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PubMed2001

B7 interactions with CD28 and CTLA-4 control tolerance or induction of mucosal inflammation in chronic experimental colitis.

CD28-B7 interaction plays a critical costimulatory role in inducing T cell activation, while CTLA-4-B7 interaction provides a negative signal that is essential in immune homeostasis. Transfer of CD45RB(high)CD4(+) T cells from syngeneic mice induces transmural colon inflammation in SCID recipients. This adoptive transfer model was used to investigate the contribution of B7-CD28/CTLA-4 interactions to the control of intestinal inflammation. CD45RB(high)CD4(+) cells from CD28(-/-) mice failed to induce mucosal inflammation in SCID recipients. Administration of anti-B7.1 (but not anti-B7.2) after transfer of wild-type CD45RB(high)CD4(+) cells also prevented wasting disease with colitis, abrogated leukocyte infiltration, and reduced production of proinflammatory cytokines IL-2 and IFN-gamma by lamina propria CD4(+) cells. In contrast, anti-CTLA-4 treatment led to deterioration of disease, to more severe inflammation, and to enhanced production of proinflammatory cytokines. Of note, CD25(+)CD4(+) cells from CD28(-/-) mice similar to those from the wild-type mice were efficient to prevent intestinal mucosal inflammation induced by the wild-type CD45RB(high) cells. The inhibitory functions of these regulatory T cells were effectively blocked by anti-CTLA-4. These data show that the B7-CD28 costimulatory pathway is required for induction of effector T cells and for intestinal mucosal inflammation, while the regulatory T cells function in a CD28-independent way. CTLA-4 signaling plays a key role in maintaining mucosal lymphocyte tolerance, most likely by activating the regulatory T cells.

Abatacept↗
PubMed2003

Reduced inflammation and tissue damage in transgenic rabbits overexpressing 15-lipoxygenase and endogenous anti-inflammatory lipid mediators.

PGs and leukotrienes (LTs) mediate cardinal signs of inflammation; hence, their enzymes are targets of current anti-inflammatory therapies. Products of arachidonate 15-lipoxygenases (LO) types I and II display both beneficial roles, such as lipoxins (LXs) that stereoselectively signal counterregulation, as well as potential deleterious actions (i.e., nonspecific phospholipid degradation). In this study, we examined transgenic (TG) rabbits overexpressing 15-LO type I and their response to inflammatory challenge. Skin challenges with either LTB(4) or IL-8 showed that 15-LO TG rabbits give markedly reduced neutrophil (PMN) recruitment and plasma leakage at dermal sites with LTB(4). PMN from TG rabbits also exhibited a dramatic reduction in LTB(4)-stimulated granular mobilization that was not evident with peptide chemoattractants. Leukocytes from 15-LO TG rabbits gave enhanced LX production, underscoring differences in lipid mediator profiles compared with non-TG rabbits. Microbe-associated inflammation and leukocyte-mediated bone destruction were assessed by initiating acute periodontitis. 15-LO TG rabbits exhibited markedly reduced bone loss and local inflammation. Because enhanced LX production was associated with an increased anti-inflammatory status of 15-LO TG rabbits, a stable analog of 5S,6R,15S-trihydroxyeicosa-7E,9E,11Z,13E-tetraenoic acid (LXA(4)) was applied to the gingival crevice subject to periodontitis. Topical application with the 15-epi-16-phenoxy-para-fluoro-LXA(4) stable analog (ATLa) dramatically reduced leukocyte infiltration, ensuing bone loss as well as inflammation. These results indicate that overexpression of 15-LO type I and LXA(4) is associated with dampened PMN-mediated tissue degradation and bone loss, suggesting that enhanced anti-inflammation status is an active process. Moreover, they suggest that LXs can be targets for novel approaches to diseases, e.g., periodontitis and arthritis, where inflammation and bone destruction are features.

Administration, Topical↗
PubMed2004

Ectopic CD40 ligand expression on B cells triggers intestinal inflammation.

