Summary Fourteen mares and their foals were attended at parturition. After mare‐foal bonding, 8 colostrum‐deprived (CD) foals were removed from their dams, deprived of colostrum, and provided with an alternative milk source for the first 24 h of life. The mares were milked out every 2–4 h during this period to remove colostrum, after which the CD foals were returned to their mares and allowed to nurse. Six colostrum‐fed (CF) foals were allowed to suck colostrum in the normal manner. Foal serum IgG concentration was determined by single radial immunodiffusion (means, CD = 0 mg/dl; CF = 1,508 mg/dl). Accepted methods were used to minimise infections in the neonatal foals. Of the 8 CD foals, 7 demonstrated clinical signs of sepsis. Septicaemia was confirmed in 5 of the 7 septicaemic CD foals by ante‐mortem blood culture or by culture of tissue at necropsy. Organisms isolated included: Actinobacillus equuli, Escherichia coli, undifferentiated coliforms, Pseudomonas spp., and Actinomyces pyogenes. Clinically ill foals were treated with antimicrobial drugs, intravenous fluid therapy, flunixin meglumine, and anti‐endotoxin hyperimmune serum. Three septicaemic CD foals survived. Four of 7 septicaemic CD foals died or were destroyed. Post‐mortem lesions included bacterial embolic pneumonia, glomerulonephritis/nephritis, lymphoid depletion/atrophy, splenic and lymphoid necrosis, hepatitis, septic arthritis, and systemic bacterial embolism. None of the CF foals bècame septicaemic. One CF foal had foal heat diarrhoea and 1 CF foal had a serum IgG concentration of 160 mg/dl (i.e. failure of passive transfer), but both foals were otherwise normal. Despite the precautions taken to prevent infection in these foals, the severity, rapidity of disease onset, and extent of this outbreak of septicaemia in CD foals demonstrate the importance of colostral immunity in protecting neonatal foals from opportunistic and pathogenic bacterial infection.
A rat hepatoma cell line was shown to synthesize heparan sulfate and chondroitin sulfate proteoglycans . Unlike cultured hepatocytes, the hepatoma cells did not deposit these proteoglycans into an extracellular matrix, and most of the newly synthesized heparan sulfate proteoglycans were secreted into the culture medium . Heparan sulfate proteoglycans were also found associated with the cell surface . These proteoglycans could be solubilized by mild trypsin or detergent treatment of the cells but could not be displaced from the cells by incubation with heparin . The detergent-solubilized heparan sulfate proteoglycan had a hydrophobic segment that enabled it to bind to octyl-Sepharose . This segment could conceivably anchor the molecule in the lipid interior of the plasma membrane . The size of the hepatoma heparan sulfate proteoglycans was similar to that of proteoglycans isolated from rat liver microsomes or from primary cultures of rat hepatocytes . Ion-exchange chromatography on DEAE-Sephacel indicated that the hepatoma heparan sulfate proteoglycans had a lower average charge density than the rat liver heparan sulfate proteoglycans . The lower charge density of the hepatoma heparan sulfate can be largely attributed to a reduced number of Nsulfated glucosamine units in the polysaccharide chain compared with that of rat liver heparan sulfate. Hepatoma heparan sulfate proteoglycans purified from the culture medium had a considerably lower affinity for fibronectin-Sepharose compared with that of rat liver heparan sulfate proteoglycans . Furthermore, the hepatoma proteoglycan did not bind to the neoplastic cells, whereas heparan sulfate from normal rat liver bound to the hepatoma cells in a timedependent reaction . The possible consequences of the reduced sulfation of the heparan sulfate proteoglycan produced by the hepatoma cells are discussed in terms of the postulated roles of heparan sulfate in the regulation of cell growth and extracellular matrix formation .Heparan sulfate proteoglycans are present in a large variety ofvertebrate tissues and appear to be preferentially located at the surface of cells, either directly associated with the cell membrane (1) or in close contact with cells, as in basement membranes (2) and in the pericellular matrix ofcultured cells (3,4).Previous studies in our laboratory have indicated that heparan sulfate proteoglycans are associated with the plasma membrane of rat liver cells by two independent mechanisms (5). The proteoglycan may be bound via its polysaccharide portion to cell surface receptors, or the core protein may be inserted into the lipid interior of the membrane (6). The mechanisms responsible for the anchorage of heparan sulfate in the basement membrane or in extracellular matrices are not clear. Immunofluorescent studies have shown a codistribution between heparan sulfate proteoglycans and fibronectin in the extracellular matrix (7, 8) and a direct binding of heparan sulfate chains to fibronectin has been demonstrated (7, 9).Transformed cells usually do not...
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