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At least 109 records · Page 6Linked to original sources
PubMed1994

The inflammatory/immune response in critical illness: role of the systemic inflammatory response syndrome.

The inflammatory/immune response is designed to protect the body and limit the extent of injury. In the setting of critical illness, however, regulation of this exquisite response is often lost for reasons that remain to be elucidated. Loss of regulation combined with shock, infection, inflammation, and/or ischemia often leads to the development of the systemic inflammatory response syndrome (SIRS), which frequently is associated with the development of septic shock, disseminated intravascular coagulation (DIC), multiple organ dysfunction (MODS), and other complications of critical illness.

Critical Care↗
PubMed2000

[Study on the modulation of the inflammatory response in mouse hepatic vasculitis with sodium selenite and vitamin E antioxidants].

OBJECTIVE: To identify the regulatory effect of sodium selenite and vitamin E on complement-neutrophil-reactive oxygen species (ROS)-activation feedback mechanism-mediated inflammatory response. METHODS: The modulation of inflammatory response through the complement-neutrophil-ROS-activation feedback cycle with sodium selenite and alpha-tocopherol was verified both in vitro tests by chemiluminescense technique and complement fixation to detect ROS production and complement activation as well as in vivo mouse hepatic vasculitis models to test for the regulation of the inflammatory response. RESULTS: Convincing results were observed as the incidence of hepatic vasculitis dropped from 100% in the control group down to 20% in the seleno-antioxidant vitamin E treated group, indicating down regulation of the inflammatory response. CONCLUSIONS: Elucidation of the mechanism of complement mediated inflammatory response is a promising area for new therapeutic developments in the modulation of inflammatory response. This study suggests that selenium, vitamin E and other antioxidants may be the useful therapeutic agents in those disorders in which upregulation of inflammatory response has been implicated, e.g. ischemia, reperfusion injury, severe sepsis, rheumatoid arthritis and hepatitis.

Animals↗
PubMed1995

The influence of surface morphology and wettability on the inflammatory response against poly(L-lactic acid): a semi-quantitative study with monoclonal antibodies.

In this study, the influence of surface morphology and wettability of both degradable and nondegradable polymer films on the inflammatory response after subcutaneous implantation in the rat was investigated. Degradable non-porous, porous, and "combi" (porous with a nonporous layer on one side) poly(L-lactic acid) (PLLA) films and nondegradable polytetrafluoroethylene (PTFE) and (porous) expanded PTFE (e-PTFE) were used. Contact angles measurements indicate that PLLA is more hydrophillic than PTFE. Assessment of the inflammatory response was performed after various periods of implantation (up till 180 days), with both conventional light microscopy and immunohistochemistry using monoclonal antibodies (mAbs). The inflammatory response observed initially can largely be considered as part of the wound healing reaction, and up till day 40 the inflammatory response against PLLA was minimally more intense than against PTFE (porous as well as nonporous). From day 40 on, the PLLA films provoke a more intense inflammatory response as compared to the PTFE films. Both porous PLLA and the porous side of the "combi" PLLA film provoke a more intense inflammatory response than nonporous PLLA and the nonporous side of the "combi" PLLA film, respectively. In general, PTFE and e-PTFE films provoke an inflammatory response which is minimally more intense than the one provoked by the sham operation. Almost no ingrowth of tissue was observed in the porous e-PTFE films. In contrast, there was abundant tissue ingrowth in and an inflammatory response against porous PLLA. It can be concluded that biodegradable PLLA films provoke a more intense inflammatory response than nondegradable PTFE films. Also, porosity enhances the inflammatory response. However, porosity enhances the inflammatory response only when the wettability of a biomaterial permits cellular ingrowth.

Animals↗
PubMed1987

The effects of capsaicin denervation on leucocyte and complement components of the inflammatory response.

Primary afferent unmyelinated nerves containing substance P modulate the inflammatory response to injury through a process known as neurogenic inflammation. Rats treated as neonates with capsaicin, to destroy these nerves permanently, have a reduced capacity to mount an inflammatory response as measured by swelling or plasma extravasation. In this study we examined some aspects of the immunological response to injury in capsaicin-treated rats. One question addressed was whether changes in the inflammatory response are due to abnormal innervation or to a direct toxic effect of capsaicin. It was observed that the histological appearance of thymus, splenic white pulp and popliteal lymph nodes was unaltered in capsaicin-treated rats. However, there was an increase in leucocyte number in splenic red pulp. There was also an increase in the white cell numbers in the peripheral circulation (7 +/- 1 X 10(6)/mL for normal rats and 14 +/- 2 X 10(6)/mL in capsaicin-treated rats, p less than 0.001, Student's t-test). This affected all white cell subgroups. Complement levels in capsaicin-treated rats were not different from normals and both groups showed a similar depletion 6 days following antigenic stimulation with sheep red cells. These data support the view that the reduced cellular response to injury in the capsaicin-treated rat is secondary to the effect of the chemical on afferent nerves and not to a primary toxic effect on cells of the inflammatory response.

