Increased expression of CD11a and CD45 on leukocytes and decreased serum TNF-alpha levels in patients with isolated coronary artery ectasia.

BACKGROUND: Aneurysm and ectasia have similar pathological pathways. TH2-associated cytokines are stimulated by aneurismal tissue and correspondingly lack mediators associated with TH1 response. In this study, we measured serum TNF-alpha and IL-18 levels which are strong TH1 stimulating cytokines and also investigated the expression of CD11a, CD11b, CD18 adhesion molecules and CD45 on leukocytes in patients with coronary artery ectasia (CAE) and controls with normal coronary arteries (NCA). METHODS: A total of 51 isolated CAE patients free of atherosclerosis and 37 NCA controls were included in the study. Cell counts and cell surface adhesion molecules were detected by flow cytometry using fluorescence conjugated monoclonal antibodies. Serum TNF-alpha, IL-18 levels, and Chlamydophila pneumoniae IgG and IgM and Helicobacter pylori IgG levels were detected by ELISA methods. RESULTS: The mean fluorescence intensities of CD11a on granulocytes, monocytes and lymphocytes and CD45 on granulocytes and monocytes were significantly higher in CAE patients when compared with the NCA group (10.01 +/- 8.2 vs. 6.79 +/- 3.49, p = 0.04; 15.84 +/- 8.64 vs. 11.56 +/- 5.27, p = 0.016; 29.58 +/- 9.98 vs. 20.02 +/- 9.66, p < 0.001; 7.58 +/- 5.03 vs. 4.57 +/- 3.05, p = 0.003; 18.73 +/- 1238 vs. 10.74 +/- 738, p = 0.004; respectively) detected by flow cytometry. TNF-alpha levels were significantly lower in the patient group (18.76 +/- 7.07 vs. 24.29 +/- 8.46; p < 0.001) when compared with controls. The percentage of granulocytes was higher in the CAE group when compared with the NCA group (65.52 +/- 14.91 vs. 52.28 +/- 1537; p = 0.002). Contrarily, the percentage of monocytes was higher in the control group when compared with the CAE group (18.12 +/- 15.69 vs. 934 +/- 733 p = 0.008). Among the infection markers studied, only C. pneumoniae IgG levels were significantly higher in patients when compared with controls (81.62 +/- 48.53 RU/mL vs. 63.79 +/- 33.83 RU/mL; p = 0.045). In CAE patients, TNF-alpha levels significantly correlated with mean fluorescence intensity levels of CD45+ granulocyte (0.525, p < 0.001), monocyte (0.469, p = 0.001) and lymphocytes (0376, p = 0.013). CONCLUSIONS: The decreased levels of TNF-alpha may indicate predominance of TH2 and lack of TH1 type immunity in CAE patients, similar to patients with aortic aneurysms. Increased levels of cell surface adhesion molecules in CAE are an indicator of activation of leukocytes for adherence and transmigration through the vessels for the initiation of inflammation.

The role of helper and regulatory T cells in the pathogenesis of vitiligo.

BACKGROUND: Alterations in cellular immunity, including CD4(+) T and CD8(+) T lymphocytes, have been proposed in the pathogenesis of vitiligo. There is also a proposed role for cytokines in the depigmentation observed in vitiligo. However, previous reports on the role of cytokines in the pathogenesis of vitiligo have been few in number. OBJECTIVE: The purpose of this investigation was to assess the role of the major cytokines produced by T-helper 1 and 2 cells as well as T-helper 17 and regulatory T cells in the pathogenesis of vitiligo. METHODS: Forty patients with vitiligo and 40 age- and sex-matched healthy control subjects were enrolled in the study. Serum interleukin (IL)-4, IL-6, IL-10, IL-17, interferon-gamma, tumor necrosis factor-beta, and transforming growth factor-beta levels were detected by enzyme-linked immunosorbent assay in both groups. The correlations of serum cytokine levels with age of onset, sex, duration of disease, type and activity of vitiligo, percentage of involved body area, Koebner positivity, family history, and the presence of associated autoimmune diseases were assessed. RESULTS: Serum transforming growth factor-beta levels were significantly decreased in the vitiligo group compared with the control group (P = .004). No difference was detected between the patient and control groups in mean levels of serum IL-6, IL-10, and tumor necrosis factor-beta. In the patients with vitiligo, serum IL-17 levels were positively correlated with the extent of body area involvement (rho = 0.329, P = .038). LIMITATIONS: Tissue cytokines compared with those in the peripheral blood were not measured. CONCLUSION: Although multiple factors have been implicated in the pathogenesis of vitiligo, reduced serum transforming growth factor-beta levels, as observed in patients in the current investigation, may contribute to enhanced cellular immunity. This may facilitate the occurrence of vitiligo by leading to diminished maturation of regulatory T cells, followed by impaired inhibition of inflammation.

