Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The infusion of 10 microgram of endotoxin lipopolysaccharide from Escherichia coli into the mammary gland of four cows 16 h before inoculation with ureaplasmas did not prevent, or even diminish, the subsequent ureaplasmal mastitis. There was no reduction in the severity or duration of the inflammatory cell response in milk or in the clinical appearance of the resulting mastitis. Also, the excretion of ureaplasmas was not reduced. A similar experiment with Mycoplasma dispar in two cows demonstrated that endotoxin was again ineffective in preventing the mastitis. Furthermore, there was some indication that the proliferation and excretion of this mycoplasma was enhanced in endotoxin-treated quarters.
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PMID:The effect of an intramammary infusion of endotoxin on experimentally induced mycoplasmal mastitis. 39 46

This study examined recognition of heterologous Gram-negative endotoxin by antibodies recognizing common lipopolysaccharide core antigens. Gram-negative endotoxins from 11 heterologous bacterial strains were tested for recognition by antibodies against common lipopolysaccharide core antigens. Serum was harvested from a calf immunized with the Rc mutant, Escherichia coli O111:B4 (J5), and affinity purified against endotoxin derived from an Ra mutant, Salmonella typhimurium, producing an antibody reagent recognizing homologous Gram-negative core antigens present in the Rc mutant vaccinal antigen. This reagent demonstrated reactivity against 11 chemically purified Gram-negative endotoxins. Included were endotoxins derived from 3 smooth E. coli species, 2 Salmonella spp., Shigella flexneri, Klebsiella pneumoniae, Pseudomonas aeruginosa, Serratia marcescens, and lipid A. Endotoxin derived from K. pneumoniae had significantly higher ELISA reactivity with core antigen specific antibodies than did endotoxin derived from either E. coli O111:B4 (J5) or P. aeruginosa. These results suggest immunization with R mutant bacterins may have utility in the prevention of Gram-negative mastitis even when whole bacteria react poorly with antibodies recognizing common core antigens.
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PMID:Antigenic homology of endotoxin with a coliform mastitis vaccine strain, Escherichia coli O111:B4 (J5). 150 May 77

Experimental intramammary infections were induced in five post-parturient Holstein cows by inoculation of low numbers (5000 colony forming units) of virulent Salmonella dublin via the teat canal of mammary gland quarters. Rectal temperature, pulse and respiratory rates, milk yield, and milk quality as assessed by the California Mastitis Test (CMT) and somatic cell counts (SCC) were recorded every 12 hours at milking. Bacteriologic cultures of foremilk quarter samples and feces were obtained daily, as were complete blood counts. ELISA titers for IgG and IgM recognizing S. dublin lipopolysaccharide (LPS) were obtained weekly on serum and quarter milk samples. All cows excreted S. dublin intermittently from infected quarters, but no changes were detected in rectal temperature, appearance of the mammary gland or secretions, CBC, milk yield, and pulse and respiratory rates. Somatic cell counts were modestly increased in infected quarters as compared with uninfected quarters (P = .015, paired t test); however, CMT scores after infection remained low, and were not significantly different from pre-infection scores (P greater than .10, sign test). After infection, administration of dexamethasone resulted in signs of clinical mastitis and increased excretion of S. dublin from mammary quarters (P = .0004, paired t test). One cow had necrotizing mastitis and S. dublin septicemia and was euthanatized. In the four surviving cows, clinical improvement was observed after systemic gentamicin therapy and intramammary infusion with polymyxin B, but all cows continued to excrete S. dublin intermittently from one or more quarters and occasionally from feces for the remaining period of observation. All infected cows demonstrated a rise in IgG and IgM ELISA titers recognizing S. dublin LPS in serum and milk. At necropsy (13-25 weeks postinfection), S. dublin was recovered only from the mammary tissue or supramammary lymph nodes in three of four cows. In one cow, mammary gland and lymph-node samples were negative for S. dublin despite positive milk cultures. In all cows, histopathologic examination revealed multifocal areas of chronic active mastitis. These lesions were similar to histopathologic findings from mammary gland carriers with naturally acquired S. dublin infection.
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PMID:Persistent experimental Salmonella dublin intramammary infection in dairy cows. 177 28

