and modeling with ordinary differential equations. Some of the advantages and disadvantages of these modeling approaches are presented, and methods for calibration and validation of these models are discussed. Finally, the usefulness of mathematical models to evaluate the prospective therapeutic strategies in clinical trials of sepsis and trauma is examined. SUMMARY: Simulations using various methods can shed insight into the pathophysiology of the acute inflammatory response and may lead to better design of clinical trials in sepsis and trauma.

Acute Disease↗
PubMed2005

Redox regulation of neutrophil apoptosis and the systemic inflammatory response syndrome.

SIRS (systemic inflammatory response syndrome) may result from a wide variety of non-infective insults. Surgery is a recognized cause of SIRS, the onset of which can have adverse prognostic significance. Neutrophil activation is a key histopathological feature of SIRS, and neutrophil clearance through programmed cell death or apoptosis is an essential step in its resolution. Increasingly, it is recognized that ROS (reactive oxygen species), such as those generated by activated neutrophils during cardiac surgery, may have a regulatory role, influencing neutrophil lifespan and thus inflammation. In this review, we discuss the continuing importance of SIRS as a herald of inflammation and the role of neutrophil longevity in the resolution of inflammation, and we consider recent evidence for the regulation of neutrophil apoptosis by ROS.

Apoptosis↗
PubMed2004

Preeclampsia and the systemic inflammatory response.

Normal pregnancy is associated with a systemic inflammatory response. The response is exacerbated in preeclampsia and can account for its clinical features. Many of the physiologic changes of normal pregnancy are part of an acute-phase reaction, which is generated by an inflammatory response. The placenta is the proximal cause of these problems. There are several possible placental factors that may evoke the inflammatory responses that currently are being investigated. The special susceptibility of obese women, or those with diabetes or chronic hypertension, to preeclampsia is explained by the chronic systemic inflammatory responses that these women have. The clinical implications of these concepts are discussed.

Female↗
PubMed1998

Periapical inflammatory responses and their modulation.

Periapical inflammatory responses occur as a consequence of bacterial infection of the dental pulp, as a result of caries, trauma, or iatrogenic insult. Periapical inflammation stimulates the formation of granulomas and cysts, with the destruction of bone. These inflammatory responses are complex and consist of diverse elements. Immediate-type responses--including vasodilatation, increased vascular permeability, and leukocyte extravasation--are mediated by endogenous mediators, including prostanoids, kinins, and neuropeptides. Non-specific immune responses--including polymorphonuclear leukocyte and monocyte migration and activation, and cytokine production--are elicited in response to bacteria and their products. Interleukin-1 and prostaglandins in particular have been implicated as central mediators of periapical bone resorption. Chronic periapical inflammation further involves specific T- and B-cell-mediated anti-bacterial responses, and activates a network of regulatory cytokines which are produced by Th1- and Th2-type T-lymphocytes. Various naturally occurring and genetically engineered models of immunodeficiency are beginning to help elucidate those components of the immune system which protect the pulpal/periapical complex. Both specific and non-specific responses interface with and are regulated by the neural system. The modulation of these responses by immune response modifies, cytokine antagonists, and other novel therapeutic agents is discussed. As an experimental model, periapical inflammation has many advantages which permit it to be used in studies of microbial ecology and pathogenesis, host response, neuroimmunology, and bone resorption and regeneration.

Cytokines↗
PubMed2006

Effects of atorvastatin on systemic inflammatory response after coronary bypass surgery.