Short-term relative antibacterial effect of octenidine dihydrochloride on the oral microflora in orthodontically treated patients.

OBJECTIVE: To evaluate the efficacy of common antiseptic mouth rinses and octenidine dihydrochloride (OCT). METHODS: The antibacterial activities of antiseptics against total and cariogenic bacteria (Streptococcus mutans and Lactobacillus species) in saliva were studied in vitro and in vivo. After unstimulated saliva was collected, one of the mouth rinse solutions was applied for 30seconds. Saliva samples were collected 15, 30, 60, and 120min later and evaluated for their bacterial count. RESULTS: OCT had a significantly greater inhibitory effect on the studied bacteria than 0.2% chlorhexidine gluconate (CHX) and 7.5% polyvinylpyrrolidone-iodine complex (PVP-I) from 15min to 120min following the application (p<0.01). The antiseptic efficacy of 0.2% CHX on total bacteria and Lactobacillus species was very similar to the efficacy observed with 7.5% PVP-I mouth solution from 15min up to 120min. Streptococcus mutans was completely inhibited by 0.15mg/ml PVP-I, 0.5mg/ml CHX, and 0.1mg/ml OCT concentrations, while Streptococcus salivarius was inhibited by 0.15mg/ml PVP-I, 2mg/ml CHX, and 0.8mg/ml OCT concentrations. Lactococcus lactis subspecies lactis was inhibited with 0.00313mg/ml OCT, 30mg/ml PVP-I, and 0.0063mg/ml CHX concentrations. CONCLUSIONS: OCT compared favorably with CHX and PVP-I in its antibacterial effects, both in vitro and in vivo (p<0.01).

The effect of Nomega-nitro-L-arginine methyl ester and L-arginine on lung injury induced by abdominal aortic occlusion-reperfusion.

PURPOSE: The aim of this study was to examine the effects of Nomega-nitro-L-arginine methyl ester (L-NAME) and L-arginine on lung injury after aortic ischemia-reperfusion (IR). METHODS: Twenty-four Wistar-Albino rats were randomized into four groups (n = 6) as follows: Control (sham laparotomy), Aortic IR (30 min ischemia and 120 min reperfusion), L-Arginine (intraperitoneal 100 mg kg(-1) live weight)+aortic IR, and L: -NAME (intraperitoneal 10 mg kg(-1) live weight)+aortic IR. In the lung specimens, the tissue levels of malondialdehyde (MDA), vascular endothelial growth factor (VEGF), and nitric oxide (NO) were measured and a histological examination was done. RESULTS: Aortic IR increased MDA, VEGF, and NO. L-Arginine further significantly increased MDA and NO, and decreased VEGF (P < 0.05 vs aortic IR). L-NAME significantly decreased MDA and NO (P < 0.05 vs L-arginine+aortic IR) and increased VEGF (P < 0.05 vs other groups). A histological examination showed the aortic IR to significantly increase (P < 0.05 vs control) while L-arginine also further increased (P > 0.05 vs aortic IR), whereas L-NAME caused a significant decrease in pulmonary leukocyte infiltration (P < 0.05 vs aortic IR). CONCLUSIONS: Our results indicate that L-arginine aggravates the lung injury induced by aortic IR, while L-NAME attenuates it.

Quantitative correlation of Helicobacter pylori stool antigen (HpSA) test with the severity of H. pylori-related gastritis.

