Helicobacter pylori infection and seasickness susceptibility among naval sailors: is there any association?

BACKGROUND: Vomiting is a very common and bothersome expression of seasickness. Previous works have shown that Helicobacter pylori infection may be related to vomiting resulting from nongastrointestinal causes, and physiological research has revealed that H. pylori may alter gastric motility. These findings, along with anecdotal case histories, led us to suspect that H. pylori infection may be related to the vomiting of seasickness. The objective of this study was to evaluate the association between H. pylori infection and seasickness susceptibility. METHODS: Participants were 90 healthy, male, naval crew members 19.5 to 25 years of age. Forty-five were susceptible to seasickness, and 45 were nonsusceptible control subjects. Quantitative analysis of IgG levels for H. pylori was performed with an enzyme-linked immunosorbent assay. RESULTS: The rate of H. pylori infection was 38% in the susceptible group, compared with 31% in the nonsusceptible group (p = 0.5). The titer of antibodies to H. pylori among case subjects was 81.2 U/mL (95% confidence interval, 11.5-151.1 U/mL), compared with 31.1 U/mL (95% confidence interval, 0.1-65.1 U/mL) for control subjects (p = 0.2). CONCLUSION: The current study does not support an association between H. pylori infection and seasickness susceptibility among sailors.

Expression of matrix metalloproteinases, sICAM-1 and IL-8 in CSF from children with meningitis.

The combined expression of the inflammatory mediators, matrix metalloproteinases (MMPs), soluble form of intracellular adhesion molecule ICAM-1 (sICAM-1) and interleukin (IL)-8, was evaluated in children infected with bacterial or viral meningitis. MMP-2 and IL-8 were detected in all CSF samples and were enhanced in both bacterial and viral infected samples, compared to those from control children. The expression of MMP-9 as well as sICAM-1 was not detected in control CSF while observed in viral infected and further elevated in bacterial infected samples. This pilot study supports a role for MMPs, IL-8 and sICAM in infectious meningitis and suggests further research to determine their possible use as biomarkers for various forms of meningeal infection as well as the use of their specific antagonists as potential therapeutic agents for central nervous system (CNS) inflammatory processes.

ELISA of anti-endomysial antibodies in the diagnosis of celiac disease: comparison with immunofluorescence assay of anti-endomysial antibodies and tissue transglutaminase antibodies.

BACKGROUND: Celiac disease is common in both children and adults. Small intestinal biopsy is mandatory for establishing a diagnosis. Anti-endomysial antibodies, detected by immunofluorescence, have a sensitivity and specificity close to 100% in the diagnosis of CD. Recently, tissue transglutaminase has been identified as the target autoantigen of antibodies against endomysium, and TTG antibodies are comparable to EMA-IMF in the diagnosis of CD. OBJECTIVE: To evaluate a new enzyme-linked immunosorbent assay kit for EMA, compared to EMA-IMF and TTG antibodies in the diagnosis of CD. METHODS: Our study population included all subjects with positive EMA-IMF who underwent intestinal biopsy (n = 21). From the same sera, TTG antibodies and EMA-ELISA were determined, and all antibody results were compared to the biopsy findings. RESULTS: EMA-IMF was able to predict biopsy findings of CD in 19 of 21 cases (90.5%). When patients with biopsy findings compatible with CD and positive EMA-IMF (n = 19) were tested for EMA-ELISA and TTG antibodies, 18 of the 19 were positive for both EMA-ELISA and TTG antibodies. A significant correlation was found between EMA-ELISA and TTG antibody titers (r = 0.74, P < 0.001). CONCLUSIONS: Our study demonstrates that EMA-ELISA is comparable to TTG antibodies in the diagnosis of CD, and supports the use of EMA-ELISA as a serologic marker for this disease.

Intravenous gamma globulin inhibits the production of matrix metalloproteinase-9 in macrophages.

BACKGROUND: Degradation of the extracellular matrix (ECM) is essential for progression and metastasis of cancer cells. The ECM-degrading enzymes, matrix metalloproteinases (MMPs), are produced mainly by intratumor monocytes/macrophages. MMPs, particularly MMP-9, are reported to be of crucial significance for both growth and tumor invasiveness. Inhibition of the expression of MMP-9 may prevent tumor development. High-dose intravenous gamma globulins (IVIG) effectively inhibit metastatic spread of tumors in mice and humans and a variety of mechanisms have been suggested to explain this effect. METHODS: We studied the effect of purified IVIG on MMP-9 secretion and mRNA expression by in vitro differentiated human monocytic cells (cell lines and peripheral blood monocytes). Zymography was employed to measure gelatinase secretion and Northern blot analysis was used to detect mRNA expression. Involvement of F(ab)(2) and Fc components in IVIG activity was also evaluated. RESULTS: IVIG dose dependently and significantly reduced the amount of secreted MMP-9 and its mRNA expression. F(ab)(2), but not Fc fragments, led to suppressed MMP-9 activity. However, competitive experiments demonstrated that Fc, but not F(ab)(2) fragments, reversed the IVIG-induced inhibitory effects. CONCLUSIONS: These results suggest that the whole IgG molecule may be needed for pertinent IVIG-induced MMP-9 down-regulation. This study points to an additional new mechanism whereby IVIG may play a beneficial role in the prevention of tumor spread in humans.

The use of a single serological marker underestimates the prevalence of celiac disease in Israel: a study of blood donors.

OBJECTIVES: Recent studies suggest that celiac disease was previously underdiagnosed. To find out whether antiendomysial antibodies underestimate the prevalence of celiac disease, we elected to use a strategy combining multiple serological markers to explore the prevalence of celiac disease in Israel and the usefulness of the various antibodies in screening for celiac disease. METHODS: Serum samples from 1571 healthy blood donors were tested. A small intestinal biopsy was offered to all patients who tested positive for either human tissue transglutaminase antibodies, an ELISA kit based on antiendomysium (EMA-ELISA), immunoglobulin A antigliadin verified by antiendomysial immunofluorescence antibodies, and to patients who were IgA deficient with elevated antigliadin IgG. RESULTS: A total of 59 subjects (3.8% of study population) were offered an intestinal biopsy based on serological findings, and 30 of 59 patients agreed to undergo intestinal biopsy (1.9% of study population). Celiac disease was diagnosed in 10 patients, establishing a prevalence of at least 1:157 in the general population (0.6%, CI = 0.3-1.1%). Using any serological marker alone would have underestimated the prevalence of celiac disease, as it was diagnosed in only two patients who tested positive for endomysial immunofluorescence antibodies (prevalence of 1:786, 0.1%, CI = 0.02-0.5%), six patients positive for tissue transglutaminase (prevalence of 1:262, 0.4%, CI = 0.1-0.9%), and seven patients positive for ELISA-EMA (prevalence of 1:224, 0.45%, CI = 0.2-0.9%). CONCLUSIONS: The prevalence of celiac disease in Israel is at least 1:157 in the general population, confirming its underdiagnosis in previous studies. The disparity between the various serological markers suggest that the use of one serological marker is insufficient for establishing the true prevalence of celiac disease.