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At least 469 records · Page 26Linked to original sources
PubMed1999

Idiopathic maxillary pain: prevalence of maxillary sinus hyperreactivity in relation to allergy, chronic mucosal inflammation, and eosinophilia.

OBJECTIVE: In patients with chronic orofacial pain, an underlying sinus hyperreactivity may contribute to the clinical symptoms of a diagnosis of atypical odontalgia, trigeminal neuralgia, or temporomandibular disorders. The purpose of this study was to assess the prevalence of histamine-related maxillary sinus hyperreactivity in patients manifesting signs and symptoms of idiopathic maxillary pain and to correlate the respective findings with the presence or absence of chronic maxillary sinusitis-related diagnoses such as allergy, chronic mucosal inflammation, and eosinophilia. STUDY DESIGN: Fifty patients who had been assigned a diagnosis of idiopathic maxillary pain underwent skin allergy tests, maxillary sinus histamine provocation tests, and maxillary sinus mucosa biopsy. Histamine challenge to a selected area was performed during transoral sinuscopy of the maxillary sinus; a positive test result was defined as the development of a significant local mucosa response such as reddening and swelling. RESULTS: Comparison of the data showed most patients (38%) to have an absence of chronic maxillary sinusitis-related diagnoses, whereas the most common multiple diagnosis was found to be chronic mucosal inflammation in combination with eosinophilia (22%). Regarding the prevalence rates of positive histamine provocation test outcomes, a significant difference was found between the diagnostic subgroup "absence of chronic maxillary sinusitis-related diagnoses" (36.9%) and the diagnostic subgroups "chronic mucosal inflammation" (20%; P< .05), "chronic mucosal inflammation in combination with eosinophilia" (18.2%; P< .05), and "chronic mucosal inflammation in combination with eosinophilia and allergy" (14.3%; P < .01). An analysis of the distribution of chronic maxillary sinusitis-related diagnoses revealed absence of chronic mucosal inflammation-related diagnoses to be significantly more frequently associated with positive histamine provocation test outcomes than with negative histamine provocation test outcomes (41.2% vs 19.7%; P< .01), whereas chronic maxillary sinusitis (41.0% vs 29.4%), eosinophilia (26.2% vs 17.6%), and allergy (13.1% vs 11.8%) were found to be more prevalent in patients with negative histamine provocation test outcomes. CONCLUSIONS: The findings of this study suggest patients with idiopathic maxillary pain to be associated with a low rate of sinus hyperreactivity, whereas a positive test outcome with histamine provocation may not be linked to the presence of chronic maxillary sinusitis-related diagnoses such as allergy, chronic mucosal inflammation, and eosinophilia. Further investigations using a larger sample size of patients with idiopathic maxillary pain and nonidiopathic maxillary pain are necessary to demonstrate the presence or absence of an idiopathic maxillary pain-specific prevalence of maxillary sinus hyperreactivity.

Adult↗
PubMed2004

Ex vivo histology-correlated optical coherence tomography in the detection of transmural inflammation in Crohn's disease.

BACKGROUND AND AIMS: Distinguishing Crohn's disease (CD) from ulcerative colitis (UC) can be difficult. Transmural inflammation, a key feature of CD, cannot be assessed by conventional colonoscopy with biopsy. Optical coherence tomography (OCT) provides high-resolution, cross-sectional images of the gut wall and might become a new diagnostic tool. The aims of this study were to perform histology-correlated OCT on surgical specimens of CD and UC and to determine its diagnostic accuracy. METHODS: Colectomy specimens from patients with a preoperative diagnosis of CD (N = 24) or UC (N = 24) were studied with OCT in the operating room. OCT and histopathology were assessed blindly, and diagnostic accuracy of OCT was assessed. RESULTS: Eight preoperatively identified UC patients (33%) with transmural inflammation on postoperative histology were diagnosed with CD, and all 8 had a disrupted layered structure on OCT, a characteristic feature of transmural disease. Sixteen UC patients (67%) had superficial inflammation on histology; of them, 13 (81%) had an intact layered structure on OCT. All 24 preoperative CD patients had transmural inflammation on histology, and 23 (96%) had a disrupted layered structure on OCT. Of 585 histology-OCT image sets from the 48 patients, 152 sets (26%) had transmural inflammation on histology. The sensitivity and specificity for OCT to detect transmural disease were 86% and 91%, respectively. CONCLUSIONS: Transmural inflammation, as characterized by disruption of the layered structure of colon wall on OCT, is an accurate marker for the diagnosis of CD. Ex vivo OCT predicted transmural inflammation on postoperative histopathology.