Animals↗
PubMed1996

[Lipopolysaccharide (LPS) induced pulmonary inflammatory response and effects of TNF in immunocompromised host (ICH)].

OBJECTIVE: To investigate the pulmonary inflammatory response and TNF-mediated effects in ICH. METHODS: ICH models of guinea pigs were induced successfully by receiving daily intraperitoneal injections of cyclophosphamide (15mg.kg-1.d-1) plus daily subcutaneous injection of cortisone acetate (100mg.kg-1.d-1) for a total of 7 consecutive days. On the day after the final dose of drugs, guinea pigs were challenged intratracheally with LPS (200 micrograms/animal) and were lavaged before and 1, 3, 5, 8, 24 hours after challenged, respectively. RESULTS: Five hours after LPS challenged, total counts of bronchoalveolar fluid (BALF) cells and the proportion of PMN increased significantly. Although the counts of both PAM and PMN increased, the proportion of PAM decreased gradually accompanied by increase of the proportion of PMNs. Hematoxylin eosin stained lung sections after challenged with LPS showed an acute intraalveolar inflammatory response. After intra-tracheal injection of LPS, the TNF level in BALF progressively increased. Both the TNF level and PMN count started to increase at 1 hour after LPS challenge, peaked at 5 hours. The TNF level in serum did not increase markedly after intratracheal injection of LPS. In the development of an inflammatory response, a large amount of TNF were released in BALF, the level of TNF in BALF was closely matched the influx of PMN. CONCLUSIONS: The data suggested that TNF was one of the cytokines which mediated influx of PMNs and inflammation. High level of TNF released in BALF of ICH could induce the lung injury. The systemic inflammatory response of ICH was involving immunosuppressed state after intratracheal injection of LPS, however, strong intraalveolar inflammatory response still occurred, which reflected the phenomenon of "compartmentalization" in inflammatory response.

Animals↗
PubMedDate not supplied

P-selectin monoclonal antibody may attenuate the whole body inflammatory response induced by cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) is known to induce an inflammatory response in association with neutrophil mediated lung injury. P-Selectin has been reported to be involved in the initiation of this inflammatory response by promoting the adhesion of neutrophils to endothelial cells in postcapillary venules. However, the role of P-selectin in the inflammatory response induced by CPB has never been clarified. To elucidate its role, we evaluated the effect of an anti-rat specific P-selectin monoclonal antibody (ARP2-4; Sumitomo Pharmaceutical) on the response of inflammatory cytokines and lung injury in a rat-CPB model. Twenty Sprague-Dawley rats underwent CPB for 30 minutes (80 ml/kg per minute, 34 degrees C) under one of two conditions. In group P, ARP2-4 (3 mg/kg) was added to the priming solution of the bypass circuit (n = 10). Saline alone was given to group C (n = 10). Inflammatory cytokines (tumor necrosis factor-alpha [TNF-alpha], interleukin[IL]-1beta, IL-6, and IL-8) and respiratory index (RI) as a marker of pulmonary gas-exchange ability were measured 1) before the initiation of CPB, 2) at the termination of CPB, and 3) 2 hours after the termination of CPB. Neither TNF-alpha nor IL-1beta was detected during the experimental period in either group. The plasma levels of IL-6 and IL-8 increased after CPB in both groups, but they were significantly lower in group P than in group C. The RI value increased in a pattern similar to that of the inflammatory cytokines and was significantly lower in group P. These data demonstrate that the addition of an anti-rat specific monoclonal antibody inhibits the abnormal release of inflammatory cytokines and attenuates CPB induced lung injury in rats. Thus, P-selectin may play a role in the augmentation of CPB induced inflammatory response, and the use of its inhibitory monoclonal antibody seems to be a promising strategy for the treatment of CPB induced lung injury.

Animals↗
PubMed2006

Characterizing the inflammatory response to cardiopulmonary bypass in children.