Several studies indicate that CD4(+) T cells, macrophages, and dendritic cells initially mediate intestinal inflammation in murine models of human inflammatory bowel disease. However, the initial role of B cells in the development of intestinal inflammation remains unclear. In this study we present evidence that B cells can trigger intestinal inflammation using transgenic (Tg) mice expressing CD40 ligand (CD40L) ectopically on B cells (CD40L/B Tg). We demonstrated that CD40L/B Tg mice spontaneously developed severe transmural intestinal inflammation in both colon and ileum at 8-15 wk of age. In contrast, CD40L/B TgxCD40(-/-) double-mutant mice did not develop colitis, indicating the direct involvement of CD40-CD40L interaction in the development of intestinal inflammation. The inflammatory infiltrates consisted predominantly of massive aggregated, IgM-positive B cells. These mice were also characterized by the presence of anti-colon autoantibodies and elevated IFN-gamma production. Furthermore, although mice transferred with CD4(+) T cells alone or with both CD4(+) T and B220(+) B cells, but not B220(+) cells alone, from diseased CD40L/B Tg mice, develop colitis, mice transferred with B220(+) B cells from diseased CD40L/B Tg mice and CD4(+) T cells from wild-type mice also develop colitis, indicating that the Tg B cells should be a trigger for this colitis model, whereas T cells are involved as effectors. As it has been demonstrated that CD40L is ectopically expressed on B cells in some autoimmune diseases, the present study suggests the possible contribution of B cells in triggering intestinal inflammation in human inflammatory bowel disease.

Adoptive Transfer↗
PubMed2006

Cutting edge: B and T lymphocyte attenuator and programmed death receptor-1 inhibitory receptors are required for termination of acute allergic airway inflammation.

T cell activation is regulated by coordinate interaction of the T cell Ag receptor and costimulatory signals. Although there is considerable insight into processes that regulate the initiation of inflammation, less is known about the signals that terminate immune responses. We have examined the role of the inhibitory receptors programmed death receptor-1 and B and T lymphocyte attenuator in the regulation of allergic airway inflammation. Our results demonstrate that there is a temporally regulated expression of both the receptors and their ligands during the course of allergic airway inflammation. Following a single inhaled challenge, sensitized wild-type mice exhibit peak inflammation on day 3, which resolves by day 10. In contrast, mice deficient in the expression of programmed death receptor-1 or B and T lymphocyte attenuator have persistent inflammation out to 15 days following challenge. Thus, these receptors are critical determinants of the duration of allergic airway inflammation.

Acute Disease↗
PubMed1997

[Interleukin-8, a regulator of inflammation in gingival crevicular fluid].

The role of interleuking-8 (IL-8), a neutrophil-attracting and-activating cytokine, was investigated in gingival crevicular fluid (GCF). ELISA was used to detect the levels of IL-8 in GCF collected from 54 adult periodontitis (AP) patients (105 teeth) and 24 healthy subjects (54 teeth). The results showed that 1. The role of IL-8 was dependent upon the concentration of IL-8 in GCF. IL-8, in the low concentration (< or = 30 micrograms/L), was positively correlated with bleeding index (r = 0.36, P < 0.01). While in the high concentration (> 30 micrograms/L), was negatively correlated with bleeding index and probing depth (r = -0.54 and r = -0.65 respectively, P < 0.01). In the majority of periodontitis sites (91%), the concentration of IL-8 in GCF were lower than 30 microliters/L. IL-8 most likely acted as pro-inflammatory factor in these teeth. 2. IL-8 was a two-way regulator of inflammation, pro-inflammation and anti-inflammation. The threshold of IL-8 between inducing and suppressing inflammation was approximately 30 micrograms/L. Within the confined range, IL-8 concentration greater than 30 micrograms/L could be inflammation suppressive, while a less-than-30 micrograms/L concentration of IL-8 might become inflammation inducing.

Adult↗
PubMed2001

Intestinal inflammation enhances the inhibitory effects of opioids on intestinal permeability in mice.

