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Inflammation Scores (inflammation + score)
Selected AbstractsScoring Total Inflammation Is Superior to the Current Banff Inflammation Score in Predicting Outcome and the Degree of Molecular Disturbance in Renal AllograftsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2009M. Mengel Emerging molecular analysis can be used as an objective and independent assessment of histopathological scoring systems. We compared the existing Banff i-score to the total inflammation (total i-) score for assessing the molecular phenotype in 129 renal allograft biopsies for cause. The total i-score showed stronger correlations with microarray-based gene sets representing major biological processes during allograft rejection. Receiver operating characteristic curves showed that total-i was superior (areas under the curves 0.85 vs. 0.73 for Banff i-score, p = 0.012) at assessing an abnormal cytotoxic T-cell burden, because it identified molecular disturbances in biopsies with advanced scarring. The total-i score was also a better predictor of graft survival than the Banff i-score and essentially all current diagnostic Banff categories. The exception was antibody-mediated rejection which is able to predict graft loss with greater specificity (96%) but at low sensitivity (38%) due to the fact that it only applies to cases with this diagnosis. The total i-score is able to achieve moderate sensitivities (60,80%) with losses in specificity (60,80%) across the whole population. Thus, the total i-score is superior to the current Banff i-score and most diagnostic Banff categories in predicting outcome and assessing the molecular phenotype of renal allografts. [source] Antiviral maintenance treatment with interferon and ribavirin for recurrent hepatitis C after liver transplantation: Pilot studyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2007Arno Kornberg Abstract Background:, The aim of this pilot study was to evaluate efficacy of a long-term antiviral maintenance therapy (AMT) with interferon-,2b and ribavirin in liver transplant recipients with recurrent hepatitis C. Methods:, Twenty-one patients with recurrent hepatitis C after liver transplantation received AMT with interferon and ribavirin, following 12 months of a basic antiviral combination treatment. Allograft function, viremia loads and allograft morphology were evaluated continuously. Results:, After 12 months of basic antiviral therapy, 14 patients (66.6%) had achieved initial clearance of viremia levels, and 17 recipients (81%) demonstrated normalization of allograft function, respectively. Inflammation score declined significantly (6.0 vs 3.9; P = 0.002), while stage of fibrosis remained unchanged. In virological responders maintenance therapy led to further regression of inflammation score (4.0 at baseline vs 3.1 at 24 months AMT) and fibrosis score (1.6 at baseline vs 1.1 at 24 months AMT). Despite persistence of viremia levels, continued antiviral therapy prevented progression to severe allograft inflammation in virological non-responders. Hematologic adverse effects resulted in treatment discontinuation in seven patients (33.3%). Conclusion:, Long-term AMT, if tolerable, might be an effective approach for preventing progression to severe allograft fibrosis and thereby improving long-term survival in liver transplant recipients with recurrent hepatitis C. [source] Is leptin a predictive factor in the end of therapy response in chronic hepatitis B?PEDIATRICS INTERNATIONAL, Issue 4 2005Mukadder Ayle Selimo}lu Abstract, Background:,The purpose of this study was to determine the leptin levels in children with chronic hepatitis B virus (HBV) infection, and to evaluate the effect of serum leptin levels on the end of therapy response (ETR). It is known that leptin stimulates T-cell immunity and so T-cell mediated immune response is critical in the outcome of chronic HBV infection. Methods:,Leptin levels in children with chronic HBV infection were investigated and its effects on the ETR in 24 children who were treated with interferon-, and lamivudine combination therapy were evaluated. Results:,The mean leptin level of the patients was higher than that of healthy children (P = 0.034). Of the patients, seven (29.2%) had ETR. The mean hepatic activity index and portal inflammation score were higher, the HBV DNA was lower, and the leptin level was similar in children with ETR when compared to others (P = 0.017, P = 0.04, P = 0.007, P = 0.34, respectively). HBV DNA and the fibrosis score were positively correlated (P = 0.016). Conclusion:,Although the higher leptin value observed in children with ETR was not statistically significant, because of close interactions between leptin, cytokines and lymphocytes, it is thought that leptin should be investigated as a predictive factor of ETR in further studies. [source] Association between blood flow and inflammatory state in a T-cell transfer model of inflammatory bowel disease in miceINFLAMMATORY BOWEL DISEASES, Issue 5 2010Norman R. Harris PhD Abstract Background: Adoptive transfer of naive T-lymphocyte subsets into lymphopenic mice initiates chronic gut inflammation that mimics several aspects of inflammatory bowel disease (IBD). Patients with IBD can have profound alterations in intestinal blood flow, but whether the same is true in the T-cell transfer model has yet to be determined. Methods: In the current study, chronic intestinal inflammation was induced in recombinase-activating gene-1-deficient (RAG,/,) mice by adoptive transfer of CD4+ T-lymphocytes obtained from interleukin-10 deficient (IL-10,/,) mice. Results: Four weeks later, widespread colonic inflammation was observed in the reconstituted recipients, in contrast to 2 control sets of mice injected with a different subset of lymphocytes or with vehicle alone. We observed that the resulting pathology induced in the reconstituted RAG,/, mice was divided distinctly into 2 subsets: 1 with blood flow near normal with very high inflammation scores, and the other with severely attenuated blood flow but with much lower signs of inflammation. Colonic and ileal blood flow rates in the latter subset of CD4+ mice averaged only ,30% compared to the mice with higher inflammation scores. The lower blood flow rates were associated with greatly reduced red blood cell concentrations in the tissue, suggesting a possible loss of vascular density. Conclusions: In this model of chronic intestinal inflammation, mild inflammation was associated with significant decreases in blood flow. Inflamm Bowel Dis 2009 [source] Dextran sodium sulfate strongly promotes colorectal carcinogenesis in ApcMin/+ mice: Inflammatory stimuli by dextran sodium sulfate results in development of multiple colonic neoplasmsINTERNATIONAL JOURNAL OF CANCER, Issue 1 2006Takuji Tanaka Abstract The mouse model for familial adenomatous polyposis, ApcMin/+ mouse, contains a truncating mutation in the Apc gene and spontaneously develops numerous adenomas in the small intestine but few in the large bowel. Our study investigated whether dextran sodium sulfate (DSS) treatment promotes the development of colonic neoplasms in ApcMin/+ mice. ApcMin/+ and Apc+/+ mice of both sexes were exposed to 2% dextran sodium sulfate in drinking water for 7 days, followed by no further treatment for 4 weeks. Immunohistochemistry for cyclooxygenase-2, inducible nitric oxide synthase, ,-catenin, p53, and nitrotyrosine, and mutations of ,- catenin and K- ras and loss of wild-type allele of the Apc gene in the colonic lesions were examined. Sequential observation of female ApcMin/+ mice that received DSS was also performed up to week 5. At week 5, numerous colonic neoplasms developed in male and female ApcMin/+ mice but did not develop in Apc+/+ mice. Adenocarcinomas developed in ApcMin/+ mice that received DSS showed loss of heterozygosity of Apc and no mutations in the ,- catenin and K- ras genes. The treatment also significantly increased the number of small intestinal polyps. Sequential observation revealed increase in the incidences of colonic neoplasms and dysplastic crypts in female ApcMin/+ mice given DSS. DSS treatment increased inflammation scores, associated with high intensity staining of ,-catenin, cyclooxygenase-2, inducible nitric oxide synthase and nitrotyrosine. Interestingly, strong nuclear staining of p53 was specifically observed in colonic lesions of ApcMin/+ mice treated with DSS. Our results suggest a strong promotion effect of DSS in the intestinal carcinogenesis of ApcMin/+ mice. The findings also suggest that strong oxidative/nitrosative stress caused by DSS-induced inflammation may contribute to the colonic neoplasms development. © 2005 Wiley-Liss, Inc. [source] Periodontal attachment loss over 14 years in cleft lip, alveolus and palate (CLAP, CL, CP) subjects not enrolled in a supportive periodontal therapy programJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 9 2003Giovanni E. Salvi