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PubMed1976

Differences in the mode of exucative reaction between early phase and late phase of carrageenin-induced inflammation in rats.

Differences in the mode of vascular permeability change induced by some stimulants such as chemical mediators between the early phase and the late phase of the carrageenin-induced granulomatous inflammation were investigated with the aid of 131I-human serum albumin as an indicator for the measurement of vascular permeability. In the early pregranulomatous phase of the inflammation, histamine injection into the inflammation locus markedly elevated local vascular permeability, while prostaglandins E1 and E2 showed no effect. On the other hand, in the late phase of the inflammation, where permanent granuloma tissue had been formed, prostaglandins E1 and E2 significantly enhanced the local vascular permeability, while histamine was inert.

Animals↗
PubMed1996

Up-regulation of cyclooxygenase-2 mRNA in the rat spinal cord following peripheral inflammation.

Prostaglandins (PG) have been described as mediators in spinal nociceptive processing after peripheral inflammation. Enzymes essential for PG biosynthesis, cyclooxygenase isozymes COX-1 and COX-2, have not yet been investigated in the spinal cord. In two studies on rats with adjuvant-induced peripheral inflammation levels of mRNA expression of both COX isoforms were analyzed in the lumbar section of the spinal cord using reverse transcription-polymerase chain reaction (RT-PCR) technique. We could show that mRNA of both COX isoforms is expressed constitutively in the spinal cord with COX-2 as the predominant isoform. Six hours after induction of peripheral inflammation, levels of COX-2 mRNA expression were raised significantly in respect to untreated control rats and returned to baseline within 3 days after induction of inflammation. COX-2 might therefore be regarded as the COX isozyme responsible for spinal PG release in nociceptive processing under a peripheral inflammatory stimulus.

Animals↗
PubMed1985

Transcortin and alpha 2u-globulin messenger RNA activities during turpentine-induced inflammation in the rat.

Previously we have shown that the serum concentration of transcortin and alpha 2u-globulin markedly decreases during turpentine-induced inflammation. In the present study transcortin and alpha 2u-globulin mRNA from healthy rats and from animals with inflammation was translated in a rabbit reticulocyte lysate system. Female rats had higher levels of translatable transcortin mRNA than male animals and the level of mRNA for transcortin and alpha 2u-globulin decreased rapidly during inflammation. These results indicate that the sex difference in the serum level of transcortin and the changes in serum transcortin and alpha 2u-globulin during inflammation are mainly determined by differences in the mRNAs in the liver.

Alpha-Globulins↗
PubMed1989

Changes in activity of the renin-angiotensin system of the rat by induction of acute inflammation.

Angiotensinogen is the precursor of biologically active peptide angiotensin II and its hepatic synthesis is increased by the induction of acute inflammation. Studies were carried out to know whether the rise in plasma angiotensinogen is actually involved in the activity of the renin-angiotensin system during acute inflammation. The plasma level of angiotensinogen in rats was increased to 2.5 times the normal level 16 h after the induction of acute inflammation by administration of lipopolysaccharide (LPS). The plasma renin concentration (PRC) was decreased to about 40% of the normal level concomitantly with a reduction of plasma renin activity (PRA) at 4 h after LPS administration. In contrast, 16 h after LPS injection, when plasma angiotensinogen showed a high level and PRC had recovered to the normal range, PRA was increased to 1.7 times the normal level. These results indicate that acute inflammation induced by LPS causes a biphasic change in the generation of angiotensin I, i.e., an early decrease depending upon the reduction of PRC and later increase depending upon elevation of the angiotensinogen concentration.

Acute Disease↗
PubMed1991

The role of chronic acanthosis and subacute inflammation in tumor promotion in CD-1 mice by petroleum middle distillates.

An initiation-promotion bioassay using CD-1 mice was conducted to examine the role of chronic acanthosis and inflammation in tumor promotion by petroleum middle distillates (MD). Test groups were initiated with 7,12-dimethylbenz[a]anthracene (DMBA). Promotion with MD consisted of twice weekly treatments for 25 weeks with either 25 or 50 microliters, 50 microliters + daily treatment with 15 micrograms dexamethasone, 50 microliters + postapplication washings, or 100 microliters. Three mice from each group were euthanized at 21-day intervals (24 total per group). The skin from interim euthanized mice was examined histopathologically for tumors, acanthosis, and subacute inflammation. Tumor incidence at study termination was as follows: 25 microliters (45%), 50 microliters (43%), 50 microliters + dexamethasone (0%), 50 microliters + washing (70%), and 100 microliters (81%). A correlation of greater than 0.93 was observed at all intervals between tumor incidence and cumulative group mean degrees of acanthosis in interim euthanized mice. The correlation between subacute inflammation at early through midstudy interval weeks and tumor incidence at study termination was poor. These results support the hypothesis that induction of a lasting, albeit mild, hyperplasia is an essential, but not sufficient requirement for tumor promotion. Furthermore, subacute inflammation does not appear to be a significant factor in tumor promotion by petroleum MD.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

Monocyte production during inflammation.