Acyloxyacyl hydrolase, a lysosomal enzyme that deacylates and thus detoxifies lipopolysaccharide (endotoxin) has been identified in bovine peripheral blood and milk neutrophils. Enzymatic activity increases on a per neutrophil basis during cases of experimental Escherichia coli mastitis. The objective of this study was to quantify acyloxyacyl hydrolase activity from milk neutrophils collected from mammary glands naturally infected with a variety of bacteria. Acyloxyacyl hydrolase activity was detectable in milk neutrophils isolated from cases of both Gram-negative and Gram-positive bacterial infections, with highest activities found in milk neutrophils from glands infected with organisms known to cause the most severe forms of mastitis. In addition, acyloxyacyl hydrolase activity was inhibited to varying degrees in mastitic milk by a nonprotein inhibitory substance. Nonenzymatic deacylation of endotoxin also occurred in mastitic milk, but to a lesser degree than enzymatic deacylation. Nonenzymatic deacylation of endotoxin was not found to occur in clinically normal milk. Severity of coliform mastitis in individual cows may be dependent in part on the interaction of endotoxin with milk neutrophil acyloxyacyl hydrolase activity, inhibition of acyloxyacyl hydrolase activity by an inhibitory substance, and the inherent ability of milk to deacylate endotoxin nonenzymatically.
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PMID:Deacylation of endotoxin during natural cases of bovine mastitis. 186 Sep 71

This study examined the degree of serologic homology among mastitis pathogens. Antibodies were raised against the Rc mutant, Escherichia coli O111:B4 (strain J5) and affinity purified against lipopolysaccharide derived from the Ra mutant, Salmonella typhimurium TV119. These antibodies reacted with a battery of unrelated Gram-negative bacteria in whole cell ELISA. Bacteria with strong cross-reactions included a heterologous, smooth E. coli, Salmonella dublin, S. typhimurium, Salmonella newport, and Pseudomonas aeruginosa. Recognition of Klebsiella pneumoniae and Bordetella bronchisepticum was observed, but reactions were weaker than with the other isolates. The reduced recognition of these isolates probably reflects a masking effect of the bacterial capsule and variations in lipopolysaccharide structure. The polyclonal antibody did not recognize a Gram-positive isolate, Staphylococcus aureus. These immunoglobulins were then tested using whole cell ELISA against a panel of bacteria recovered from the mammary glands of cattle with clinical mastitis. Marked reactivity was noted against a variety of Gram-negative pathogens. Gram-positive isolates had lower recognition by Gram-negative core antigen specific immunoglobulin. The results suggest immunization with rough mutant bacteria may have broad application in the prevention of coliform mastitis.
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PMID:Antigenic homology among gram-negative organisms isolated from cattle with clinical mastitis. 190 3

Pasteurella haemolytica is represented by two biotypes (A and T), 15 serotypes, and numerous untypable strains. Specific biotypes and serotypes are associated with fibrinous pleuropneumonia (pneumonic pasteurellosis) in cattle, sheep, and goats, septicemic pasteurellosis in lambs, and mastitis in ewes. Four virulence factors have been associated with P. haemolytica: fimbriae, a polysaccharide capsule, endotoxin [lipopolysaccharide (LPS)], and leukotoxin (LKT). The interactions of these virulence factors with components of the pulmonary alveolus are discussed as a model for the pathogenesis of pasteurellosis. Fimbriae on P. haemolytica may enhance colonization of the upper respiratory tract. The capsule of P. haemolytica varies in composition among serotypes. It inhibits complement-mediated serum killing as well as phagocytosis and intracellular killing of P. haemolytica. The capsule enhances neutrophil directed migration and adhesion of P. haemolytica to alveolar epithelium. Pasteurella haemolytica LPS can alter bovine leukocyte functions, by dose-dependent inhibition or augmentation; it is directly toxic to bovine endothelium; it modifies cardiopulmonary hemodynamics; and it elevates circulatory prostanoids, serotonin, cAMP, and cGMP. Leukotoxin is produced by all known serotypes and many untypable strains. Leukotoxin is a poreforming cytolysin that affects ruminant leukocytes and platelets by altering function at low levels but causing lysis at high levels.
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PMID:Molecular aspects of virulence of Pasteurella haemolytica. 197 1

Alterations in the various leukocyte populations in milk, blood, and mammary lymph were studied by use of the flow cytometric method during acute mastitis episodes induced by endotoxin infusion (50 micrograms of lipopolysaccharide of Salmonella typhimurium SH 4809) via the teat canal. Lymph samples were collected via a semipermanent catheter from an afferent duct to the supramammary lymph node. Milk somatic cell count increased at 4 hours after infusion of endotoxin. Neutrophils were the predominant cell population for up to 59 hours after infusion. Numbers of lymphocytes and monocytes-macrophages in milk also increased after the endotoxin infusion. The total cell count in milk started to decrease during the third postinfusion day and returned to preinfusion values during the fourth day. Lymphocyte numbers remained high for about 1 week after the infusion, and lymphocytes were the predominant cell population between postinfusion days 4 and 8. Total blood leukocyte count decreased during the first 6 hours after infusion, followed by an increase until postinfusion hour 31. The proportion of neutrophils in blood increased during the first day, whereas that of lymphocytes decreased. Lymph flow rate and leukocyte numbers in lymph increased after endotoxin infusion. The proportion of neutrophils in the lymph increased during the first 6 hours, whereas that of lymphocytes decreased. After postinfusion hour 6, the inverse course of events was seen.
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PMID:Flow cytofluorometric studies on the alteration of leukocyte populations in blood and milk during endotoxin-induced mastitis in cows. 224 Jul 83