The inhibitory effects of central and peripherally acting opioid agonists on intestinal permeability (PER) were evaluated during acute and chronic intestinal inflammation in mice. Inflammation was induced by the intragastric (p.o.) administration of one (acute) or two (chronic) doses of croton oil (CO), whereas controls received saline (SS). Intestinal PER was assessed by the blood-to-lumen transfer of 51Cr-ethylenediaminetetraacetate (51Cr-EDTA). CO significantly increased PER during acute (2.5 times) and chronic (3.2 times) inflammation. The potency of s.c. morphine-inhibiting PER was enhanced 3.8 and 8.7 times in acute and chronic CO, whereas that of s.c. fentanyl was increased 2.0 and 4.3 times, respectively, compared with SS. Similarly, s.c. [D-Pen(2,5)]-enkephalin was 4.7 and 11.1 times more potent during acute and chronic CO, and the E(max) values of the dose-response curves increased 35% during inflammation. The potency of s.c. U50,488H was 5.6 (acute) and 6.7 times (chronic) greater compared with SS. All effects were reversed by specific antagonists. The i.p. administration of beta-funaltrexamine differentially blocked morphine effects during acute and chronic CO, suggesting that the effects are mediated by different populations of functional mu-opioid receptors (OR). The increase in potencies of s.c. PL017 and ICI-204,448 during CO were comparable to those observed with fentanyl and U50,488H and their effects were antagonized by s.c. naloxone methiodide. Moreover, the potency of the agonists during inflammation was unaltered when administered i.c.v. The results show that intestinal inflammation enhances the effects of delta- > mu- > kappa-opioid agonists on PER by activation of peripheral OR.

Analgesics, Opioid↗
PubMed2001

Inhibitory effect of low density lipoprotein on the inflammation-inducing activity of calcium pyrophosphate dihydrate crystals.

OBJECTIVE: It has been proposed that low density lipoprotein (LDL) plays a role in the self-limiting nature of pseudogout inflammation. We investigated changes of LDL concentration in rat air pouch fluid during periods of acute and subsiding inflammation to evaluate whether LDL contributes to inhibiting inflammation of pseudogout. We examined whether LDL binds to calcium pyrophosphate dihydrate (CPPD) crystals as a possible mechanism for reduction of inflammation. METHODS: In this in vivo study, 5 mg suspensions of CPPD crystals and saline were injected into the rat air pouch. Fluid samples were taken from rat air pouch at 0, 3, 6, 12, 24, and 48 h after injection. White blood cells in the samples were counted; the remaining fluid was centrifuged and concentrations of beta-glucuronidase and PGE2 in the supernatant were measured as inflammatory markers. LDL in the supernatant was immunochemically identified by Western blotting, then pellets containing crystals were examined by the same technique. RESULTS: LDL was identified in the air pouch 3 h after CPPD crystal injection, and its concentration increased and reached a peak level after 24 h. Inflammatory markers reached maximal level from 6 to 12 h, then decreased after 24 h. In the pellets containing crystals, LDL could not be identified in every specimen. CONCLUSION: LDL in the rat air pouch increased during the inflammatory course induced by CPPD crystal and the inflammation subsided as the LDL increased. Since some reports indicate LDL was related to reduction of crystal induced inflammation such as gout or pseudogout, we concluded that LDL could contribute to the resolution of acute pseudogout arthritis in vivo with or without binding to CPPD crystals.

Animals↗
PubMed2002

Norepinephrine from synovial tyrosine hydroxylase positive cells is a strong indicator of synovial inflammation in rheumatoid arthritis.

