Gram-negative Rod Bacteraemia: function of phagocytic cells and opsonic activity of serum

1979 ◽  
Vol 45 (3) ◽  
pp. 517-517
Author(s):  
Willemien C. van Dijk ◽  
H. A. Verbrugh ◽  
Marijke E. van der Tol ◽  
J. Verhoef
Keyword(s):  
Phagocytic Cells ◽  
Opsonic Activity ◽  
Gram Negative

Serum amyloid A is an innate immune opsonin for Gram-negative bacteria

Blood ◽  
2006 ◽  
Vol 108 (5) ◽  
pp. 1751-1757 ◽  
Author(s):  
Chandrabala Shah ◽  
Ranjeeta Hari-Dass ◽  
John G. Raynes
Keyword(s):  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Reactive Oxygen Intermediate ◽  
Gram Negative Bacteria ◽  
Phagocytic Cells ◽  
Peripheral Blood Mononuclear ◽  
Gram Negative ◽  
E Coli ◽  
Amyloid A ◽  
Innate Recognition

Serum amyloid A (SAA) is the major acute-phase protein in man and most mammals. Recently we demonstrated that SAA binds to many Gram-negative bacteria including Escherichia coli and Pseudomonas aeruginosa through outer membrane protein A (OmpA) family members. Therefore we investigated whether SAA altered the response of innate phagocytic cells to bacteria. Both the percentage of neutrophils containing E coli and the number of bacteria per neutrophil were greatly increased by SAA opsonization, equivalent to the increase seen for serum opsonization. In contrast, no change was seen for Streptococcus pneumoniae, a bacteria that did not bind SAA. Neutrophil reactive oxygen intermediate production in response to bacteria was also increased by opsonization with SAA. SAA opsonization also increased phagocytosis of E coli by peripheral blood mononuclear cell-derived macrophages. These macrophages showed strong enhancement of TNF-α and IL-10 production in response to SAA-opsonized E coli and P aeruginosa. SAA did not enhance responses in the presence of bacteria to which it did not bind. These effects of SAA occur at normal concentrations consistent with SAA binding properties and a role in innate recognition. SAA therefore represents a novel innate recognition protein for Gram-negative bacteria.

Opsonic activity of intravenous immune globulin on Gram-negative bacteria exposed to a monobactam antibiotic

1989 ◽  
Vol 3 (4) ◽  
pp. 241-248 ◽  
Author(s):  
Maria Teresa Lun ◽  
Giammarco Raponi ◽  
Alessandra Giordano ◽  
Paola Cipriani ◽  
Cristina Nazzari ◽  
...  
Keyword(s):  
Immune Globulin ◽  
Intravenous Immune Globulin ◽  
Gram Negative Bacteria ◽  
Opsonic Activity ◽  
Gram Negative

scholarly journals Variation, Modification and Engineering of Lipid A in Endotoxin of Gram-Negative Bacteria

2021 ◽  
Vol 22 (5) ◽  
pp. 2281
Author(s):  
Kazuyoshi Kawahara
Keyword(s):  
Fatty Acids ◽  
Lipid A ◽  
Hydroxy Fatty Acids ◽  
Hydroxyl Groups ◽  
Gram Negative Bacteria ◽  
Vaccine Adjuvants ◽  
Phagocytic Cells ◽  
Gram Negative ◽  
Electrostatic Charges ◽  
Lipid A Structure

Lipid A of Gram-negative bacteria is known to represent a central role for the immunological activity of endotoxin. Chemical structure and biosynthetic pathways as well as specific receptors on phagocytic cells had been clarified by the beginning of the 21st century. Although the lipid A of enterobacteria including Escherichia coli share a common structure, other Gram-negative bacteria belonging to various classes of the phylum Proteobacteria and other taxonomical groups show wide variety of lipid A structure with relatively decreased endotoxic activity compared to that of E. coli. The structural diversity is produced from the difference of chain length of 3-hydroxy fatty acids and non-hydroxy fatty acids linked to their hydroxyl groups. In some bacteria, glucosamine in the backbone is substituted by another amino sugar, or phosphate groups bound to the backbone are modified. The variation of structure is also introduced by the enzymes that can modify electrostatic charges or acylation profiles of lipid A during or after its synthesis. Furthermore, lipid A structure can be artificially modified or engineered by the disruption and introduction of biosynthetic genes especially those of acyltransferases. These technologies may produce novel vaccine adjuvants or antagonistic drugs derived from endotoxin in the future.