Adult↗
PubMed2003

Identification of parasite antigen, correlation of parasite density and inflammation in skin lesions of post kala-azar dermal leishmaniasis.

BACKGROUND: Post kala-azar dermal leishmaniasis (PKDL) is an unusual dermatosis following kala-azar (KA). Demonstration of the amastigotes in lesions plays an important role in the diagnosis of PKDL. It was aimed to evaluate the utility of an antibody G2D10 in detecting leishmania parasite antigen, to correlate the parasite number/percentage of parasites with the inflammation, and to assess the epidemiological significance associated with the location of the parasites. MATERIAL AND METHODS: The study was conducted on 50 cases. Hematoxylin and eosin (H & E) stains and immunohistochemical (IHC) stains, using G2D10 antibody, was performed on the skin biopsies. The number of parasites and density of inflammation were semiquantitatively assessed. RESULTS: Leishmania donovan bodies (LDBs) were identified in 50% of cases with the H & E compared to 80% positivity with the IHC. All 50 cases showed inflammation in the superficial dermis (SD). About 44% showed dense inflammation compared to 16% sparse and 40% moderate inflammation. Parasite percentage was maximum in the SD (100%) compared to 75 and 42% in the mid and deep dermis, respectively. CONCLUSIONS: The IHC showed a higher percentage of LDB localization (80 vs. 50%). Density of inflammation was maximum in the SD. The parasite percentage was correlated with the inflammation. Location of parasites could have an epidemiological significance.

Adolescent↗
PubMed2004

Vascular endothelial growth factor (VEGF) induces remodeling and enhances TH2-mediated sensitization and inflammation in the lung.

Exaggerated levels of VEGF (vascular endothelial growth factor) are present in persons with asthma, but the role(s) of VEGF in normal and asthmatic lungs has not been defined. We generated lung-targeted VEGF(165) transgenic mice and evaluated the role of VEGF in T-helper type 2 cell (T(H)2)-mediated inflammation. In these mice, VEGF induced, through IL-13-dependent and -independent pathways, an asthma-like phenotype with inflammation, parenchymal and vascular remodeling, edema, mucus metaplasia, myocyte hyperplasia and airway hyper-responsiveness. VEGF also enhanced respiratory antigen sensitization and T(H)2 inflammation and increased the number of activated DC2 dendritic cells. In antigen-induced inflammation, VEGF was produced by epithelial cells and preferentially by T(H)2 versus T(H)1 cells. In this setting, it had a critical role in T(H)2 inflammation, cytokine production and physiologic dysregulation. Thus, VEGF is a mediator of vascular and extravascular remodeling and inflammation that enhances antigen sensitization and is crucial in adaptive T(H)2 inflammation. VEGF regulation may be therapeutic in asthma and other T(H)2 disorders.

Airway Obstruction↗
PubMed1997

Reversal of tolerance to the antitransit effects of morphine during acute intestinal inflammation in mice.