The Helicobacter pylori (H. pylori) load in both stomach and stool and the resulting severity of gastritis are important criteria in validating the status of H. pylori infection. We aimed to assess the reliability of the H. pylori stool antigen (HpSA) test for the primary diagnosis of H. pylori infection by calculating the best cut-off value to obtain the highest sensitivity and specificity in dyspeptic patients. We also investigated the correlation of HpSA test with the severity of gastritis and H. pylori load. The H. pylori statuses of 95 patients were evaluated by the positivity of both rapid urease test and microscopic detection of H. pylori in biopsy specimens, 88 subjects of whom were H. pylori positive. The sensitivity and specificity of the HpSA test were 51.1% (45/88) and 100% (7/7), respectively, according to the manufacturer's recommended cut-off value of 0.16. However, with the best cut-off value of 0.048, calculated by receiver operator characteristics analysis, the sensitivity of the test increased to 92.0% (81/88) with the same specificity. High values of the HpSA test were correlated with high scores of corpus H. pylori load and the severity of antrum and corpus inflammation (p < 0.05). With the best cut-off value of the HpSA test, the primary diagnosis of H. pylori infection can be made with higher sensitivity and specificity. The HpSA test is a helpful tool that evaluates the severity of H. pylori infection and the degree of gastric inflammatory activity and gastric H. pylori load.

Detection of Helicobacter pylori and Chlamydia pneumoniae DNA in human coronary arteries and evaluation of the results with serologic evidence of inflammation.

OBJECTIVE: Atherosclerosis is pathologically similar to a chronic inflammatory response. Recent reports have suggested that Chlamydia pneumoniae (C. pneumoniae) and Helicobacter pylori (H. pylori) play a role in the pathogenesis of atherosclerosis but this relation has not been confirmed on an inflammatory background. METHODS: Twenty-nine consecutive patients admitted to Suleyman Demirel University Medical School Cardiovascular Surgery Department, Isparta, Turkey between May 2002 to June 2003 were included in the study and the presence of C. pneumoniae and H. pylori DNA in atherosclerotic plaques of 14 coronary endarterectomy specimens and 15 left internal mammarian artery (LIMA) specimens as control subjects were determined by polymerase chain reaction. Serologic evidence of infection and inflammatory markers were also determined in both groups. RESULTS: Two C. pneumoniae DNA cases from the plaque group (14.3%) and 4 H. pylori DNA cases; 3 from plaque (21.4%) and one from the LIMA groups (6.7%) were detected. The C-reactive protein (mg/L) were higher in DNA positive samples of C. pneumoniae (66.58) and H. pylori (21.93) compared to DNA negatives of C. pneumoniae (8.49) and H. pylori (10.98), similarly interleukin-6 (U/L) levels were higher in DNA positive samples of C. pneumoniae (42.25) and H. pylori (56.37) compared with DNA negatives of C. pneumoniae (17.52) and H. pylori (13.28), but the differences were not statistically significant. Apolipoprotein B levels were significantly higher in C. pneumoniae immunoglobulin M positive cases (0.844 g/L) compared with negatives (0.661 g/L) (p=0.004). CONCLUSION: Chronic infections modify the serum lipid profile in a way that increases the risk of atherosclerosis. The increased titers of inflammation markers in DNA positive patients support inflammation in atherosclerosis, however, the results should be reproduced in a larger cohort.

Ectasia and severe atherosclerosis: relationships with chlamydia pneumoniae, helicobacterpylori, and inflammatory markers.

To date, there has been no convincing evidence for an association between Chlamydia pneumoniae or Helicobacter pylori and ectasia. In this case-control study, we have investigated the association of H. pylori and C. pneumoniae seropositivity with ectasia, severe coronary atherosclerosis, and normal vessels, which were so classified by coronary angiography. We have also evaluated the influence of these infections on inflammatory markers such as high-sensitive C-reactive protein (hsCRP) and interleukin 6 (IL-6). Of the 796 patients undergoing coronary angiography for suspected ischemic heart disease, 244 patients were recruited. Of these, 91 had normal vessels, 88 had 3 or more obstructed vessels, and 65 had ectatic vessels without atherosclerosis. Eighty-seven atherosclerotic patients (98.9%) were positive for C. pneumoniae IgG, as were 64 ectatic patients (98.5%) and 76 controls (83.5%) (P < 0.001). Forty-two atherosclerotic patients (47.7%) were positive for C. pneumoniae IgM, as were 43 ectatic patients (66.2%) and 43 controls (47.3%) (P = 0.036). Seventy-two atherosclerotic patients (81.8%) were positive for H. pylori IgA, as were 26 ectatic patients (40.0%) and 44 controls (48.4%) (P < 0.001). High-sensitive CRP levels were significantly higher in ectatic patients (5.639 mg/L) than in controls (4.390 mg/L) (P = 0.032), and IL-6 levels were significantly higher in atherosclerotic patients (33.92 U/L) than in controls (14.01 U/L) (P < 0.001). Interleukin-6 levels were higher in H. pylori seropositive patients, and hsCRP levels were higher in C. pneumoniae seropositive patients, when compared with seronegatives. We suggest that, as in atherosclerosis, C. pneumoniae infection is related to ectasia, with raised CRP levels.