Abstract Objectives: (i) To assess the overall and (ii) cleft-associated rate of periodontal disease (PD) progression in subjects with cleft lip, alveolus and palate (CLAP) and (iii) to compare these rates with those of subjects with cleft lip (CL) and cleft palate (CP). Material and methods: Twenty-six subjects not enrolled in a supportive periodontal therapy (SPT) program were examined in 1979, 1987 and 1993. PD progression was assessed as increase in pocket probing depth (PPD in mm) and probing attachment loss (PAL in mm). Results: Extensive plaque accumulation and high frequencies of gingival units bleeding on probing were observed at all three examinations. A statistically significant increase in mean PPD of 0.57±0.21 mm (SD) in both groups as well as a statistically significant loss of PAL of 1.85±0.23 mm (SD) in the CLAP group and of 1.72±0.21 mm (SD) in the CL/CP group occurred over the observation period (p<0.05). In subjects with CLAP, statistically significant increases in PPD and loss of PAL were recorded over time at sites adjacent to the cleft as well as at control sites (p<0.05). Over 14 years, however, PPD increased 1.72±1.08 mm (SD) at cleft sites versus 0.72±1.14 mm (SD) at control sites (p<0.05), and PAL amounted to 3.19±1.35 mm (SD) at cleft sites versus 2.41±1.52 mm (SD) at control sites (p<0.05). Conclusion: Both the CLAP and the CL/CP subjects are at high risk for PD progression if no SPT program is provided. This also suggests that alveolar cleft sites in subjects with high plaque and gingival inflammation scores underwent more periodontal tissue destruction than control sites over a 14-year period. Zusammenfassung Ziele: 1. Beurteilung der gesamten und 2. der mit der Spalte assoziierten Progressionsrate der Parodontalerkrankung (PD) bei Patienten mit Lippen-Kiefer-Gaumenspalten (CLAP) und 3. der Vergleich dieser Progressionsraten mit denen von Patienten mit Lippenspalten (CL) sowie Gaumenspalten (CP). Material und Methoden: 26 Patienten, die nicht an einem SPT-Programm teilnahmen wurden in 1979, 1987 und 1993 untersucht. Die PD-Progression wurde über die Zunahme der Sondierungstiefe (PPD in mm) und den klinischen Attachmentverlust (PAL in mm) beurteilt. Ergebnisse: Bei allen drei Untersuchungszeitpunkten wurde eine ausgedehnte Plaqueakkumulation und eine große Häufigkeit von Gingivabereichen, die bei Sondierung bluteten beobachtet. Während der Beobachtungsperiode fand in beiden Gruppen ein statistisch signifikanter Anstieg der mittleren PPD von 0.57±0.21 mm (SD) als auch ein statistisch signifikanter Attachmentverlust von 1.85±0.23 mm (SD) in der CLAP-Gruppe sowie von 1.72±0.21 mm (SD) in der CL/CP-Gruppe statt (p<0.05). Bei den Patienten mit CLAP wurde im Laufe der Zeit sowohl an den Parodontien neben der Spalte als auch an den Kontrollstellen (p<0.05) ein statistisch signifikanter Anstieg der PPD und Attachmentverlust registriert. Während der 14 Jahre jedoch nahm die PPD an Stellen mit Spalte um 1.72±1.08 mm (SD) zu im Gegensatz zu den Kontrollstellen (p<0.05) wo dieser Wert 0.72±1.14 mm (SD) betrug. Für den Attachmentverlust lag dieser Wert bei 3.19±1.35 mm (SD) an den Stellen mit Spalte im Gegensatz zu den Kontrollstellen (p<0.05) mit 2.41±1.52 mm (SD). Schlussfolgerung: Wenn keine parodontale Erhaltungstherapie zur Verfügung gestellt wird haben beide Personen, die mit CLAP und die mit CL/CP ein hohes Risiko hinsichtlich der Parodontitisprogression. Dies läßt annehmen, dass bei Personen mit viel Plaque und ausgeprägter Entzündung der Gingiva, die Stellen mit Kieferspalten während einer 14-jährigen Zeitperiode eine stärkere Zerstörung der parodontalen Gewebe erfahren als die Kontrollstellen. Résumé Les buts de cette étude ont été de suivre la progression du taux de la maladie parodontale associée au bec de lièvre (CLAP) et de comparer ces taux avec ceux de sujets ayant lèvre fendue (CL) et palais fendu (CP). Vingt-six sujets non-soumis à un programme parodontal de maintien (SPT) ont été examinés en 1979, 1987 et 1993. La progression PD a été enregistrée telle une augmentation de la profondeur au sondage (PPD en mm) et une perte d'attache au sondage (PAL en mm). Une énorme accumulation de plaque dentaire et de très hautes fréquences dans les nombres d'unités gingivales avec saignement au sondage ont été observées lors des trois examens. Une augmentation statistiquement significative dans la moyenne PPD de 0.57±0.21 mm (SD) dans les deux groupes ainsi qu'une perte significative de PAL de 1.85±0.23 mm (SD) dans le groupe CLAP et de 1.72±0.21 mm (SD) dans le groupe CL/CP apparaîssaient durant cette période d'observation (p<0.05). Chez les sujets avec CLAP, les augmentations statistiquement significatives de PPD et la perte de PAL ont été enregistrées avec le temps sur les sites adjacents au bec de lièvre ainsi qu'au niveau des sites contrôles (p<0.05). Sur les quatorze années, cependant, PPD augmentait de 1.72±1.08 mm (SD) au niveau des sites bec de lièvre vs 0.72±1.14 mm (SD) au niveau des contrôles (p<0.05), et PAL s'élevait à 3.19±1.35 mm (SD) au niveau des sites bec de lièvre vs 2.41±1.52 mm au niveau des contrôles (p<0.05). Tant les sujets CLAP que les CL/CP étaient à haut risque pour la progression PD si un programme SPT n'était pas suivi. Ceci suggère également que les sites alvéolaires associés au bec de lièvre avec des scores de plaque et de gingivite importants s'accompagnaient de plus de destruction que les sites contrôles sur une période de quatorze années. [source] Promoter hypomethylation of protease-activated receptor 2 associated with carcinogenesis in the stomachJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2007Tomiyasu Arisawa Abstract Background and Aim:, Trypsin acting at protease-activated receptor 2 (PAR2) contributes to a progression of malignant tumors. An abnormal DNA methylation has been recognized as an important molecular mechanism for the genesis of various types of cancers. We attempted to clarify the relationship between the promoter methylation of PAR2 and gastric cancer. Method:, We estimated the methylation of the PAR2 promoter in both antral non-cancerous mucosa and cancer lesions in 94 patients with gastric cancer. We employed a methylation-specific PCR method. Results:, Regarding the methylation ratio (MR) of antral-non-cancerous mucosa, no significant difference was despite among gender, age and Helicobacter pylori infection status, whereas MR increased rising inflammation scores. The MR of cancer lesions was significantly lower than that of antral non-cancerous mucosa. This finding was not dependent on tumor staging, but also histological classification. In venous invasion, lymph node metastasis, or peritoneal dissemination negative cases, this significant lower MR was also seen. Conclusion:, The promoter methylation of PAR2 seems to be increased with a progression of chronic inflammation and has an inhibitory effect on carcinogenesis of the stomach. [source] Nitric Oxide-Mediated Intestinal Injury Is Required for Alcohol-Induced Gut Leakiness and Liver DamageALCOHOLISM, Issue 7 2009Yueming Tang Background:, Alcoholic liver disease (ALD) requires endotoxemia and is commonly associated with intestinal barrier leakiness. Using monolayers of intestinal epithelial cells as an in vitro barrier model, we showed that ethanol-induced intestinal barrier disruption is mediated by inducible nitric oxide synthase (iNOS) upregulation, nitric oxide (NO) overproduction, and oxidation/nitration of cytoskeletal proteins. We hypothesized that iNOS inhibitors [NG-nitro- l -arginine methyl ester (l -NAME), l -N6 -(1-iminoethyl)-lysine (l -NIL)] in vivo will inhibit the above cascade and liver injury in an animal model of alcoholic steatohepatitis (ASH). Methods:, Male Sprague,Dawley rats were gavaged daily with alcohol (6 g/kg/d) or dextrose for 10 weeks ± l -NAME, l -NIL, or vehicle. Systemic and intestinal NO levels were measured by nitrites and nitrates in urine and tissue samples, oxidative damage to the intestinal mucosa by protein carbonyl and nitrotyrosine, intestinal permeability by urinary sugar tests, and liver injury by histological inflammation scores, liver fat, and myeloperoxidase activity. Results:, Alcohol caused tissue oxidation, gut leakiness, endotoxemia, and ASH. l -NIL and l -NAME, but not the d -enantiomers, attenuated all steps in the alcohol-induced cascade including NO overproduction, oxidative tissue damage, gut leakiness, endotoxemia, hepatic inflammation, and liver injury. Conclusions:, The mechanism we reported for alcohol-induced intestinal barrier disruption in vitro , NO overproduction, oxidative tissue damage, leaky gut, endotoxemia, and liver injury , appears to be relevant in vivo in an animal model of alcohol-induced liver injury. That iNOS inhibitors attenuated all steps of this cascade suggests that prevention of this cascade in alcoholics will protect the liver against the injurious effects of chronic alcohol and that iNOS may be a useful target for prevention