C. Caroline Blackwell

ABO blood group, secretor state, and susceptibility to recurrent urinary tract infection in women.

ABO blood group and secretor state was determined in 319 women with recurrent urinary tract infection and compared with those of a control group of 334 women of similar age ranges. Women of blood groups B and AB who are non-secretors of blood group substances showed a significant relative risk of recurrent urinary tract infection of 3.12 (95% confidence limits, 1.49 and 6.52) in comparison with other types. This appears to be a genuine example of synergy in which absence of anti-B isohaemagglutinin and secretor substances combines to give an increased risk of recurrent urinary tract infection. Determination of blood group and secretor state may provide additional information in identifying those at risk.

Cytokine responses and sudden infant death syndrome: genetic, developmental, and environmental risk factors

Despite the success of the campaigns to reduce the risk of sudden infant death syndrome (SIDS), it still remains the major cause of postneonatal mortality. The incidence of SIDS is higher among ethnic groups in which there are also high incidences of serious infectious diseases. The risk factors for SIDS parallel those for susceptibility to infection, and recent data have provided evidence to support the mathematical model of the common bacterial toxin hypothesis. One current hypothesis for the etiology of SIDS is that the deaths are a result of overwhelming proinflammatory responses to bacterial toxins; as in inflammatory responses to sepsis, cytokines, induced by bacterial toxins, cause physiological changes leading to death. The genetic, developmental, and environmental risk factors for SIDS are reviewed in relation to colonization by potentially harmful bacteria and the inflammatory responses induced in the nonimmune infant to microorganisms or their products.

Isolation of a Cell Surface Component of Helicobacter pylori That Binds H Type 2, Lewis a , and Lewis b Antigens

BACKGROUND & AIMS Individuals of blood group O and nonsecretors of ABO blood group antigens are more susceptible to peptic ulcers. The aim of this study was to determine if blood group antigens associated with group O or secretor status are epithelial cell receptors for Helicobacter pylori. METHODS Bacterial binding and binding of monoclonal antibodies to H type 2, Lewis(a), and Lewis(b) to Kato III, buccal epithelial, and gastric mucosal cells were shown by flow cytometry. Bacterial outer membrane proteins eluted from H type 2, Lewis(a), or Lewis(b) were shown by polyacrylamide gel electrophoresis. RESULTS Kato III and human epithelial cells bound each monoclonal antibody; O cells bound more anti-H type 2 (P < 0.05). Binding indices for H. pylori correlated with those for anti-H type 2 (P < 0.005) and anti-Lewis(b) (P < 0.001) but not anti-Lewis(a). A 61-kilodalton protein was eluted from H type 2, Lewis(a), or Lewis(b). CONCLUSIONS Our results indicate that H type 2 is an important receptor for the 61-kilodalton bacterial adhesin, partly explaining increased susceptibility of individuals of blood group O to ulcers. Lewis(b) binds H. pylori more efficiently than Lewis(a). If these interactions occur in vivo, lack of Lewis(b) in mucosal fluids of nonsecretors may contribute to colonization by H. pylori.

ABO blood group, secretor status and detection of Helicobacter pylori among patients with gastric or duodenal ulcers.

Patients (454) referred for gastroscopy to the General Hospital of Athens were examined to determine (1) if non-secretors were over-represented among patients with ulcers and (2) if there was an association with ABO blood group or secretor status and carriage of Helicobacter pylori. Compared with the local population, among patients with either gastric ulcer (51) or duodenal ulcer (96) there was a significant increase in the proportion of those who were blood group O (P less than 0.025); however, there were no significant differences in the proportions of non-secretors. H. pylori was identified in 62% of the 454 patients: 59.5% of those without evidence of ulcers; 62.5% of those with gastric ulcer; 88% of those with duodenal ulcer (P less than 0.0005). These bacteria were cultured more often and in higher numbers from patients with duodenal ulcer (P less than 0.025). There was no association between ABO blood group and prevalence of H. pylori. The prevalence of H. pylori among non-secretors with gastric ulcer (12.5%) was significantly lower than that for non-secretors with duodenal ulcer (100%) (P less than 0.0005). This was not observed for secretors.

Association between secretor status and respiratory viral illness.