OBJECTIVE: Density of sympathetic nerve fibers in synovial tissue was lower in patients with rheumatoid arthritis (RA) compared to those with osteoarthritis (OA). This was accompanied by norepinephrine (NE) release from synovial tyrosine hydroxylase positive cells (TH+ cells). We investigated the role of TH+ cells and NE in synovial inflammation. METHODS: Synovial tissue of 34 patients with RA and 36 with OA who underwent knee joint replacement surgery was characterized using immunohistochemistry and a synovial tissue superfusion technique, respectively. In culture experiments with mixed synoviocytes, the effect of NE on secretion of interleukin 6 (IL-6), IL-8, tumor necrosis factor (TNF), and matrix metalloproteinase-3 (MMP-3) was investigated. RESULTS: Tissue density of TH+ cells was higher in RA compared to OA (63.9 vs 34.2 cells/mm2; p = 0.017). Basal NE release from synovial tissue correlated highly significantly with density of TH+ cells in RA (Rrank = 0.573, p = 0.001) but not in OA (Rrank = 0.102, NS). Basal NE release correlated with the degree of inflammation in RA (Rrank = 0.420, p = 0.021) but not in OA (Rrank = 0.174, NS), and with spontaneous IL-8 secretion in RA (Rrank = 0.581, p = 0.001) but not in OA (Rrank = 0.160, NS). Only in RA, density of TH+ cells correlated positively with spontaneous secretion of IL-6, IL-8, and MMP-3. We confirmed the extensive loss of sympathetic nerve fibers in RA compared to OA (0.32 vs 3.1 nerve fiber/mm2; p < 0.001). The ratio of sympathetic to sensory nerve fibers was 1 to 5 in RA and 2 to 1 in OA. A ratio of 1.0 separates almost all patients into 2 diseases groups (RA vs OA). Prior prednisolone treatment of RA patients was related to decreased spontaneous cytokine secretion, a lower density of T cells, CD163+ macrophages and TH+ cells, a lower degree of inflammation, and reduced synovial NE secretion. NE was able to inhibit secretion of IL-6 (in OA), IL-8 (in RA), and TNF (in RA and OA) in culture experiments. CONCLUSION: TH+ cells and release of NE are strongly linked to a higher degree of synovial inflammation. Culture experiments indicate that NE has antiinflammatory properties at higher concentrations (10(-5) M). NE secretion of TH+ cells may be an antiinflammatory mechanism to counteract local inflammation. Thus, TH+ cell derived NE can be an important local factor of immunomodulation in synovial inflammation.

Adrenergic Fibers↗
PubMedDate not supplied

Eosinophilia in the ethmoid mucosa and its relationship to the severity of inflammation in chronic rhinosinusitis.

BACKGROUND: The aim of this study was to analyze histopathologically mucosal inflammation in patients with chronic rhinosinusitis. In addition, we assessed tissue eosinophilia in relation to the severity of inflammation and to the computer tomographic (CT) findings. METHODS: Forty-eight pathological sinus mucosa specimens obtained during functional endoscopic sinus surgery were stained by hematoxvlin and eosin. Total inflammatory cells and eosinophils were quantified. The preoperative CT scans were scored by the staging system of Lund-MacKay. RESULTS: The grade of the eosinophilic infiltration in the diseased sinus mucosa correlated significantly with the severity of the mucosal inflammation. Allergy or asthma had no effect on the proportion of the eosinophilic infiltrate. The CT scan scores assessed by the Lund-MacKay system correlated significantly with the severity of the inflammatory cellular infiltrate. The correlation between the CT scan scores and the eosinophilic infiltrate of the mucosa was close to significant. CONCLUSION: Eosinophilic mucosal inflammation represents the most severe inflammatory changes of the mucosa. Twenty to forty percent of the patients with chronic rhinosinusitis had no eosinophilic inflammation of the mucosa. The CT-staging system of Lund-Mackay correlated with the extent of mucosal inflammation.

Adolescent↗
PubMed2003

[Microbial inflammations of the orbit in children].

The author evaluates in a retrospective study the incidence, diagnosis and causal agent and therapeutic results of microbial inflammations of the orbit. During the period from Jan. 1 1997 till Dec. 31 1999 66 children were hospitalized with the diagnosis of inflammation of the orbit. The mean age of the children was 6.2 years, the mean period of hospitalization 10.2 days. Chandler's classification of inflammations of the orbit was used. The diagnosis was established in collaboration by an ophthalmologist, otolyryngologist and roentgenologist. The main cause of inflammations of the orbit was inflammation of the paranasal sinuses. The most frequent microbial agents were streptococci, staphylococci and Haemophilus influenzae. All patients were treated during hospitalization by antibiotics administered by the i.v. route. Surgery was necessary in 8 patients--in 4 patients with an orbital abscess and in 4 patients with a subperiostal abscess not responding to conservative treatment. The operation was performed by an otolaryngologist using always the endonasal approach. The authors did not record in their group any permanent ophthalmological complications resulting from the inflammation of the orbit.

Abscess↗
PubMed1992

[The significance of lobular inflammation in chronic active hepatitis].