The majority of the resident macrophages in non-inflamed organs and serous cavities derive from circulating monocytes, but a small proportion originate from immature mononuclear phagocytes that only divide once in the tissues and originate from the bone marrow as well. During an acute inflammation the number of circulating monocytes increases, and a large proportion of these cells migrate to the site of inflammation and differentiate into exudate macrophages. The monocyte production during an acute inflammation is controlled by humoral factor, FIM, which is a protein that is synthesized and secreted by macrophages at the site of inflammation.

Animals↗
PubMed1985

The failure of cyclosporin to inhibit granulomatous inflammation in acute Arthus-like panophthalmitis.

Acute Arthus-like panophthalmitis (AP) was induced in Lewis rat eyes by lens injury after immunization with whole rabbit lens extract. AP consists of an acute anterior ocular inflammation, followed by a posterior choroidal granulomatous reaction. Neither inflammatory response was inhibited by daily treatment with cyclosporin, 10 mg/kg, beginning on the day of lens injury. Cyclosporin would not be expected to interfere with the lens-induced anterior Arthus-like inflammation. The lack of inhibition of the choroidal inflammation was unexpected. The results are interpreted to indicate that the posterior granulomatous choroidal inflammation is a non-immune reaction initiated by the severe lens-induced Arthus-like reaction.

Animals↗
PubMed1993

Foreign body granulomatous inflammation increases the sensitivity of splenocytes to immunomodulation by 1,25-dihydroxyvitamin D3.

1,25-dihydroxyvitamin D3, the active metabolite of vitamin D, partially inhibits antigen and mitogen-driven lymphocyte stimulation. We studied the effect of granulomatous inflammation on the sensitivity of lymphocytes to 1,25-dihydroxyvitamin D3 in vitro, measuring the inhibitory effect of 1,25-dihydroxyvitamin D3 on mitogenesis of splenocytes of mice with chronic inflammation induced by subcutaneous injection of talc. Systemic manifestations of the local inflammation included loss in body weight, splenomegaly, enhanced DNA synthesis by freshly isolated splenocytes and enhanced prostaglandin secretion by activated splenocytes. Splenocytes from animals with local inflammation were more susceptible to inhibition by 1,25-dihydroxyvitamin D3, but not by prostaglandin E2. This increased sensitivity to 1,25-dihydroxyvitamin D3 was abolished by blocking prostaglandin synthesis in splenocyte cultures with indomethacin and was restored by adding prostaglandin E2. This effect cannot be attributed to enhanced prostaglandin synthesis in the presence of 1,25-dihydroxyvitamin D3, but is probably due to a qualitative change in the response of splenocytes from inflamed animals to the combined action of 1,25-dihydroxyvitamin D3 and prostaglandin E2.

Adjuvants, Immunologic↗
PubMed1995

Sensory denervation with capsaicin attenuates inflammation and nociception in arthritic rats.

The relatively few studies that have investigated the effects of the nervous system on chronic joint disease have reported conflicting results. We have reassessed the effects of capsaicin on experimental polyarthritis with particular reference to the relationship between changes in nociception and changes in process and outcome measures of disease activity. Capsaicin pretreatment significantly attenuated both joint swelling and disease outcome as determined by quantitative radiology and histology. There was a close correlation between process measures of inflammation and mechanical hyperalgesia in both the untreated and capsaicin treated arthritic groups. The results confirm a suppression of inflammation by capsaicin and imply that the nociceptive and pro-inflammatory (neurogenic inflammation) activities of capsaicin-sensitive fibres are closely linked such that stimuli which cause pain will also induce neurogenic inflammation and vice versa.

Animals↗
PubMed1996

Basal and touch-evoked fos-like immunoreactivity during experimental inflammation in the rat.