Cardiopulmonary bypass is known to trigger a global inflammatory response. Age-dependent differences in the inflammatory response, the increased susceptibility to injury of immature organ systems, and the larger extracorporeal circuit to patient size ratio results in greater susceptibility of younger and smaller patients to the damaging effects of cardiopulmonary bypass. In this review the components of the inflammatory response to cardiopulmonary bypass are reviewed with special reference to the pediatric age group, including the age-specific impact on organ systems. In addition the current and evolving strategies to prevent, limit, and treat the inflammatory response to cardiopulmonary bypass in children are examined.

Age Factors↗
PubMed2005

Seprafilm does not aggravate intraperitoneal septic conditions or evoke systemic inflammatory response.

PURPOSE: To determine whether Seprafilm aggravates the systemic inflammatory response and adversely affects the outcome of postoperative intraperitoneal septic conditions. METHODS: We retrospectively analyzed the relationship between the intraperitoneal placement of Seprafilm and the rate of intraperitoneal septic complications in 278 consecutive patients. Experimentally, 40 rats were subjected to laparotomy with or without the intraperitoneal placement of Seprafilm. Bacterial peritonitis was induced by cecal ligation and puncture (CLP) and the serum cytokine levels were measured. RESULTS: Seprafilm did not increase the rate of septic complications or aggravate inflammatory responses in patients with or without postoperative intraperitoneal inflammatory complications. Experimentally, there was no significant difference between the serum inflammatory cytokine levels after CLP with or without Seprafilm. CONCLUSIONS: Seprafilm did not adversely affect postoperative inflammatory response or clinical outcomes, even in patients with intraperitoneal septic complications.

Adult↗
PubMed1997

Interleukin 1 receptor antagonist gene expression in rat pituitary in the systemic inflammatory response syndrome: pathophysiological implications.

The systemic inflammatory response syndrome (SIRS) is characterized by endothelial cell activation causing a generalized inflammatory response and cytokine-mediated pathophysiological alterations. The pathophysiology of SIRS involves changes in the functioning of several endocrine glands, including the pituitary. SIRS-induced alterations in pituitary function include activation of the hypothalamic-pituitary adrenal (HPA) axis causing hypercortisolemia, the euthyroid sick syndrome, and cessation of reproductive function. These changes are in part mediated by cytokines, such as tumor necrosis factor alpha (TNF-alpha) and interleukin 1 (IL-1). IL-1 function depends on the local ratio of bioactive IL-1 and IL-1 receptor antagonist. Here we review our studies on IL-1 beta and IL-1ra mRNA levels in the pituitary in a rat model of SIRS. We have found that IL-1 beta mRNA peaked at 2 h after lipopolysaccharide (LPS) administration, increasing twelvefold over control values in the posterior pituitary and fivefold over controls in the anterior pituitary. IL-1ra mRNA levels peaked at 6 h post-LPS administration, later than those of IL-1 beta mRNA. IL-1ra mRNA levels increased tenfold in the anterior pituitary, but were induced only threefold in the posterior pituitary. IL-1ra gene expression is profoundly induced in the pituitary in vivo during systemic inflammation and its induction follows that of IL-1 beta, but it is differentially regulated and tissue-specific, occurring predominantly in the anterior pituitary. Future studies of the effects of IL-1 in the pituitary should take into account the local levels of IL-1ra.

Animals↗
PubMed1981

Genetic linkage of resistance to Listeria monocytogenes with macrophage inflammatory responses.

The mobilization of adequate numbers of mononuclear phagocytes to inflammatory foci was measured in Listeria-resistant and Listeria-sensitive mice. Resistant strains, such as B10.A, were found to have a 2- to 3-fold greater accumulation of peritoneal macrophages after i.p. treatment with a variety of nonspecific inflammatory stimuli in comparison to sensitive strains, such s A/J. In addition to low macrophage inflammatory responses, A/J mice had fewer resident peritoneal macrophages. Moreover, measurement of chemotaxis in vitro of equal numbers of thioglycollate-induced macrophages showed cells from A/J mice to be less responsive to complement-derived chemotactic factors. Thus, the mononuclear phagocyte systems of resistant B10.A and sensitive A/J mice were quantitatively and qualitatively different. A survey of inbred mouse strains revealed that these differences were not peculiar to A strain mice and that, in general, the level of the in vivo macrophage inflammatory response correlated with the level of resistance to Listeria in a given strain. Like resistance to Listeria, the macrophage inflammatory response was found to be genetically controlled by an autosomal, non-H-2-linked gene(s) expressed as incompletely dominant. Backcross analysis showed genetic linkage of the macrophage inflammatory response with resistance to Listeria. Thus, the results of this study provide formal evidence that the cellular basis of the genetically determined, enhanced resistance to Listeria is an augmented pool size of mononuclear phagocytes, and the prompt mobilization of these cells to foci of infection.