Authors have performed an anatomo-clinico-biological comparison of two groups of hepatitis with lobular inflammation: group I with a simple lobular inflammation, called lobular hepatitis, and group II with a lobular inflammation associated with portal and periportal hepatitis, called chronic active hepatitis (CHA) with lobular hepatitis. Furthermore, a comparative study of these forms with a group of CHA without lobular inflammation was performed. Both forms of lobular inflammation appeared in young patients, the large majority of whom were infected with the hepatitis B virus; in 5 cases of CHA with lobular hepatitis the presence of the delta agent in the liver, possibly responsible of the lobular inflammation, was detected. The two forms of lobular hepatitis are differentiated by: the fivefold increase of ALAT over the normal value, with usually normal gamma-globulins and albumin, in the first group; in the lobular hepatitis, HBsAg was present in 33% of cases in the first group and in none of the patients of the second group, suggesting the integration of HBsAg within the hepatocytic genome; the clinical picture was generally asymptomatic in the first group and noisier, with hepatomegaly, in the second group; the period elapsed since the acute hepatitis was shorter in the first group (4-11 months) in 8 of 15 patients and longer in the second group. The clinical course of these forms of hepatitis if unforeseeable and the diagnosis is established on the basis of the morphological examination.

Adult↗
PubMedDate not supplied

Recent insights into the relationship between airway inflammation and asthma.

There have been important recent advances in our understanding of the relationship between eosinophilic airway inflammation and airway dysfunction. Observational studies have shown that eosinophilic airway inflammation is not always present in asthma nor is it an exclusive feature of asthma. Its presence seems to be more closely linked to the presence of corticosteroid responsive airways disease and the occurrence of severe exacerbations than the presence of symptoms or the extent of airway dysfunction--indeed recent evidence suggests that in asthma these features may be more closely linked to the site of localisation of mast cells in the airway wall. One implication of this new understanding of the significance of eosinophilic airway inflammation is that it predicts that measuring airway inflammation might provide information that it is not readily available from a more traditional clinical assessment, and that patients might do better if this information is available. Recent studies support this view, showing a marked reduction in asthma exacerbation in patients with moderate to severe disease who are managed with reference to markers of airway inflammation as well as symptoms and simple tests of airway function. The development of new agents that have the potential to modulate specific aspects of airway inflammation, together with refinements in non-invasive techniques to assess the efficacy of these agents offers the prospect of further refining our understanding of the role of this aspect of the inflammatory response in asthma and other airway diseases.

Asthma↗
PubMed2005

[Demonstration of a mechanism of anti-inflammatory effect of erythromycin on allergic airway inflammation in rat].

OBJECTIVE: To investigate whether erythromycin exerts anti-inflammatory effect on allergic airway inflammation and whether erythromycin modulate allergic airway inflammation by inhibiting nuclear factor kappa B (NF-kappa B) activation. METHODS: Ovalbumin (OVA) together with aluminum hydroxide and Bordetella Pertussis was injected intraperitoneally to immunize SD rats and two weeks later 1% OVA was inhaled to challenge them for consecutive 7 days to mimic allergic airway inflammation. In treatment group, erythromycin was given orally (180 mg/kg.d) during the course of allergen exposure. WBC counts in bronchoalveolar lavage fluid (BALF) and lung specimen analysis were used to describe lung tissue inflammation. The expression of NF-kappa B subunit p65 in cell nucleus of lung tissue was measured by immunohistochemistry and NF-kappa B binding activation in lung tissue by electrophoresis mobility shift assay (EMSA). RESULTS: Lung tissue specimen analysis indicated that the severity of allergic inflammation was reduced in treatment group. The number of total WBC in BALF (x 10(8)/L) (31 +/- 22) was lower than that in model group animals (66 +/- 28), P < 0.01. The number (x 10(3)/mm(2)) of cells with nuclear staining of NF-kappa B per square millimeter of submucosal region around large bronchus (1.4 +/- 0.4) was lower than that in model group animals (2.6 +/- 0.6), P < 0.01. NF-kappa B binding activity (32 +/- 14) was lower than that of model group (46 +/- 17), P < 0.05. CONCLUSION: Erythromycin had an obvious protective role in allergic airway inflammation. Erythromycin inhibited NF-kappa B transcriptional activity to exert anti-inflammatory effect.

Animals↗
PubMed2005

[Effects of budesonide on chronic airway inflammation in guinea pigs sensitized with repeated exposure to allergen].