Fos-immunoreactivity can readily be induced in spinal cord neurones by noxious, but to a much more limited extent, by innocuous peripheral stimuli. The present study has investigated whether low intensity stimuli and electrical stimulation of A beta afferents elicit greater c-fos expression during the behavioural sensory hypersensitivity generated by experimental peripheral inflammation. We have examined the time-course of c-fos expression after inflammation produced by either an intra-plantar injection of the irritant turpentine oil or of complete Freund's adjuvant (CFA). In the former case, a significant initial expression in all dorsal horn laminae was followed by a gradual decrease, whereas after CFA injection, an initial expression limited to the superficial laminae subsequently extended into the deep laminae, with a decrease at 24 h and an increase in labelling at later times. Low intensity touch stimuli repeated for 10 min, when applied at 24 h and 48 h after CFA injection, elicited a significant increase in the number of Fos-immunoreactive neurons in both the superficial and deep laminae of the dorsal horn compared to non-inflamed animals. Electrical stimulation of the sciatic nerve 24 h post-CFA injection, at a strength sufficient only to activate A beta-afferents fibres (100 microA, 50 microseconds, 10 min), also elicited a significant increase in labelling relative to the same stimuli applied in control animals, especially in laminae V-VI. The present results demonstrate that low intensity cutaneous stimuli elicit a significantly greater increase in c-fos expression in dorsal horn neurons during peripheral inflammation and that A beta-afferent input contributes to this, a finding that may relate to the allodynia experienced during inflammation.

Afferent Pathways↗
PubMed1990

Utilization of vitamin A in rats with inflammation.

Reductions in the concentration of retinol (vitamin A) in serum, lung and kidney were observed in rats subjected to inflammation-inducing treatments (turpentine oil injection of thermal injury). At the same time, the liver showed an almost normal vitamin A content. Feeding of retinol to vitamin A-depleted rats with inflammation revealed that intestinal absorption of retinol was still active in the inflamed state, and the livers of these rats showed good incorporation of retinol. The livers of normal and vitamin A-depleted rats subjected to the inflammatory treatments showed a normal RBP content (retinol-binding protein) and hepatic release of holo-RBP into the serum was not impaired functionally. These results suggest the possibility that the decreases of vitamin A in the lung, serum and kidney may be due primarily to enhanced local consumption of vitamin A related to the inflammation, rather than to a reduced supply of vitamin A from the liver or to decreased intestinal absorption. In bovine serum albumin (BSA)-sensitized rats produced by direct intubation of BSA into the lungs, the level of vitamin A in the lung decreased prior to that in the liver or serum, supporting the hypothesis that the decrease in vitamin A in the inflamed lungs of these rats may be due mainly to the consumption of vitamin A in the lung in response to inflammation.

Animals↗
PubMed1992

Preproenkephalin mRNA in spinal dorsal horn neurons is induced by peripheral inflammation and is co-localized with Fos and Fos-related proteins.

Increased levels of preproenkephalin mRNA in spinal cord neurons induced by peripheral tissue inflammation were examined using in situ hybridization histochemistry. In addition, in situ hybridization histochemistry was combined with immunocytochemistry to determine whether increases in preproenkephalin mRNA were co-localized in spinal cord neurons with increases in immunoreactivity for Fos and Fos-related proteins coded by the immediate-early proto-oncogene, c-fos, and related genes. Dorsal horn laminae I-II, V-VI and VII showed a greater than 200% increase in preproenkephalin mRNA-labeled neurons on the inflamed side as compared to the contralateral control. Inflammation also induced Fos-like immunoreactivity in cell nuclei, mainly in the superficial laminae I-II and the neck of the dorsal horn (laminae V-VI). Few labeled nuclei were detected on the contralateral side. Inflammation resulted in double-labeling of neurons ipsilateral to the inflamed limb whereas they were almost completely absent on the contralateral side. Double-labeled neurons were most frequently found in laminae V-VI. Double-labeled laminae I-II neurons were concentrated in the medial two-thirds of the dorsal horn, the site that receives innervation from the inflamed limb. There were also many double-labeled neurons in laminae VII. Over 90%, 82% and 69% of all neurons expressing preproenkephalin mRNA co-localized Fos immunoreactivity in laminae V-VI, I-II, and VII, respectively. However, the number of neurons expressing increased Fos immunoreactivity was substantially greater than the subpopulation of double-labeled neurons. Our findings indicated that peripheral inflammation induces an increase in preproenkephalin mRNA levels in spinal cord neurons and that most neurons exhibiting preproenkephalin mRNA labeling also co-localized Fos and Fos-related immunoreactivity. These data are consistent with evidence supporting the role of Fos and Fos-related proteins in the regulation of transcription of the preproenkephalin gene in spinal neurons.

Animals↗
PubMed1993

Inflammation of the rat paw enhances axonal transport of opioid receptors in the sciatic nerve and increases their density in the inflamed tissue.