1. The aim of investigation was to establish and compare the reversibility of tolerance to the antitransit effects of morphine by three different procedures: (a) acute inflammation of the gut, (b) lorglumide a cholecystokininA (CCKA) receptor antagonist, or (c) MK-801, an N-methyl-D-aspartate (NMDA) receptor ion channel blocker. The type of interaction between morphine and lorglumide or MK-801 on the inhibition of gastrointestinal transit (GIT) in naive animals was also evaluated. 2. Male Swiss CD-1 mice were implanted with 75 mg of morphine base or placebo pellets. Gastrointestinal transit was assessed with a charcoal meal and results expressed as % inhibition of GIT. Inflammation was induced by the intragastric (p.o.) administration of croton oil (CO), while controls received castor oil (CA) or saline (SS). Morphine was administered by subcutaneous (s.c.) or intracerebroventricular (i.c.v.) injection, to naive and tolerant animals treated with CO, CA or SS. Dose-response curves for s.c. morphine were also performed in naive and tolerant mice receiving 5.2 or 7.4 nmol (s.c.) lorglumide or MK-801, respectively. 3. The ED50 values for inhibition of GIT by s.c. morphine were: 45.9 +/- 2.7 and 250.1 +/- 3.1 nmol in naive and tolerant animals, respectively, demonstrating a five fold decrease in the potency of morphine. In naive animals, inflammation (CO) decreased the ED50 of morphine three times (14.4 +/- 2.2 nmol). However, no tolerance to s.c. morphine (ED50 16.4 +/- 2.6 nmol) was manifested during intestinal inflammation. After i.c.v. administration, a similar degree of tolerance to morphine was observed (4.8 fold decrease in potency). Intestinal inflammation had no effect on the ED50 values of i.c.v. morphine in naive and tolerant animals, showing that reversal of tolerance is related to local mechanism/s. Mean values for intestinal pH were 6.9 +/- 0.04 and 6.2 +/- 0.04 in SS and CO treated mice, respectively. In addition, morphine was 74 times more potent by the i.c.v. than by the s.c. route (naive-SS). 4. Morphine and lorglumide interacted synergistically in naive animals; in addition, the administration of lorglumide reversed tolerance to s.c. morphine. No interaction (additivity) was observed in naive animals when morphine and MK-801 were administered in combination. However, the drug completely reversed tolerance to the antitransit effects of morphine. 5. The present investigation shows that acute inflammation of the gut reverses tolerance to the antitransit effects of s.c. morphine by a peripheral mechanism. Qualitatively similar results were obtained after the administration of lorglumide or MK-801. Our results suggest that a local decrease in pH could play an important role during inflammation, while antagonism of endogenous compensatory systems would explain the reversal of tolerance induced by lorglumide or MK-801.

Acute Disease↗
PubMed2003

Pulmonary fluorodeoxyglucose uptake in infants of very low birth weight with and without intrauterine inflammation.

OBJECTIVE: We compared early pulmonary (18)fluorodeoxyglucose ((18)FDG) uptake in infants who had very low birth weight with and without exposure to intrauterine inflammation by using positron emission tomography (PET). A secondary goal was to correlate (18)FDG uptake with later death or bronchopulmonary dysplasia. METHODS: Within 72 hours of birth, 22 singleton infants between 25 and 30 weeks of gestation had a thoracic PET scan after intravenous (18)FDG. Influx constants (K(i)) for (18)FDG were determined. Placental histology assessed exposure to intrauterine inflammation. RESULTS: Chorioamnionitis was found in 13 infants. Seven of these infants also had evidence of funisitis. No inflammation was detected in the remaining nine infants. Median (minimum, maximum) thoracic K(I) was 0.008 (0.006, 0.011) mL/min/mL in infants with funisitis, 0.006 (0.002, 0.008) in infants with chorioamnionitis only, and 0.006 (0.001, 0.015) in infants with no evidence of intrauterine inflammation (P=.16). No relation was found between K(i) and later death or bronchopulmonary dysplasia. Cord blood interleukin-6 was elevated in newborns with placental inflammation (P=.014). CONCLUSION: Early thoracic PET scanning for metabolically active inflammatory cells does not differ between infants with and without exposure to intrauterine inflammation. Evidence of early intrapulmonary sequestration of inflammatory cells in some infants without chorioamnionitis points to the complex etiology of postnatal inflammation.