Effects of intramammary infusion of prednisolone (40 mg) or intramuscular injection of dexamethasone (30 mg) or flumethasone (5 mg) on local and systemic signs in Escherichia coli endotoxin-induced mastitis were studied. The effect of varying intervals (0, 2, and 4 h) between intramammary infusion of endotoxin and prednisolone in the same quarter was determined. Intramammary infusion of endotoxin (.01 mg lipopolysaccharide of E. coli) produced inflammation of the infused quarter, fever, tachycardia, and leukopenia followed by a neutrophilic leukocytosis in the blood and a decrease in plasma zinc and iron concentrations. All corticosteroid treatments, except intramammary administration of prednisolone 4 h after endotoxin infusion, enhanced leukocytosis and diminished local signs of inflammation. Intramuscular injection of dexamethasone or flumethasone together with intramammary infusion of endotoxin and intramammary administration of prednisolone 2 h after lipopolysaccharide infusion completely abolished the febrile response. Abolishment of fever and attenuation of several hematologic and blood biochemical changes may be explained by diminished synthesis of endogenous mediators within the inflamed quarters due to glucocorticosteroid action.
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PMID:Effect of steroidal anti-inflammatory drugs on Escherichia coli endotoxin-induced mastitis in the cow. 264 98

Forty-six Escherichia coli isolates of serotype O2:K1 from human urinary tract infections, chicken sepsis, and bovine mastitis were obtained from laboratories in England, Denmark, Sweden, and Finland. The bacteria were compared for outer membrane protein (OMP) pattern, lipopolysaccharide pattern, electrophoretic mobilities of enzymes, and flagellar serotype and were tested for fimbriation, biotype, hydroxamate production, hemolysin production, antibiotic resistance, plasmid content, colicin production, and virulence in neonatal rats. Isolates from humans were assigned to two clonal groups; poultry isolates belonged to one of these clonal groups, whereas bovine isolates belonged to the other. Poultry and human isolates of the same clonal group could be distinguished only by their plasmid content. Strains within this group were heterogeneous with respect to biotype, fimbriation, virulence, and flagellar serotype. Human and bovine isolates of the second clonal group were distinguished by a minor change in OMP pattern and by their plasmid content. It is concluded that meaningful clonal groupings are best recognized by the combination of OMP and electrophoretic enzyme patterns. The O:K serotype can aid in the recognition of important subclones, whereas the other microbiological properties tested can vary widely within clonal groupings. Furthermore, we conclude that certain O:K serotypes can contain very different clonal groupings having little genetic relatedness.
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PMID:Clonal analysis of Escherichia coli O2:K1 isolated from diseased humans and animals. 351 Jan 71

Milk whey immunoglobulins (Ig) and phagocytosis of staphylococci by milk polymorphonuclear neutrophilic leukocytes (PMN) were measured in 12 cows (allotted to 6 pairs) during acute bovine mastitis induced by intramammary inoculation of endotoxin. Six of these cows (or 1 in each pair) were treated with flunixin meglumine and were compared with the others (given only saline solution). The endotoxin inoculation comprised 10 micrograms of Escherichia coli O26:B6 lipopolysaccharide injected into one of the rear quarters (mammae). Flunixin meglumine was administered parenterally at a dosage of 1.1 mg/kg every 8 hours (total of 7 doses) beginning at 2 hours after endotoxin was injected. Milk samples were obtained, and whey samples were prepared from each quarter of each cow 3 times before inoculation and at 2, 4, 8, 12, 24, 48, 72, 96, 120, 144, 168, and 336 hours after endotoxin was inoculated. Significant increases (P less than 0.05) in milk whey IgG1, IgG2, IgM, and IgA concentrations were observed in whey samples from endotoxin-inoculated quarters. Greatest relative increase was seen for IgG2. Increased whey Ig concentrations were not observed in quarters which were not inoculated with endotoxin. Concentrations of whey IgG1 and IgM in endotoxin-inoculated quarters were significantly (P less than 0.05) decreased in flunixin meglumine-treated cows, compared with those in saline solution-treated cows. Significant increases in phagocytosis of staphylococci by milk PMN were observed in whey samples from endotoxin-inoculated quarters. Significant differences in PMN phagocytosis were not found in whey samples from cows given flunixin meglumine when compared with whey samples from cows given saline solution.
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PMID:Endotoxin-induced bovine mastitis: immunoglobulins, phagocytosis, and effect of flunixin meglumine. 353 54


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