The effect of inflammation, induced by unilateral intraplantar injection of Freund's adjuvant, on opioid receptors transported in the sciatic nerve and on opioid receptors present in the paw of the rat was studied by means of in vitro receptor autoradiography using [125I]beta-endorphin (human) as ligand. In the absence of inflammation, human beta-endorphin binding sites accumulated proximally and distally to a ligature placed on the sciatic nerve in a time-dependent manner, indicating bidirectional axonal transport. Some human beta-endorphin binding was also visible in non-inflamed paw tissue. Inflammation of the paw tissue massively increased human beta-endorphin binding on both sides of the sciatic nerve ligature and in the ipsilateral paw tissue. In inflamed paw tissue, beta-endorphin binding accumulated in the cutaneous nerve fibers as well as in the immune cells infiltrating the surrounding tissue. In the sciatic nerve and paw tissue, beta-endorphin binding was displaced by (D-Ala2, N-methyl-Phe4, Gly-ol5)enkephalin and (D-Pen2, D-Pen5)enkephalin, selective mu- and delta-opioid receptor agonists, respectively, and by the universal opioid antagonist naloxone, but not by U-50,488H, a k-selective receptor agonist. Taken together, these data provide neuroanatomical evidence for local inflammation-induced enhanced axonal transport of opioid receptors in rat sciatic nerve and accumulation in paw tissue.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Inflammation, an inducer of metallothionein, inhibits carbon-tetrachloride-induced hepatotoxicity in rats.

Inflammation, induced by turpentine (0.1 ml i.m.), protected against carbon tetrachloride (CCl4)-induced hepatotoxicity based on serum activities of sorbitol dehydrogenase. Inflammation was confirmed by elevated serum ceruloplasmin activities, and was associated with high hepatic levels of metallothionein, a zinc protein proposed to protect against CCl4-induced injury. Inflammation suppressed cytochrome P-450 activities, but this was not associated with protection against CCl4-promoted liver microsomal injury as assessed by glucose-6-phosphatase activity loss. Thus, protection against plasma membrane injury did not result primarily from depressed microsomal activation of CCl4. Each effect of inflammation reported here resembled effects of zinc injections. This similarity strengthens the hypothesis that metallothionein protects against CCl4-induced hepatic plasma membrane injury.

Animals↗
PubMed2005

Erythrocyte adhesiveness/aggregation: a novel biomarker for the detection of low-grade internal inflammation in individuals with atherothrombotic risk factors and proven vascular disease.

BACKGROUND: We have introduced a concept of using the erythrocyte as a sensor for the detection of enhanced inflammation-sensitive protein concentrations. We presently evaluated the capability of this new biomarker to detect the presence of inflammation in individuals with a history of a vascular disease as opposed to individuals with atherothrombotic risk factors but no clinically evident vascular disease. METHODS: The degree of erythrocyte adhesiveness/aggregation was determined in the peripheral venous blood by using a simple blood test. Blood was drawn into a syringe containing sodium citrate and trickled onto a slide at an angle of 30 degrees. The slides were than scanned by a blinded technician by using an image analyzer to determine the area that is covered by the erythrocytes. RESULTS: One hundred fifty-six subjects (61 women and 95 men) of 2586 (1238 women and 1348 men) met the criteria of a definite vascular disease (history of stroke, myocardial infarction, coronary artery bypass grafting, or peripheral vascular disease). The degree of erythrocyte aggregation was significantly (P = .008) higher in men, but not in women, with vascular disease as opposed to these without a vascular disease. The results of receiver operating characteristic curve analysis confirmed the diagnostic superiority of the erythrocyte aggregation biomarker over other commonly used markers of the acute phase in men. Similar results were obtained by using discriminant analysis. Finally, a significant correlation was found between the degree of erythrocyte aggregation and other markers of the acute phase suggesting its relevance for the detection and quantitation of low-grade inflammation in individuals with atherothrombosis. CONCLUSION: Erythrocyte adhesiveness/aggregation may be a useful biomarker to detect internal inflammation in individuals with atherothrombosis.

Adhesiveness↗
PubMed2006

Inflammation and long-term mortality in acute congestive heart failure.

BACKGROUND: Systemic inflammation has long been recognized as a precipitator of acute congestive heart failure (CHF). The impact of inflammation on prognosis in acute CHF, however, is unknown. METHODS: This study evaluated the prognostic role of inflammation among 214 consecutive patients presenting with acute CHF to the emergency department. Patients were stratified according to C-reactive protein (CRP) levels determined on admission. The primary end point was all-cause mortality during 24-month follow-up. RESULTS: The median CRP level was 13.0 mg/L, with an intertertile range of 6.0 to 25.0 mg/L. Initial and long-term outcomes were significantly different to the detriment of patients with higher CRP levels. Patients in the highest CRP tertile significantly more often required admission to the intensive care unit (33% vs 14% in patients in the first tertile, P = .028) and died inhospital (15% vs 2% in patients in the first tertile, P = .027). Cumulative 24-month mortality rates were 33.5% in the first, 42.4% in the second, and 53.6% in the third tertile (P = .0265 by log-rank test). After multivariate adjustment, CRP remained an independent predictor of death (hazard ratio 1.4, 95% CI 1.1-1.8 for each step up in tertile, P = .044). CONCLUSIONS: Inflammation is a significant and independent predictor of long-term mortality in patients with acute CHF.