Bronchopulmonary Dysplasia↗
PubMed1997

Interleukin (IL) 1beta, IL-1 receptor antagonist, IL-10, and IL-13 gene expression in the central nervous system and anterior pituitary during systemic inflammation: pathophysiological implications.

The pathophysiology of systemic inflammation and sepsis involves peripheral organs, causing gastrointestinal, renal, and cardiovascular alterations, as well as the central nervous system (CNS), affecting sleep, temperature regulation, behavior, and neuroendocrine function. The molecular basis of the CNS effects of systemic inflammation are not fully elucidated. Here we show that the CNS responds to systemic inflammation with pronounced IL-1beta gene expression and limited IL-1 receptor antagonist (IL-1ra), IL-10, and IL-13 gene expression. This pattern occurs throughout the CNS, including areas such as the subfornical organ, pineal gland, neurohypophysis, and hypothalamus. In contrast, in the anterior pituitary, we found limited IL-1beta gene expression but marked induction of the mRNA encoding for the secreted isoform of IL-1ra, secreted IL-1ra. We conclude that the central manifestations of peripheral inflammation are mediated by endogenous brain IL-1beta synthesized during systemic inflammation in the context of limited central cytokine counter regulation of IL-1. As IL-1beta is a potent stimulus for inducible nitric oxide synthase expression and activity, these findings explain our previous observation that systemic inflammation promotes inducible nitric oxide synthase gene expression in the brain and the spillover of NO metabolites into cerebrospinal fluid. The CNS transcription of the HIV-1 replication factor IL-1beta in the context of limited transcription of the IL-1 replication inhibitors IL-1ra, IL-10, and IL-13 might help explain the negative impact of systemic inflammation on the clinical course of AIDS. In addition, we propose that IL-1ra may be secreted by the anterior pituitary as a systemic anti-inflammatory hormone that is released in response to IL-1beta originated from multiple sources.

Animals↗
PubMed2001

Regulation of experimental mucosal inflammation.

Studies conducted over the past 10 years have provided ample evidence that many types of inflammations arising from basic abnormalities of immune regulation are ultimately 'funneled' through a Th1 or Th2 T cell-mediated immune reaction. Thus, by understanding these types of reactions and, in particular, by identifying their natural checkpoints, one can control the inflammation regardless of its more basic causes. A case in point is the inflammatory disease of the intestine known as Crohn disease, a disease now thought to be due to one or more abnormalities leading to an excessive immune response to elements of the bacterial microflora of the gut. Both in murine models and by study of Crohn disease itself, we have shown that Crohn inflammation is due to a Th1 T-cell abnormality involving overproduction of interleukin (IL)-12, interferon (IFN-gamma, and tumor necrosis factor (TNF)-alpha. In addition, we and others have shown that treatment of mice with anti-IL-12 or other agents that downregulate the level of IL- 12 secretion can have a dramatic effect on the inflammation. This is because anti-IL-12 administration leads to apoptosis of activated Th1 T cells. A second checkpoint of Th1 T-cell-mediated inflammation involves its downregulation by the suppressor cytokine, transforming growth factor (TGF)-beta. We have been delivering TGF-beta to mice with experimental intestinal inflammation, using several novel approaches. In particular, we have successfully treated such mice with intranasally administered DNA encoding active TGF-beta. Another approach currently under investigation is delivery of TGF-beta by gene therapy. These and other developments in the understanding of inflammation paint a bright future for cytokine-based therapeutic agents. It is now apparent that these therapies are not only effective and safe but also potentially long-lasting.