Infection with Chlamydia pneumoniae but not Helicobacter pylori is related to elevated apolipoprotein B levels.

OBJECTIVE: Results of many studies show that apolipoprotein B (apo B) is a better marker of risk of vascular disease than other lipid markers including LDL and HDL-cholesterol and triglycerides. We investigated the association between two infectious agents: C. pneumoniae and H. pylori, known to have an atherogenic effect, and apo B, to evaluate the effects of chronic infections on apo B levels. METHODS AND RESULTS: The study group consisted of 257 patients in whom diagnostic coronary angiography was performed. C. pneumoniae IgG and IgM and H. pylori IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay and apo B levels were measured by the nephelometry method. Established risk factors of atherosclerosis were recorded. Of 257 patients recruited, 104 had normal vessels, 88 had 3 or more vessels obstructed and 65 had ectatic vessels without atherosclerosis. Mean apo B concentration was significantly higher in C. pneumoniae IgG and IgM positive healthy subjects compared with C. pneumoniae negatives (0.954 vs. 0.722 and 0.973 vs. 0.851, p < 0.001 and p = 0.007, respectively). Apo B levels were significantly higher in severe atherosclerotic patients (0.985 +/- 0.234 g/l) compared with control subjects (0.892 +/- 0.244 g/l) (p = 0.008), but the difference was not significant in ectatic subjects (0.946 +/- 0.272 g/l) when compared with controls (p = 0.18). Apo B levels were higher but not statistically significant in H. pylori antibody positive cases when compared with negatives. CONCLUSIONS: Apo B levels increased with C. pneumoniae infection. This finding supports the hypothesis that lipid profiles change to atherogenic lipid profile in chronic infections.

[Case report: nosocomial Ralstonia pickettii infection in neonatal intensive care unit]. / Olgu raporu: yenidogan yogun bakim unitesinde hastane kaynakli Ralstonia pickettii enfeksiyonu.

Although Ralstonia pickettii was known as a saprophytic species, it has been isolated in nosocomial infections in recent years. In this case report, R. pickettii infection of a neonate in the neonatal intensive care unit (ICU) was presented. R. pickettii was isolated from the blood cultures of the neonate and also from the incubator and distilled water of the incubator. The isolates revealed identical biochemical and physiological characteristics. The strains were identified by conventional tests and by API ID32 GN system. There was no other newborn infected by R. pickettii in the ICU during the same period. In conclusion, R. picketti should be taken into consideration as an etiologic agent especially in ICU infections. To prevent outbreaks, sterile solutions used for patient care and other possible sources must be investigated regularly.

Gastroduodenal Helicobacter pylori infection diagnosed by Helicobacter pylori stool antigen is related to atherosclerosis.

OBJECTIVE: The causative relation between Helicobacter pylori (H. pylori) and atherosclerosis has been determined as seropositivity or determination of H. pylori from atherome plaques by molecular methods. The site of entrance and the reservoir of the bacteria in the body is still a subject of discussion. In this study Helicobacter pylori stool antigen (HpSA) which shows gastrointestinal system colonization and infection with high specificity and sensitivity was determined in atherosclerotic, ectatic and angiographically normal groups. METHODS AND RESULTS: A total of 62 patients was categorized according to diagnostic coronary angiography as 12 had normal coronary arteries, eight had one, 18 had two, and 12 had three atherosclerotic coronary arteries. Twelve patients had ectatic vessels. There were 27 (44%) HpSA positive and 35 (56%) HpSA negative patients. There was a statistically significant relation between HpSA positivity and the degree of vessel involvement in coronary artery disease (CAD) patients, essentially between the group with three vessels (83%) obstructed and the normal group (25%). Ectatic vessel group had a higher incidence (50%) of HpSA positivity compared to the control group but not enough for statistical significance. CONCLUSIONS: The results indicate that gastrointestinal system H. pylori colonization increases the risk of atherosclerosis. We may speculate that the reservoir and spread of H. pylori is via gastrointestinal tract. Studies may be performed to detect whether gastrointestinal tract H. pylori infection treatment will decrease the risk of coronary artery damage caused by H. pylori.