of ALD. [source] Clinical significance of TT virus infection in children with chronic hepatitis BPEDIATRICS INTERNATIONAL, Issue 3 2005Erhun Kasirga AbstractBackground:,The pathogenic role of TT virus (TTV) is not clear in patients with chronic hepatitis B. The aims of the present study were to determine the frequency of TTV positivity in serum and saliva samples and the possible role of TTV in children with chronic hepatitis B. Methods:,Sera and saliva from 29 healthy children and 25 children with chronic hepatitis B were tested for TTV-DNA by means of real-time polymerase chain reaction (PCR). Results:,Fifty-two percent (13/25) of the serum samples and 32% (8/25) of the saliva samples were positive for TTV-DNA in children with chronic hepatitis B. In healthy non-transfused children, TTV-DNA was detected in 58% (17/29) of the serum samples and 41% (12/29) of the saliva samples. Six (46%) of 13 children with chronic hepatitis and 10 (59%) of 17 healthy children had TTV-DNA positivity both in serum and saliva samples. Two serum samples were negative for TTV-DNA while the saliva samples were positive for TTV-DNA in chronic hepatitis B and control groups. Mean age, sex, serum alanine aminotransferase levels, hepatitis B virus (HBV)-DNA values were similar in TTV-positive and -negative children with chronic hepatitis B. However, total histologic activity index (HAI), periportal necrosis and portal inflammation scores were significantly higher in children with HBV-DNA and TTV-DNA viremia (P = 0.013, P = 0.008, P = 0.015, respectively). Conclusions:,Because total HAI, periportal necrosis and portal inflammation scores were higher in children with TTV coinfection, TTV infection may contribute to the progression of liver damage in children with chronic hepatitis B. [source] Effects of pneumoperitoneum with or without colostomy on rat colonic anastomotic healingANZ JOURNAL OF SURGERY, Issue 3 2004Hedef Özgün Background: Elevated intra-abdominal pressure and colostomy have adverse effects on colonic anastomoses. The aim of the present study was to investigate the effects of laparoscopic colon surgery with and without diverting colostomy on healing of colonic anastomoses in an experimental model. Methods: Thirty-six male rats were divided into three equal groups: group 1, control (colonic anastomosis and anaesthesia for 180 min only); group 2, 180 min pneumoperitoneum and colonic anastomosis; and group 3, similar to group 2 with a proximal colostomy. On day 7, bursting pressures, tissue hydroxyproline and nitric oxide concentrations and histopathological inflammation scores were determined and compared. Results: Mean bursting pressures were higher in the control group than the two pneumoperitoneum groups (P = 0.0003). Mean tissue hydroxyproline concentrations showed no difference (P > 0.05). Mean tissue nitric oxide concentrations were significantly increased in the control group (P = 0.0013). Histopathological scores demonstrated increased inflammatory response in group 3 compared to the controls (P = 0.0009). Conclusion: Pneumoperitoneum delays collagen maturation and impairs anastomotic strength in the colon. Following pneumoperitoneum, performance of a diverting loop colostomy to protect the anastomosis will not have additional detrimental effects on anastomotic healing. [source] Association of interleukin-18 expression with enhanced levels of both interleukin-1, and tumor necrosis factor , in knee synovial tissue of patients with rheumatoid arthritisARTHRITIS & RHEUMATISM, Issue 2 2003Leo A. B. Joosten Objective To examine the expression patterns of interkeukin-18 (IL-18) in synovial biopsy tissue of patients with rheumatoid arthritis (RA), and to determine whether expression of this primary cytokine is related to the expression of other cytokines and adhesion molecules and related to the degree of joint inflammation. Methods Biopsy specimens of knee synovial tissue either without synovitis (n = 6) or with moderate or severe synovitis (n = 11 and n = 12, respectively) were obtained from 29 patients with active RA. Paraffin-embedded, snap-frozen sections were used for immunohistochemical detection of IL-18, tumor necrosis factor , (TNF,), IL-1,, IL-12, and IL-17. Furthermore, adhesion molecules, such as intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin, and cell markers CD3, CD14, and CD68 were stained. Results IL-18 staining was detectable in 80% of the RA patients, in both the lining and sublining of the knee