OBJECTIVE: Inhaled glucocorticosteroids (ICS) remains the first line controller medication for chronic airway inflammation in asthma till now. If the impact of allergen could not be eliminated, how would the improvement of airway inflammation be achieved with inhaled glucocorticosteroids therapy? What was its effect on airway remodeling? In this study, an animal model of asthma was established and the effects of budesonide on airway allergic inflammation and extracellular matrix (ECM) deposition in sensitized guinea pigs with repeated exposure to allergen were investigated. METHODS: Thirty-two male Hartley guinea pigs were randomly divided into four groups with 8 in each group: (A) Group of repeated exposure to ovalbumin (OVA), (B) Group of repeated exposure to OVA plus budesonide (BUD) intervention, (C) Group of stopping repeated exposure to OVA plus stopping BUD intervention, (D) Control group. At 24 h after the last OVA challenge (8 weeks after the first OVA challenge), bronchoalveolar lavage fluid (BALF) was collected from each animal. Total and differential leukocyte counts in BALF was performed on cell suspension smear stained with May-Grünwald-Giemsa (MGG) method. The upper lobe of right lung was removed and regularly fixed, then paraffin embedded lung tissues sections were prepared. The count of eosinophils infiltrated in the airway wall was performed on H&E stained lung tissue sections with LEICA Q500IW computerized image analysis system. Fibronectin and collagen type III (Col-III) deposited in the airway wall were detected by immunohistochemical staining on the paraffin embedded lung tissues sections. The intensity of positive reaction of fibronectin or Col-III deposited in the airway wall was analyzed with LEICA Q500IW computerized image analysis system. RESULTS: The count of eosinophils in BALF (x 10(5)/ml) of group A and B were higher than that of group C and D (35.70 +/- 25.22, 11.49 +/- 5.51 vs. 1.00 +/- 0.90, 1.02 +/- 0.78, P < 0.01), the difference between group A and B, group B and C was significant. The count of eosinophils infiltrated at each level of airway wall in group A and B were higher than that of group C and D (large airway: 6.95 +/- 2.28, 1.54 +/- 1.09 vs. 0.76 +/- 0.45, 0.88 +/- 0.25; medial airway: 9.22 +/- 3.89, 3.99 +/- 2.3 vs. 1.25 +/- 1.20, 0.64 +/- 0.36; small airway: 11.56 +/- 4.02, 2.67 +/- 1.15 vs. 1.32 +/- 0.83, 0.43 +/- 0.24, P < 0.01), the difference between group A and B, group B and C was significant. The gray values of fibronectin deposited in medial and small airway of group A and B were lower than those of group C and D (medial airway 122 +/- 22, 174 +/- 23 vs. 219 +/- 34, 229 +/- 20; small airway 135 +/- 29, 165 +/- 41 vs. 236 +/- 20, 220 +/- 16, P < 0.05), the difference between group A and B, group B and C was significant. The gray values of Col-III deposited in medial and small airway of group A and B were lower than those of group C and D (medial airway 153 +/- 21, 174 +/- 22 vs. 189 +/- 14, 200 +/- 18; small airway 133 +/- 23, 176 +/- 20 vs. 191 +/- 14, 198 +/- 20, P < 0.05), the difference between group A and B was significant. CONCLUSION: Inhaled budesonide could partially inhibit allergic inflammation and ECM deposition in airway wall in guinea pig chronic asthma model with repeated exposure to allergen. Early inhaled budesonide combined with avoidance of OVA exposure could completely inhibit allergic inflammation and ECM deposition. These results suggest that the inhibitory effect on airway allergic inflammation and airway remodeling of inhaled glucocorticosteroids would be limited when the allergen factor could not be avoided.

Administration, Inhalation↗
PubMedDate not supplied

Analysis of thte possible impact of inflammation severity and early and delayed loading on nitric oxide metabolism around dental implants.