Animals↗
PubMed2004

Inhaled fluticasone propionate reduces concentration of Mycoplasma pneumoniae, inflammation, and bronchial hyperresponsiveness in lungs of mice.

BACKGROUND: Mycoplasma pneumoniae has been shown to induce airway inflammation and bronchial hyperresponsiveness (BHR) in mice. Inhaled corticosteroids are the mainstay of asthma treatment, but their effects on M. pneumoniae and associated airway inflammation and BHR are poorly understood. METHODS: Four groups of mice were studied to determine whether inhaled fluticasone propionate (FP) could attenuate airway inflammation and BHR by reducing or eliminating M. pneumoniae in lungs. The active group received aerosolized FP once daily for 5 days. Control mice received aerosolized sham solution plus M. pneumoniae, sham solution alone, or FP alone. RESULTS: Mice treated with sham solution or FP alone did not develop airway inflammation or BHR. Mice infected with M. pneumoniae (no FP) developed significant lung inflammation and BHR. FP treatment of infected mice reduced neutrophils in bronchoalveolar lavage fluid (BALF), lung inflammation, and BHR. Expression of Toll-like receptor 2 in lung tissue tended to be down-regulated (P=.18) by FP in infected mice. FP reduced M. pneumoniae by up to 20-fold in lung tissue but not in BALF. CONCLUSION: Inhaled FP suppresses airway inflammation and BHR, which may be caused, in part, by its ability to reduce concentrations of M. pneumoniae in lung tissue.

Administration, Inhalation↗
PubMed1992

Inhibitory effect of tetrandrine on lens proteins-induced ocular inflammation in rabbits.

Ocular inflammation was induced by 25 microliters of lens proteins (62.5mg/ml) injected into anterior chamber of the rabbit eye. Tetrandrine (Tet) (50mg/kg ip) and Indomethacin (Ind) (20 mg/kg ip) showed marked inhibition on this ocular inflammation. Maximum inhibition rate of Tet and Ind was 65% and 66% and their anti-inflammation action lasted 5 and 4 h, respectively. In the early phase of ocular inflammation (at 2 h) the total content of prostaglandin E(PGES) in the iris was reduced by Tet and Ind. Ind showed a greater effect than Tet on PGES. Tet also inhibited leukocyte chemotaxis significantly at late phase of inflammation. No significant effect was observed on the IOP recovery following reduction by 20% NaCl iv. Topical instillation of 50 microliters of 2% Tet did not display any inhibition of ocular inflammation. These results indicate that Tet is an effective ocular antiinflammatory agent without producing ocular hypertension. The antiinflammatory mechanism of Tet in early phase (at 2 h) was related to inhibition of PGES synthesis. The relationship between ocular anti-inflammation and calcium antagonism of Tet was discussed.

Alkaloids↗
PubMed2001

Association between inflammation and changes in residual renal function and peritoneal transport rate during the first year of dialysis.