OBJECTIVES: Systemic inflammatory response occurs frequently after coronary artery bypass surgery, and it is strongly correlated with the risk of postoperative morbidity and mortality. Recent studies demonstrate that treatment with statin is associated with a significant and marked decrease in inflammation-associated variables such as the C-reactive protein, cytokines, and adhesion molecules. Therefore, we investigated the effects of preoperative atorvastatin treatment on systemic inflammatory response and perioperative morbidity after cardiopulmonary bypass. DESIGN: Double-blinded, placebo-controlled, randomized study. SETTING: University hospital. PATIENTS: Forty patients were randomized to treatment with atorvastatin (20 mg/day, group A, n=20) or placebo (group B, n=20) 3 wks before surgery. INTERVENTIONS: Three-week treatment by atorvastatin 20 mg/day. MEASUREMENT AND MAIN RESULTS: Postoperative serum levels of both interleukin-6 and interleukin-8 increased significantly over baseline, but the peak levels observed 4 hrs postoperatively were significantly lower in the atorvastatin group. In the same fashion, CD11b expression on neutrophils was significantly lower in the statin group at 4 and 24 hrs postoperatively. Finally, neutrophil-endothelial adhesion was significantly reduced in the statin patients compared with controls. The operation time, blood loss, need for inotropic support, intubation time, and length of intensive care unit or hospital stay did not differ significantly between the two groups. The systemic inflammatory response syndrome score on postoperative days 1 and 2 was comparable in both groups. CONCLUSIONS: Pretreatment with atorvastatin significantly reduces cytokine release and neutrophil adhesion to the venous endothelium in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass.

Aged↗
PubMed2005

Extracellular cyclophilins contribute to the regulation of inflammatory responses.

The main regulators of leukocyte trafficking during inflammatory responses are chemokines. However, another class of recently identified chemotactic agents is extracellular cyclophilins, the proteins mostly known as receptors for the immunosuppressive drug, cyclosporine A. Cyclophilins can induce leukocyte chemotaxis in vitro and have been detected at elevated levels in inflamed tissues, suggesting that they might contribute to inflammatory responses. We recently identified CD147 as the main signaling receptor for cyclophilin A. In the current study we examined the contribution of cyclophilin-CD147 interactions to inflammatory responses in vivo using a mouse model of acute lung injury. Blocking cyclophilin-CD147 interactions by targeting CD147 (using anti-CD147 Ab) or cyclophilin (using nonimmunosuppressive cyclosporine A analog) reduced tissue neutrophilia by up to 50%, with a concurrent decrease in tissue pathology. These findings are the first to demonstrate the significant contribution of cyclophilins to inflammatory responses and provide a potentially novel approach for reducing inflammation-mediated diseases.

Animals↗
PubMed2006

Compartmentalization of the inflammatory response in sepsis and SIRS.

Sepsis and systemic inflammatory response syndrome (SIRS) are associated with an exacerbated production of both pro- and anti-inflammatory mediators that are mainly produced within tissues. Although a systemic process, the pathophysiological events differ from organ to organ, and from organ to peripheral blood, leading to the concept of compartmentalization. The nature of the insult (e.g. burn, hemorrhage, trauma, peritonitis), the cellular composition of each compartment (e.g. nature of phagocytes, nature of endothelial cells), and its micro-environment (e.g. local presence of granulocyte-macrophage colony stimulating factor [GM-CSF] in the lungs, low levels of arginine in the liver, release of endotoxin from the gut), and leukocyte recruitment, have a great influence on local inflammation and on tissue injury. High levels of pro-inflammatory mediators (e.g. interleukin-1 [IL-1], tumor necrosis factor [TNF], gamma interferon [IFN-gamma], high mobility group protein-1 [HMGB1], macrophage migration inhibitory factor [MIF]) produced locally and released into the blood stream initiate remote organ injury as a consequence of an organ cross-talk. The inflammatory response within the tissues is greatly influenced by the local delivery of neuromediators by the cholinergic and sympathetic neurons. Acetylcholine and epinephrine contribute with IL-10 and other mediators to the anti-inflammatory compensatory response initiated to dampen the inflammatory process. Unfortunately, this regulatory response leads to an altered immune status of leukocytes that can increase the susceptibility to further infection. Again, the nature of the insult, the nature of the leukocytes, the presence of circulating microbial components, and the nature of the triggering agent employed to trigger cells, greatly influence the immune status of the leukocytes that may differ from one compartment to another. While anti-inflammatory mediators predominate within the blood stream to avoid igniting new inflammatory foci, their presence within tissues may not always be sufficient to prevent the initiation of a deleterious inflammatory response in the different compartments.

Animals↗