Expression of BPI (bactericidal/permeability-increasing protein) in human mucosal epithelia

2003 ◽  
Vol 31 (4) ◽  
pp. 795-800 ◽  
Author(s):  
O. Levy ◽  
G. Canny ◽  
C.N. Serhan ◽  
S.P. Colgan
Keyword(s):  
Antibacterial Activity ◽  
Functional Expression ◽  
Gram Negative Bacteria ◽  
Antimicrobial Proteins ◽  
Opsonic Activity ◽  
Gram Negative ◽  
The Subject ◽  
Epithelial Inflammation ◽  
Proteins And Peptides

Among the antimicrobial proteins and peptides of humans is the cationic 55 kDa bactericidal/permeability-increasing protein (BPI), which possesses antibacterial, endotoxin-neutalizing and opsonic activity against Gram-negative bacteria. Although identified originally as an abundant constituent of neutrophil granules, we have recently identified functional expression of BPI by human mucosal epithelia. BPI expression was markedly up-regulated by exposure of epithelia to lipoxins, endogenous anti-inflammatory eicosanoids that are generated in vivo in the context of aspirin treatment (aspirin-triggered lipoxins). Epithelial BPI was found to be surface expressed and fully functional, as measured by antibacterial activity against Salmonella typhimurium as well as lipopolysaccharide (LPS; endotoxin)-neutralizing activity. These results suggest a role for BPI as an effector of epithelial antibacterial activity and as a modulator of epithelial responses to LPS. Both BPI and the lipoxins are currently the subject of intensive biopharmaceutical development, raising the possibility that therapeutic use of BPI or modulation of epithelial BPI expression may be a useful adjunctive therapy for conditions in which epithelial inflammation is associated with Gram-negative infections and/or endotoxin.

scholarly journals Virulence Factors of Salmonella Typhi

2021 ◽  
Author(s):  
Noor S.K. Al-Khafaji ◽  
Ali M.K. Al-Bayati ◽  
Hussein O.M. Al-Dahmoshi
Keyword(s):  
Small Intestine ◽  
Virulence Factors ◽  
Blood Stream ◽  
Salmonella Typhi ◽  
Phagocytic Cells ◽  
Gram Negative ◽  
The Family ◽  
Gram Negative Organisms ◽  
Salmonella Pathogenicity Islands ◽  
Vi Antigen

S. Typhi is an enteric bacillus which belongs,to the genus Salmonella in the family Enterobacteriacaea and it is a multi–organs pathogen which inhibits the lymphatic tissues of the small intestine, liver, spleen, and blood stream of infected humans.S.Typhi has a mixture of features that make it an efficient pathogen. This species contains an endotoxin that is characteristic of Gram-negative organisms, as well as the virulence-enhancing Vi antigen. Many of the S. Typhi virulence factors are clustered in some areas of the chromosome known as Salmonella pathogenicity islands (SPI), such as adhesion, invasion, and toxin genes. A protein known as invasin that permits non-phagocytic cells is also produced and excreted by the bacterium., Where it is capable of intracellular living. The oxidative burst of leukocytes may also be inhibited, making innate immune reaction ineffective.

scholarly journals Putting the Jigsaw Together - A Brief Insight Into the Tularemia

2015 ◽  
Vol 10 (1) ◽  
Author(s):  
K. Kubelkova ◽  
A. Macela
Keyword(s):  
Francisella Tularensis ◽  
Severe Disease ◽  
Standard Of Care ◽  
Phagocytic Cells ◽  
Current Standard ◽  
Gram Negative ◽  
Infectious Dose ◽  
Multiple Routes ◽  
Bioterrorism Agent ◽  
Insight Into

AbstractTularemia is a debilitating febrile and potentially fatal zoonotic disease of humans and other vertebrates caused by the Gram-negative bacterium Francisella tularensis. The natural reservoirs are small rodents, hares, and possibly amoebas in water. The etiological agent, Francisella tularensis, is a non-spore forming, encapsulated, facultative intracellular bacterium, a member of the γ-Proteobacteria class of Gram-negative bacteria. Francisella tularensis is capable of invading and replicating within phagocytic as well as non-phagocytic cells and modulate inflammatory response. Infection by the pulmonary, dermal, or oral routes, respectively, results in pneumonic, ulceroglandular, or oropharyngeal tularemia. The highest mortality rates are associated with the pneumonic form of this disease. All members of Francisella tularensis species cause more or less severe disease Due to their abilities to be transmitted to humans via multiple routes and to be disseminated via biological aerosol that can cause the disease after inhalation of even an extremely low infectious dose, Francisella tularensis has been classified as a Category A bioterrorism agent. The current standard of care for tularemia is treatment with antibiotics, as this therapy is highly effective if used soon after infection, although it is not, however, absolutely effective in all cases.

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