PURPOSE: The aim of the present study was to analyze the possible impact of clinical status, presence and severity of inflammation, and loading on nitric oxide (NO) metabolism around mandibular dental implants. MATERIALS AND METHODS: A total of 34 implants in 17 patients, loaded either early (EL) or after a delay (DL), were classified according to the presence and severity of clinical inflammation in the peri-implant sites. Clinical parameters were recorded, peri-implant sulcular fluid (PISF) samples were obtained, and PISF nitrite levels were spectrophotometrically determined. Clinical measurements and nitrite analysis were repeated at 1, 3, 6, and 9 months postloading at available sites. RESULTS: Compared to noninflamed sites, inflamed sites demonstrated higher mean total nitrite levels (P = .032) that tended to increase with the severity of inflammation at both EL and DL implants. At noninflamed sites, EL implants provided significantly higher PISF volume than DL implants (P = .001). At noninflamed sites, EL implants revealed higher total nitrite levels; on the contrary, at inflamed sites, DL implants revealed higher total nitrite levels. In general, nitrite levels demonstrated a pattern of decrease followed by an increase during follow-up. DISCUSSION: Increased NO production with the presence and the severity of inflammation supports the contribution of NO in the peri-implant inflammatory process. Loading is also likely to have an impact on NO metabolism, which suggests a role for NO in remodeling and adaptation of bone around dental implants. CONCLUSION: Besides the presence of inflammation, the severity of inflammation and loading also seem to have an impact on NO metabolism around dental implants.

Adult↗
PubMed2005

[Acute inflammation of omental processes of the colon].

Results of treatment of 17 patients aged from 27 to 82 years with acute inflammation of omental processes (OP) are analyzed. The majority of them were hospitalized on day 1-3 from the beginning of the disease. In 9 cases inflammation was in the right half of the colon, in 7 -- in sigmoid colon (which in 3 patients was located in the right iliac area). In right-sided location of inflammation clinical picture looks like acute appendicitis. In some patients mainly in left-sided location of the inflammation the disease looks like renal colic, perforation of colon or peritonitis. Acute pathology of OP was suspected only in one case. All the patients underwent surgery. In 8 of them necrosis was revealed, in 7 -- phlegmonous inflammation of one OP, in 2 -- inflammatory infiltration without destruction. Surgery comes to removing of affected OP, which was supplemented with appendectomy in 9 cases. There were no complications and lethal outcomes. Problems of diagnosis and surgical treatment of acute inflammation of OP are discussed.

Acute Disease↗
PubMedDate not supplied

[The use of bronchoalveolar lavage (BAL) in the study of airway inflammation].

Bronchoscopy and bronchoalveolar lavage can be used to investigate the airways inflammation associated with chronic bronchitis. Visual inspection of the airways provides presumptive evidence of inflammation and bronchoalveolar lavage can recover samples enriched for airways epithelial lining fluid contents. The ability to sample airways inflammation may provide a means of characterizing the airways inflammation associated with chronic bronchitis and of identifying mediators of inflammation that perpetuate the inflammation. Furthermore, bronchoalveolar lavage in conjunction with pulmonary function testing may provide a means for rapidly assessing responses to new therapeutic interventions.

Adult↗
PubMed2004

[The role of Candida sp. in etiopathogenesis of esophageal, gastric and duodenal mucosa inflammation in children].

UNLABELLED: The aim of the study was to demonstrate morphological traits of Candida-induced upper alimentary tract mucosa inflammation. The material for the study comprised 18 children aged 4 to 18 years treated at the I Department of Paediatrics and Gastroenterology, Institute Polish Mother Health Centre. In these children positive mycologic cultures were obtained from alimentary tract inflammed mucosa sections. Upper alimentary tract endoscopy was performed and macroscopic and microscopic evaluation was made. Children with excluded H. pylori infection, reflux disease, lambliosis and allergy were included into the investigated group. Savara-Muller's classification was used for oesophageal mucosa inflammation evaluation, whereas gastric and duodenal mucosa inflammation were assessed according to Tytgat. RESULTS: the most frequent macro lesions concerned simultaneously gastric and duodenal mucosa (44.46%). 27.77% of patients demonstrated oesophagitis, gastritis and duodenitis. In histopathological examination inflammatory lesions in oesophageal mucosa were observed in 38.88% (most frequently I degree). Chronic gastritis was found in all children, non-active in 11 and active in 7. Duodenal mucosa demonstrated traits of chronic active inflammation in 8 children and chronic in 5 of them. CONCLUSIONS: Candida fungi may be an etiopathogenetic factor of oesophageal, gastric and duodenal mucosa inflammation, Candida-induced mucosa inflammation is most frequently of chronic nature.

Adolescent↗