BACKGROUND: Peritoneal transport rate, a major determinant of peritoneal dialysis (PD) patient survival, increases in most patients starting on PD, while in other patients peritoneal transport rate may decline. Although several factors may contribute to changes in peritoneal transport rate, inflammation is known to be associated with a high peritoneal transport rate, and residual renal function (RRF), which often declines after start of PD, may also be related to inflammation. Therefore, we hypothesized that changes in peritoneal transport rate during patients' first year on PD and declining RRF may be linked with inflammation. METHODS: A total of 76 PD patients (40 males, mean age 56.8+/-14.1 years), who underwent two peritoneal equilibration tests at a mean of 0.4 months and 1 year after beginning PD, were included in the study. Based on the change in dialysate to plasma creatinine concentration ratio at 4-h dwell (D/P Cr) during first year on PD, the patients were divided into decreased or unchanged (group DUC; n=22) and increased (group I; n=54) groups. RESULTS: Initially, group I had a lower proportion of high transporters and more often high serum C-reactive protein (sCRP, > or =10 mg/l) and lower RRF compared with the DUC group. In group I, serum albumin and RRF decreased significantly and dialysate protein loss and glucose absorption increased significantly during the first year on PD. When patients were divided into two groups based on median change in RRF (1.9 ml/min), patients with a decrease in RRF >1.9 ml/min during first year on PD had a higher proportion of high sCRP, higher D/P Cr, and higher changes in D/P Cr compared to patients with a decrease in RRF < or =1.9 ml/min. Patients with elevated sCRP at one year included a higher proportion of patients who had high sCRP at the start of PD, higher increase in D/P Cr, lower serum albumin, lower RRF, and more decrease in RRF during first year on PD compared with patients having normal sCRP. RRF was inversely correlated with changes in D/P Cr during the first year on PD (r=-0.28, P=0.02). Multiple regression analysis revealed that the only factors affecting changes in D/P Cr were high sCRP and a low RRF. CONCLUSIONS: Our preliminary short-term study suggests that changes in peritoneal transport rate during patients' first year on PD may be linked with inflammation and declining residual renal function. Inflammation and residual renal function were identified as the only independent factors determining peritoneal transport rate during the first year on PD. It is possible that inflammation may cause both an increase in peritoneal transport rate and a decline in residual renal function, or that the decline in residual renal function and the increase in peritoneal transport rate may induce or aggravate inflammation. Further studies are needed to confirm these findings.

Adult↗
PubMed2005

Persistent reduction of spinal inflammation as assessed by magnetic resonance imaging in patients with ankylosing spondylitis after 2 yrs of treatment with the anti-tumour necrosis factor agent infliximab.

OBJECTIVES: Patients with ankylosing spondylitis (AS) benefit from anti-TNF therapy both on a clinical basis and as depicted by magnetic resonance imaging (MRI). It is not known whether spinal inflammation remains suppressed over time. Our objective was to assess spinal inflammation by MRI in AS patients after 2 yr of continuous infliximab treatment. METHODS: Twenty patients with active AS were examined by MRI at baseline, after 3 months (end of placebo-controlled-phase) and after 2 yr of continuous infliximab therapy (5 mg/kg/6 weeks). T1 pre- and post-gadolinium (T1/gadolinium-diethylenetriamine-pentaacetic acid) and short tau inversion recovery (STIR) MRI sequences were performed and read by one blinded reader using the ASspiMRI score. RESULTS: Spinal inflammation, detected by MRI in all patients at baseline, decreased after 3 months only in the infliximab group in both MRI sequences. Persistent improvement of spinal inflammation was seen after 2 yr by scoring STIR sequences, with a mean score of 4.6 +/- 5.9 vs 15.2 +/- 13.2 at baseline (P = 0.01). On an individual level, inflammatory spinal lesions decreased from 6.7 +/- 5.0 per patient at baseline to 2.2 +/- 1.8 after 2 yr (P = 0.003). Improvement in spinal inflammation was found in all patients by both MRI sequences. Only a minor degree but some spinal inflammation was still present after 2 yrs. CONCLUSION: Spinal inflammation in MRI was persistently reduced in all patients constantly treated with infliximab, but it was not completely eradicated. Disease activity parameters did not directly correlate with MRI, but both pointed in the same direction. Both types of information may be useful for the definition of response to anti-TNF therapy.

Adult↗
PubMed2004

Neurogenic painful inflammation.