Acute Disease↗
PubMed2004

Assessment of systemic inflammation and infective pathogen burden in patients with cardiac syndrome X.

Inflammation plays a key role in coronary artery disease (CAD), but whether it is involved in the pathogenesis of syndrome X (SX) is not known. Thus, we assessed the presence of systemic inflammation in patients with SX and its possible relation to infections from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus. We studied 55 patients with SX (57 +/- 8 years old; 27 women), 49 with stable angina and obstructive CAD (56 +/- 8 years old; 24 women), and 60 healthy controls (57 +/- 11 years old; 24 women). Plasma levels of high-sensitivity C-reactive protein and interleukin-1 receptor antagonist were measured in all patients. Infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus was assessed in 43 patients with SX, 40 patients with CAD, and in 39 controls. Patients with SX had lower serum levels of C-reactive protein than did patients with CAD (4.06 +/- 6.8 vs 5.99 +/- 7.8 mg/L, p = 0.013) but higher levels of C-reactive protein than did controls (1.75 +/- 1.98 mg/L; p = 0.008). Plasma levels of interleukin-1 receptor antagonist were higher in patients with CAD (570 +/- 738 pg/ml) and patients with SX (494 +/- 677 pg/ml) than in controls (254 +/- 174, pg/ml; p = 0.0003 vs CAD and p = 0.013 vs SX) but did not differ significantly between patients with CAD or SX (p = 0.20). There were no differences across groups in the prevalence of infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus and in the prevalence of 1, 2, 3, and 4 infections (p = 0.99). Among patients with SX, no correlation was found between markers of inflammation and indexes of disease activity (angina episodes, exercise test results). Our data show evidence of increased low-grade systemic inflammation in patients with cardiac SX, which was unrelated to an increased infectious pathogen burden.

C-Reactive Protein↗
PubMed2004

The influence of celecoxib on muscle fatigue resistance and mobility in elderly patients with inflammation.

BACKGROUND: Acute inflammation has a negative effect on the muscular system in elderly patients, compromising the outcome of the underlying disease. OBJECTIVE: The aim of this study was to evaluate the effect of cyclooxygenase-2 (COX-2) inhibition on muscle performance and mobility in hospitalized elderly patients with acute inflammation of infectious origin. METHODS: In this single-blind, controlled trial, consecutively hospitalized elderly patients (age > or = 70 years) with inflammation (C-reactive protein [CRP] levels > or =10 mg/L) due to acute infection were randomly assigned to receive 2 weeks of treatment with the COX-2-selective inhibitor celecoxib, acetaminophen, or no supplementary medication (control). The following variables were assessed at baseline and at 1 and 2 weeks' follow-up: muscle fatigue resistance (primary outcome measure); grip strength and mobility (secondary outcome measures); and levels of the acute-phase markers CRP, interleukin (IL)-1beta, IL-6, IL-10, tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta (TGF-beta) as explanatory variables. RESULTS: Forty-three consecutively hospitalized elderly patients (31 women, 12 men; mean [SD] age, 84 [6] years) were enrolled. Fourteen patients received celecoxib, 14 received acetaminophen, and 15 received no supplementary medication. The change in fatigue resistance was significantly different between groups (P = 0.021, Kruskal-Wallis chi-square test), with significantly greater improvement in patients receiving celecoxib compared with the acetaminophen and control groups (63% increase from baseline; P < 0.05). There were no significant between-group differences in changes in grip strength, mobility, IL-1beta, IL-6, TNF-alpha, or TGF-beta. The changes in levels of IL-10 differed significantly between groups (P = 0.020, Kruskal-Wallis chi-square test), with greater improvement in the celecoxib group compared with the acetaminophen group (P = 0.032). CONCLUSION: The results of this study suggest that COX-2-selective inhibition has a beneficial effect on muscle fatigue resistance in hospitalized elderly patients with acute inflammation of infectious origin. However, until further trials are conducted, the use of COX-2-selective inhibitors for this indication is not recommended.

Acute Disease↗