OBJECTIVE--To determine whether non-secretion of blood group antigens is associated with respiratory virus diseases. DESIGN--Study of secretor status in patients with respiratory virus diseases determined by an enzyme linked immunosorbent assay (ELISA) developed to identify Lewis (Le) blood group antigen phenotypes (Le(a) non-secretor; Le(b) secretor). SUBJECTS--Patients aged 1 month to 90 years in hospital with respiratory virus diseases (584 nasal specimens). MAIN OUTCOME MEASURES--Criteria for validation of ELISA (congruence between results on ELISA testing of 1155 saliva samples from a previous study and previously established results on haemagglutination inhibition (HAI) testing, proportions of Le(a), Le(b), and Le- phenotypes in 872 samples of nasal washings from a previous study compared with the normal population). Secretor status of patients determined by ELISA and viruses isolated. RESULTS--Agreement between HAI and ELISA for 1155 saliva samples was 97%. Lewis antigens were detected by ELISA in 854 (97.9%) of nasal washings (Le(a) 233 (26.7%), Le(b) 621 (71.2%), and Le- 18 (2.1%)) in proportions predicted for a northern European population. Secretors were significantly overrepresented among patients from whom influenza viruses A and B (55/64, 86%; p less than 0.025), rhinoviruses (63/72, 88%; p less than 0.01), respiratory syncytial virus (97/109, 89%; p less than 0.0005), and echoviruses (44/44, p less than 0.0005) had been isolated compared with the distribution of secretors in the local population. CONCLUSION--Secretion of blood group antigens is associated with respiratory virus diseases.

Secretor status, smoking and carriage of Neisseria meningitidis.

A survey of ABO blood groups, secretor status and smoking habits among 389 students and staff of a school in which there was an outbreak of meningococcal disease found no difference in the distribution of the ABO blood groups but a significantly higher proportion of non-secretors (37.6%) in the population examined compared with that reported for previous surveys of the neighbouring population in Glasgow (26.2%) (P less than 0.0005). There was also a significantly higher proportion of non-secretors among carriers of meningococci (47%) compared with non-carriers (32%). Increased carriage of meningococci among non-secretors might contribute to the increased susceptibility of individuals with this genetic characteristic to meningococcal disease observed in previous studies. Although passive exposure to cigarette smoke has been associated with meningococcal disease, there was no association between passive smoking and carriage. There was, however, a significant association between active smoking and carriage.

Helicobacter pylori in the mouth - negative isolation from dental plaque and saliva

Objective To determine the colonization of Helicobacter pylori in dental plaque and saliva of individuals with H. pylori-associated gastritis. Patients and methods One hundred and twenty adult dyspeptic patients attending for outpatient endoscopy were randomly selected. Saliva, dental plaques and antral biopsies were collected and cultured in Dents medium. Antral biopsies were also taken for histological confirmation of colonization. Results Eleven patients were withdrawn owing to poor tolerance of endoscopy. Fifty-two patients (47%) were found to be H. pylori positive on culture from antral biopsies and on antral histology. H. pylori was not isolated from, saliva and dental plaques in any of the patients irrespective of their infective status. The H. pylori seropositivity rate was higher in the Japanese (72%) than in the Dutch (33%). Conclusion We failed to isolate H. pylori from saliva and dental plaque in a group of dyspeptic patients with H. py/ori-associated gastritis. We believe that our finding strongly suggests that oral to oral route is not an important mode of transmission in the adult population.

Factors enhancing adherence of toxigenic Staphylococcus aureus to epithelial cells and their possible role in sudden infant death syndrome

Toxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewis(a) antigen and infection with respiratory syncytial virus (RSV). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from nonsecretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewis(a) or anti-type-1 precursor significantly reduced bacterial binding (P < 0.01); however, attachment of the bacteria correlated only with the amount of Lewis(a) antigen detected on the cells (P < 0.01). HEp-2 cells infected with RSV bound significantly more bacteria than uninfected cells. These findings are discussed in context of factors previously associated with SIDS (mothers smoking, bottle feeding and the prone sleeping position) and a hypothesis proposed to explain some cases of SIDS.

The role of bacterial toxins in Sudden Infant Death Syndrome (SIDS)

There is increasing evidence for the involvement of bacterial toxins in some cases of sudden infant death syndrome (SIDS), particularly the pyrogenic toxins of Staphylococcus aureus. This had led to the hypothesis that some SIDS deaths are due to induction of inflammatory mediators by infectious agents or their products during a period in which the infant is unable to control these normally protective responses. The genetic, developmental and environmental risk factors identified for SIDS are assessed in relation to frequency or density of mucosal colonisation by toxigenic bacteria and their effects on induction and control of inflammatory responses to the toxins.

Increased inflammatory responses of persons of blood group O to Helicobacter pylori.

Persons of blood group O are at increased risk of peptic ulcers. Enhanced binding of Helicobacter pylori to epithelial cells of persons of blood group O has been demonstrated. Release of interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-alpha by human leukocytes from 40 donors (10 from each ABO blood group) was measured after incubation in vitro with outer membrane protein preparations of H. pylori. Isolates DU (from a patient with a duodenal ulcer), GC (from a patient with gastric cancer), NE (from a patient with normal endoscopic findings), and NCTC 11637 bound in significantly higher numbers to group O leukocytes. Bacterial binding correlated with release of IL-6 and TNF-alpha but not of IL-10. Group O cells released significantly more IL-6 in response to DU, NE, and NCTC 11637, and the cells released more TNF-alpha in response to DU and NCTC 11637. Increased density of colonization of epithelial cells and higher inflammatory responses to H. pylori of persons of blood group O might contribute to increased susceptibility to peptic ulceration.