PURPOSE OF REVIEW: Neurogenic inflammation results from the release of neuropeptides from peripheral nerve terminals. This secretion can be induced by two mechanisms: activation of afferent sensory nerves (e.g. by disease processes or experimentally by electrical stimulation) or activation of receptors expressed on peripheral nerve terminals. While the role of these mechanisms in the regulation of inflammation is well described, its significance for the generation of pain is much less clear and will be examined in this review. RECENT FINDINGS: Activation of two receptors on peripheral sensory neurons (i.e. transient receptor potential vanilloid-1 channel and proteinase activated receptor-2) has been shown to induce neurogenic inflammation. Interference with this activation can ameliorate pain, but it remains uncertain whether this effect is indeed mediated by blockage of neurogenic inflammation. Two human diseases (complex regional pain syndrome and migraine) are believed to result from aberrant neuronal activation. In complex regional pain syndrome, studies in human patients and in a recently established animal model do not support a role for neurogenic inflammation in pain. In migraine, antagonists to the receptor for calcitonin gene related peptide ameliorated headache and could be the first conclusive evidence for the role of neurogenic inflammation in the generation of pain. Lastly, spinal mechanisms also appear to regulate immune cell recruitment to a peripheral site and seem to interfere with antinociception. SUMMARY: While considerable experimental and clinical evidence supports the existence of neurogenic inflammation, it is less clear whether this process plays an important role in the generation of pain.

Journal Article↗
PubMedDate not supplied

Septal lines in pleural inflammation: multidetector computed tomography findings in 30 patients.

OBJECTIVE: The aim of the study was to evaluate the interstitial changes adjacent to pleural inflammation on multidetector computed tomography. METHODS: The multidetector computed tomography scans of 30 patients with pleural inflammation were retrospectively and blindly evaluated by 2 observers. A control group of 7 patients with documented fibrothorax was also included. The number, appearance, thickness, and extent of septal lines were analyzed. RESULTS: More than 10 septal lines immediately adjacent to the abnormal pleura were seen in 22 of the 30 patients with pleural inflammation and 2 of the 7 patients with fibrothorax (P<0.01). Septal lines that are more than 1 mm thick were seen in 13 of the 30 patients with acute inflammation and none of the patients with fibrothorax (P<0.01). Differences between focal and diffuse pleural inflammation included 10 cm or greater craniocaudal extent and more smooth septal lines with diffuse pleural inflammation. CONCLUSIONS: Pleural inflammation is associated with increased number and thickening of septal lines in the immediately adjacent lung parenchyma.

Adult↗
PubMed1995

Effect of Misoprostol on Acute and Chronic Inflammation.

Prostaglandins and their fatty acid precursors are important to regulation of cell function, and immune and inflammatory responses. Prostaglandin E compounds in particular have been shown to reduce inflammation and tissue injury. We examined the ability of misoprostol, the orally active analog of Prostaglandin E1, to influence inflammation in two animal models. In the subcutaneous air pouch model, acute inflammation was induced by tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). Misoprostol reduced pouch leukocyte counts in a dose dependent manner (33--49% v control), but did not alter fluid accumulation. The non-steroidal antiinflammatory agent, diclofenac, also reduced leukocyte counts in a dose dependent manner (28--66%) without affecting pouch fluid volume. Low dose misoprostol and low dose diclofenac used together reduced leukocyte counts by 39%, suggesting an advantageous snyergy in suppression of acute inflammation. Collagen induced arthritis (CIA) is a model of chronic inflammation. Misoprostol had no effect on the severity or course of CIA. Diclofenac reduced significantly all indices of inflammation tested, including joint swelling, number of affected joints and ability to walk. Misoprostol interfered with the antiinflammatory effect of diclofenac when the two compounds were administered together in the CIA model. These studies suggest that Misoprostol suppresses neutrophil mediated acute inflammation.

Journal Article↗
PubMed2000

Airway inflammation and remodeling in asthma.