synovial tissue. IL-18 expression in the synovial tissue was strongly correlated with the expression of IL-1, (in the sublining r = 0.72, in the lining r = 0.71; both P < 0.0001) and TNF, (in the sublining r = 0.59, P < 0.0007, and in the lining r = 0.68, P < 0.0001). In addition, IL-18 expression in the sublining correlated with macrophage infiltration (r = 0.64, P < 0.0007) and microscopic inflammation scores (r = 0.78, P < 0.0001), and with the acute-phase reaction as measured by the erythrocyte sedimentation rate (r = 0.61, P < 0.0004). Interestingly, RA synovial tissue that coexpressed IL-18 and IL-12 demonstrated enhanced levels of the Th1-associated cytokine IL-17. Conclusion Our results show that expression of IL-18 is associated with that of IL-1, and TNF, and with local inflammation in the synovial tissue of patients with RA. In addition, synovial IL-18 expression correlates with the acute-phase response. These data indicate that IL-18 is a primary proinflammatory cytokine in RA that drives the local production of IL-1, and TNF,. [source] Insulin-like growth factor 1-coated sutures improve anastomotic healing in an experimental model of colitis,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 2 2010E. Rijcken Background: Exogenously applied insulin-like growth factor (rhIGF-1) may improve normal intestinal healing. This study examined the effect of rhIGF-1-coated sutures on anastomotic healing in experimental colitis. Methods: Acute colitis was induced in rats by dextran sodium sulphate (DSS). Inflammation was assessed by clinical Disease Activity Index (DAI), myeloperoxidase (MPO) measurement and histological examination. A distal colonic anastomosis was performed using sutures coated with rhIGF-1 dissolved in poly(D,L -lactide) (PDLLA) under general anaesthetic. Anastomotic healing was evaluated histologically, and by hydroxyproline measurement and bursting parameters after 1, 3 and 7 days, and compared with healthy, DSS and DSS + PDLLA controls. Results: DAI, MPO and histological inflammation scores were significantly increased in all animals treated with DSS. Bursting occurred less often within the anastomotic line on day 3 in the IGF group than in DSS controls (three versus eight of ten). On day 7, the IGF group had significantly increased histological healing scores (mean(s.e.m.) 12·5(0·7) versus 9·2(0·8) (P < 0·050)) and hydroxyproline content (4·6(0·3) versus 3·6(0·1) mg/g tissue; P < 0·050) compared with DSS controls. Conclusion: IGF-1-coated sutures improve important aspects of anastomotic healing in rats with experimental colitis. Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Effect of proteolytic activity of Epicoccum purpurascens major allergen, Epi p 1 in allergic inflammationCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2008N. Kukreja Summary Enzymes play an important role in inducing airway inflammation, but knowledge is limited to few proteins. This study was carried out to assess the role of Epi p 1, a serine protease of Epicoccum purpurascens, in inducing allergy and inflammation in a murine model. Balb/c mice were sensitized with Epi p 1 active protease (EAP) or Epicoccum extract. Subsequently, Epi p 1 sensitized mice were boosted on day 14 with EAP or inactivated protease (EIAP). Three intranasal challenges were given and mice were killed to obtain blood, bronchoalveolar lavage fluid (BALF), spleen and lung tissues. Cellular airways infiltration, immunoglobulin E (Ig)E titres and cytokine levels in BALF and splenocyte culture supernatant were compared. Mice immunized with EAP had higher Epi p 1-specific serum IgE and IgG1 than EIAP immunized mice (P < 0·01). There was a twofold difference in the number of eosinophils in BALF of EAP mice and EIAP mice (P < 0·01). A similar trend was recorded for eosinophil peroxidase activity (P < 0·05), indicating the role of proteolytic activity in inducing inflammation. Further, lung histology revealed increased leucocyte infiltration and airway narrowing, with higher inflammation scores in the EAP group than in the EIAP group. The lungs of EAP mice showed increased mucus and goblet cell metaplasia. Interleukin (IL)-4 and IL-5 levels were higher in BALF and splenocyte culture supernatant of EAP mice than in EIAP mice (P < 0·05), indicating a T helper 2 response. Proteolytic activity of Epi p 1 plays an important role in inducing allergic inflammation. The enzymatically inactive form may be investigated for immunotherapy. [source] | ||||||||||