The severity of the clinical course in necrotizing enterocolitis (NEC) associated with Clostridium perfringens (Cp) may support the hypothesis of a specific disease. We conducted a case control study of infants diagnosed with NEC, who underwent surgical treatment over a 7-year period. Patient histories examined characteristics of the infants, bacterial infection as well as NEC's severity, antibiotic treatment, and clinical course. Infants infected with NEC associated with Cp were compared with NEC patients without Cp. The alpha toxin from Cp type A was detected in most of the isolated strains. Cp was identified as a causative agent of NEC in nine cases. As compared with the control group (n = 32), the onset of disease was earlier in life, the clinical course more severe, and patients had a larger extent of gangrene. Portal venous gas was evident in 77% of all Cp cases, as compared to 25% in the control group. The mortality rate was 44% in the Cp group, and only 18.7% in the control group. Type A Clostridium perfringens was identified in six cases. In each isolate alpha toxin production was proven, but without any correlation to the severity of the clinical course, the extent of intestinal gangrene or mortality. In premature infants NEC in conjunction with Cp seems to be more severe than other NEC cases; it also entails higher mortality and morbidity. Alpha toxin concentrations do not correlate with the severity of the disease. Portal venous gas is highly suggestive for the diagnosis of Cp infection.

Liver macrophages, which are involved in the different types of hepatitis, may indirectly induce hepatic fibrogenesis, since they have the possibility to activate hepatic stellate cells and fibroblasts by secretion of TGF-β , TNF-α and IL-1. To evaluate variations of the number of liver macrophages and their subpopulations, a quantification was carried out in normal human liver tissue, fatty liver, fatty liver hepatitis and hepatitis B. Identification was performed by the mab PG-M1 (anti-CD68) and, comparatively, four lectins, Griffonia simplicifolia agglutinin I (GSA-I), Erythrina cristagalli agglutinin (ECA), peanut agglutinin (PNA) and soybean agglutinin (SBA). A slight decrease in the frequency of macrophages in pericentral fields was observable in fatty liver and fatty liver hepatitis as compared to normal liver tissue. On the other hand, the number of CD68 cells was significantly enhanced in hepatitis B with moderate and severe inflammatory activity. The highest incidence of macrophages was found in portal tracts of liver with fatty liver hepatitis and, particularly, hepatitis B. The fraction of cells stained by ECA, PNA or SBA did not increase significantly under pathological conditions. In contrast, the percentage of GSA-I binding macrophages was higher in liver parenchyma of hepatitis B and in portal tract macrophages in fatty liver hepatitis and also hepatitis B. In conclusion, our results indicate that GSA-I may aid in the detection of the subpopulation of activated macrophages which are assumed to play a pivotal role in liver pathology.

Interactions between human haematopoietic and bone marrow stromal cells are governed by complex carbohydrate-mediated adhesion processes. In order to evaluate corresponding carbohydrate-binding sites on human myelo- and erythropoietic cells which were able to react with mono- or oligosaccharides, we established an immunocytochemical double-staining assay. In a first step, cell lineages were visualized using Lewis(x) (CD15) or glycophorin C-specific monoclonal antibodies. The second step included polyacrylamide-conjugated carbohydrate structures. According to our results, the carbohydrate-binding potential of granulopoietic cells increased during the process of maturation, contrasting a reduction of carbohydrate-binding sites on erythroid precursor cells during differentiation. With respect to previous in vitro studies, these findings shed some light on certain aspects of bone marrow homing as well as on the trafficking of mature cellular elements into circulation. It is tempting to speculate that carbohydrate-mediated adhesion mechanisms may be involved in the various functional defects of progenitor cells in chronic myelogenic leukaemia, especially regarding their complex interactions with the marrow microenvironment.

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