An important advance in our understanding of the pathophysiology of asthma has been the discovery that airway inflammation is not confined to severe asthma but also characterizes mild and moderate asthma. Inflammation in asthma may be the result of a peculiar type of lymphocytic inflammation whereby Th2 lymphocytes secrete cytokines that orchestrate cellular inflammation and promote airway hyperresponsiveness. The term "airway remodeling" in asthma refers to structural changes that occur in conjunction with, or because of, chronic airway inflammation. Airway remodeling results in alterations in the airway epithelium, lamina propria, and submucosa, leading to thickening of the airway wall. The consequences of airway remodeling in asthma may include incompletely reversible airway narrowing, bronchial hyperresponsivenesss, airway edema, and mucus hypersecretion. Airway remodeling in asthma thus may predispose persons with asthma to asthma exacerbations and even death from airway obstruction caused by smooth muscle contraction, airway edema, and mucus plugging. Although much has been learned in the past 25 years about the pathophysiology of airway inflammation and airway remodeling in asthma, important questions remain about the relation between airway inflammation and remodeling, the natural history of airway remodeling, and the effects of current asthma treatments on remodeled airways.

Airway Obstruction↗
PubMed2005

Propionibacterium acnes associated with inflammation in radical prostatectomy specimens: a possible link to cancer evolution?

PURPOSE: Inflammation is commonly observed in the prostate gland and has been implicated in the development of prostate cancer. The etiology of prostatic inflammation is unknown. However, the involvement of a carcinogenic infectious agent has been suggested. MATERIALS AND METHODS: Prostatic tissue from 34 consecutive patients with prostate cancer was cultured to detect the presence of bacterial agents. Prostatic inflammation was assessed by histological examination of wholemount tissue sections. RESULTS: The predominant microorganism detected was Propionibacterium acnes, found in 35% of prostate samples. A significantly higher degree of prostatic inflammation was observed in cases culture positive for P. acnes (p =0.007). P. acnes was separated into 3 groups based on cell surface properties, phenotype and genetic grouping. All skin control isolates were classified as group 1 whereas most prostatic isolates were classified as groups 2 and 3. CONCLUSIONS: P. acnes has been isolated from prostatic tissues in men who underwent radical prostatectomy for localized cancer and has been shown to be positively associated with prostatic inflammation. This inflammation may then be linked to the evolution of carcinoma. Furthermore, organisms infecting these patients with prostate cancer differ genetically and phenotypically from the commonly identified cutaneous P. acnes isolates, suggesting that specific subtypes may be involved in development of prostatic inflammation.

Bacteriological Techniques↗
PubMed2005

Colorectal inflammation is well predicted by fecal calprotectin in children with gastrointestinal symptoms.

OBJECTIVES: The protein calprotectin is mainly derived from neutrophils. Increased fecal excretion of calprotectin has been reported in inflammatory bowel disease. The recommended cut-off level in adults (<50 microg/g feces) seems to be applicable in children aged 4 to 17 years. The aim of this study was to evaluate the use of fecal calprotectin to detect colorectal inflammation in children with gastrointestinal symptoms. METHODS: We obtained stool samples on thirty-six children with gastrointestinal symptoms and suspected inflammation of the colon before they underwent colonoscopy. The samples were examined with an improved fecal calprotectin enzyme-linked immunosorbent assay method (Calprest, Eurospital). The results were correlated with the histopathologic findings in the colon. RESULTS: In children with colorectal inflammation (n = 22) the median fecal calprotectin concentration was 349 microg/g (range, 15.4-1860 microg/g). The most common diagnosis in this group was inflammatory bowel disease. Median fecal calprotectin was 16.5 microg/g (range, 5.0-65 microg/g) in children with no inflammation (n = 14). When <50 microg/g was used as upper reference limit the fecal calprotectin test had a sensitivity of 95%, specificity 93%, positive predictive value 95% and negative predictive value 93% to detect colorectal inflammation. CONCLUSIONS: The improved fecal calprotectin enzyme-linked immunosorbent assay is a simple test with potential use in children. Increased fecal calprotectin strongly predicted the presence of colorectal inflammation in children with gastrointestinal symptoms. Fecal calprotectin can be used to select patients who should undergo diagnostic colonoscopy for investigation of colorectal inflammation, including inflammatory bowel disease.

Adolescent↗