Animals↗
PubMed2001

Aprotinin and the systemic inflammatory response after cardiopulmonary bypass.

Cardiopulmonary bypass is associated with a systemic inflammatory response, a spectrum of pathophysiologic changes ranging from mild organ dysfunction to multisystem organ failure. Complications include coagulation disorders (bleeding diathesis, hyperfibrinolysis) from platelet defects and plasmin activation, as well as pulmonary dysfunction from neutrophil sequestration and degranulation. Diverse injuries are a consequence of multiple inflammatory mediators (complement, kinins, kallikrein, cytokines). Both plasmin and kallikrein amplify the inflammatory response by activating components of the contact activation system. The full-Hammersmith (high dose) of aprotinin, a serine protease inhibitor approved for reducing blood loss and transfusion requirements in cardiopulmonary bypass, inhibits kallikrein and plasmin, resulting in suppression of multiple systems involved in the inflammatory response. Specifically, inhibition of factor XII, bradykinin, C5a, neutrophil integrin expression, elastase activity, and airway nitric oxide production are observed. Clinical correlates include reduced capillary leak, preserved systemic vascular resistance and blood pressure, and improved myocardial recovery following ischemia. Overall, evidence indicates that aprotinin attenuates the systemic inflammatory response associated with cardiopulmonary bypass.

Animals↗
PubMed1993

T cells specific for the myelin oligodendrocyte glycoprotein mediate an unusual autoimmune inflammatory response in the central nervous system.

Myelin oligodendrocyte glycoprotein (MOG)-specific T cells mediate an autoimmune inflammatory response in the central nervous system (CNS) that differs radically from conventional models of T cell-mediated experimental allergic encephalomyelitis (EAE). Using synthetic peptides an encephalitogenic T cell epitope of MOG for the Lewis rat was identified within the extracellular IgG V-like domain of the protein, amino acids 44-53 (FSRVVHLYRN). The adoptive transfer of CD4+ T cells specific for this epitope induce an intense, dose-dependent inflammatory response in the CNS of naive syngeneic recipients. However, unlike the inflammatory response induced by myelin basic protein (MBP)-specific T cell lines, inflammation mediated by the MOG peptide-specific T cells failed to induce a gross neurological deficit. This unexpected observation was not due to a reduction in the overall inflammatory response in the CNS, but was specifically associated with a decrease in the extent of parenchymal (as opposed to perivascular) inflammation, a selective decrease in the number of ED1+ macrophages infiltrating the CNS, and a total lack of peripheral nerve inflammation. The decreased recruitment of macrophages into the CNS could not be ascribed to deficiencies in the synthesis of interferon-gamma, tumor necrosis factor-alpha, interleukin (IL)-6 or IL-2 by the T cell line. Moreover, this sub-clinical inflammatory response induced severe blood-brain barrier dysfunction as demonstrated by the induction of severe clinical disease following intravenous injection of a demyelinating MOG-specific monoclonal antibody. The neurological deficit in EAE thus exhibits an unexpected dependence on the identity of the target autoantigen, which determines the extent and nature of the local inflammatory response and ultimately the extent of the neurological deficit.

Amino Acid Sequence↗
PubMed2002

Oxidative stress in critically ill patients with systemic inflammatory response syndrome.

OBJECTIVE: To evaluate whether critically ill patients with systemic inflammatory response syndrome, on admission to an intensive care unit, had more severe oxidative stress than those without this syndrome. DESIGN: A prospective, cohort study. SETTING: A mixed medical and surgical adult intensive care unit with 12 beds. PATIENTS: A total of 68 consecutive patients admitted to the intensive care unit. INTERVENTIONS: Venous blood samples were routinely obtained within 24 hrs of admission. MEASUREMENTS AND MAIN RESULTS: Patients' plasma total antioxidant capacity, the lipid peroxidation products malondialdehyde and 4-hydroxynonenal, reduced sulfhydryl groups, and nitrites/nitrates were measured by spectrophotometric technique at admission to the intensive care unit. Myeloperoxidase (enzyme-linked immunosorbent assay) and polymorphonuclear elastase (immuno-activation assay) were also measured on admission to the intensive care unit. The patients with criteria of systemic inflammatory response syndrome (n = 20) had higher Acute Physiology and Chronic health Evaluation III scores (determined by collecting the worst value within 24 hrs after admission to the intensive care unit) and plasma concentrations of lipid peroxidation products and nitrites/nitrates and lower plasma concentration of reduced sulfhydryl groups and plasma total antioxidant capacity than patients without the syndrome (n = 48). Moreover, the markers for leukocyte activation, myeloperoxidase and polymorphonuclear elastase, presented higher concentrations in the plasma of patients with systemic inflammatory response syndrome. CONCLUSIONS: Patients admitted to the intensive care unit with criteria of systemic inflammatory response syndrome had a more severe oxidative stress than patients without this syndrome.

APACHE↗
PubMed1993

Further evidence for the involvement of prolactin in the inflammatory response.

The pro-inflammatory activity of prolactin (PRL) was clearly demonstrated in our previous research on rat paw oedema. In the present study we report our results on the activity of PRL on other animal models of acute and chronic inflammation. Repeated administration of ovine PRL provoked a significant increase in the inflammatory parameters in experimental carrageenan pleurisy (leukocytes number and prostaglandin E2 concentration in the exudate). A pro-inflammatory effect was also present after a hyperprolactinaemia induced by pituitary gland graft. Moreover, the inflammatory response to polyester sponge implantation was significantly potentiated by oPRL, whereas the hormone was completely inactive on cotton pellet granuloma test. A possible involvement of prostaglandins in the pro-inflammatory activity of PRL is suggested.

Analysis of Variance↗
PubMed2002

Inflammatory responses after surgery.

The inflammatory response after major surgery is of great importance for patients, physicians and perioperative medicine in general. This article, although not intended to be comprehensive, provides an overview of present knowledge about inflammatory mechanisms, predictive parameters and therapeutic approaches.

Blood Coagulation↗
PubMed1998

Role of the coagulation system in the local and systemic inflammatory response.

Activation of the coagulation cascade during the inflammatory response is an essential component of the host response to infection. Coagulation represents a double-edged sword. Necessary for hemostasis and the acute containment of an infective focus, it also amplifies the inflammatory response, decreases bacterial clearance, and in the critically ill patient contributes to end-organ damage and death. Evidence for these concepts is found in the fact that critically ill and septic patients consistently demonstrate marked abnormalities in their biochemical indices of coagulation. Moreover, there is excellent experimental evidence to suggest that replacement or inhibition of individual coagulation factors, either consumed or up-regulated during the inflammatory response, can attenuate both local and systemic injury and protect animals from otherwise fatal outcomes. Based on these facts, novel therapeutic approaches to the treatment of the systemic response to infection have been developed and tested in intensive care settings. Although promising results have been obtained, much work remains to be done in defining exactly which coagulation factors (or combination of factors) should be inhibited or replaced during treatment of the septic, critically ill patient. The experimental and clinical evidence linking the coagulation cascade to local and systemic inflammation is reviewed, and the status of the clinical trials performed to date is overviewed.

Animals↗
PubMed1984

Natural resistance to listeriosis: role of host inflammatory responsiveness.

The accumulation of inflammatory macrophages at the infective foci appears to represent the major host defense mechanism during the early or innate phase of resistance to infection with Listeria monocytogenes. Certain inbred strains of mice, such as A/J [A] have genetically-determined defects in macrophage mobilization in vivo in response to intraperitoneal (IP) treatment with the nonspecific inflammatory stimulus, thioglycollate. These strains of mice are also genetically-susceptible to infection with Listeria. In contrast, other strains (C57BL/6J or B10.A/SgSn [B]) are high responders for both genetically-determined traits. Linkage analysis of the two traits in backcross progeny showed that the trait of a high macrophage inflammatory response segregates with the trait of resistance to Listeria. These observations suggested that the gene(s) controlling the level of the macrophage inflammatory response is identical with or linked to the gene(s) controlling resistance to Listeria. We have found additional evidence to support this hypothesis by analyzing the expression of the two traits in 12 AXB/BXA recombinant inbred [RI] mouse strains derived from progenitor B (high macrophage response, Listeria-resistant) and A (low macrophage response, Listeria-susceptible) mice. Furthermore, those AXB/BXA strains, which like progenitor A mice, are susceptible to infection with Listeria exhibit a defect in the number of polymorphonuclear leukocytes recovered from peritoneal exudates 18 h after IP injection with thioglycollate. The strain distribution pattern of both the resistance/susceptibility to Listeria and the leukocyte inflammatory response in RI strains is concordant with that of Hc allele coding for effective/defective levels of C5 complement protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