The influence of the O and K antigens of Klebsiella aerogenes on surface hydrophobicity and susceptibility to phagocytosis and antimicrobial agents

Williams, Paul H.; Lambert, Peter A.; Haigh, C. G.; Brown, M. R. W.

doi:10.1099/00222615-21-2-125

Cited by 58 publications

(42 citation statements)

References 31 publications

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“…In addition, FACS analysis demonstrated no difference in the degree of FITC labeling of the mutants compared with that of the parent GBS strain. This finding is consistent with the concept that an increase in the binding and phagocytosis of encapsulated pathogens may occur when surface charges are altered or possible ligands are exposed (26,49) and with previous reports indicating that CPS of type III GBS may contribute to the organism's ability to evade host defense mechanisms (30).…”

Section: Nonopsonic Binding Of Type III Gbs With Human Pmnsupporting

confidence: 80%

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Nonopsonic Binding of Type III Group B Streptococci to Human Neutrophils Induces Interleukin-8 Release Mediated by the p38 Mitogen-Activated Protein Kinase Pathway

et al. 2000

Infect Immun

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Nonopsonic interaction of host immune cells with pathogens is an important first line of defense. We hypothesized that nonopsonic recognition between type III group B streptococcus and human neutrophils would occur and that the interaction would be sufficient to trigger neutrophil activation. By using a serum-free system, it was found that heat-killed type III group B streptococci bound to neutrophils in a rapid, stable, and inoculum-dependent manner that did not result in ingestion. Transposon-derived type III strain COH1-13, which lacks capsular polysaccharide, and strain COH1-11 with capsular polysaccharide lacking terminal sialic acid demonstrated increased neutrophil binding, suggesting that capsular polysaccharide masks an underlying binding site. Experiments using monoclonal antibodies to complement receptor 1 and to the I domain or lectin site of complement receptor 3 did not inhibit binding, indicating that the complement receptors used for ingestion of opsonized group B streptococci were not required for nonopsonic binding. Nonopsonic binding resulted in rapid activation of cellular p38 and p44/42 mitogen-activated protein kinases. This interaction was not an effective trigger for superoxide production but did promote release of the proinflammatory cytokine interleukin-8. The release of interleukin-8 was markedly suppressed by the p38 mitogen-activated protein kinase inhibitor SB203580 but was only minimally suppressed by the mitogen-activated protein/extracellular signal-regulated kinase inhibitor PD98059. Thus, nonopsonic binding of type III group B streptococci to neutrophils is sufficient to initiate intracellular signaling pathways and could serve as an arm of innate immunity of particular importance to the immature host.

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Section: Nonopsonic Binding Of Type III Gbs With Human Pmnsupporting

confidence: 80%

“…Changes in surface characteristics of polysaccharides of microorganisms may alter the surface charge and thus render them more susceptible to phagocytosis (49). The binding of type III GBS transposon mutant strains lacking CPS or its terminal monosaccharide, sialic acid, was enhanced.…”

Section: Discussionmentioning

confidence: 89%

Nonopsonic Binding of Type III Group B Streptococci to Human Neutrophils Induces Interleukin-8 Release Mediated by the p38 Mitogen-Activated Protein Kinase Pathway

et al. 2000

Infect Immun

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“…However, the mechanisms of cell surface polysaccharide synthesis have not been well characterized. Among the bacterial cell surface polysaccharides, CPS is the major polysaccharide and it has been considered to be a barrier against antibacterial reactions such as phagocytosis by polymorphonucleated cells in a host (29,42). Klebsiella pneumoniae is a species of gram-negative rod belonging to the family Enterobacteriaceae (9,25) that causes opportunistic infections or mixed infections of immunocompromised hosts.…”

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confidence: 99%

Genomic organization of the Klebsiella pneumoniae cps region responsible for serotype K2 capsular polysaccharide synthesis in the virulent strain Chedid

et al. 1995

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The genomic organization of the chromosomal cps region that is responsible for capsular polysaccharide synthesis in Klebsiella pneumoniae Chedid (O1:K2) was investigated. Deletion analyses and Southern hybridization studies suggested that the central region of the cloned 29-kb BamHI fragment is indispensable for K2 capsular polysaccharide synthesis. The 24,329-bp nucleotide sequence of the Klebsiella cps region was determined and deposited in the EMBL and GenBank databases through DDBJ and assigned accession number D21242. Nineteen possible open reading frames (ORFs) were identified in the sequenced area. Among them, 13 ORFs are very close to each other. Six of the 19 ORFs show considerable nucleotide sequence similarities to Salmonella typhimurium cpsG, cpsB, rfbP, and orf2.8, Escherichia coli gnd, and Haemophilus influenzae bexD, respectively. Moreover, the deduced amino acid sequence of the ORF10 product demonstrated a highly hydrophobic profile and showed putative membrane topology similarity to Rickettsia prowazekii ATP/ADP translocase. Nucleotide sequences similar to the 54 -dependent promoter, as well as the usual ؊35 and ؊10 sequences, were identified just upstream of ORF3, which is the first ORF in the polycistronic structure. Furthermore, a sequence (GGGCGGTAGCGT) found just downstream of the 54 -dependent promoter-like sequence was generally conserved among gene clusters implicated in cell surface polysaccharide synthesis, such as Salmonella rfb and viaB and E. coli kpsMT and rfaQPG. A possible transcriptional terminator with a hairpin loop structure found just downstream of ORF15 that is a homolog of E. coli gnd. K2 capsular polysaccharide biosynthesis in E. coli K-12 depends on cpsB (mannose-1-phosphate guanyltransferase gene), and Klebsiella cpsB, found in the downstream region of the polycistronic structure, was able to complement cpsB of E. coli. Results of transposon insertion and promoter-cloning analyses were consistent with the results of nucleotide sequence analysis.

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“…Although we could not rule out a role of the GTF-I N terminus in antiphagocytic effect against PMNs, our findings suggest that GTF proteins may not play an important role in antiphagocytic effect. Bacterial hydrophobicity is known to play an important role in the interaction between bacteria and phagocytic cells and subsequent phagocytosis (1,7,24,40,43). In this study, the cell surface of the serotype c-specific polysaccharide-defective mutant Xc24R is markedly more hydrophobic than that of the wild-type strain Xc (Table 2).…”

Section: Discussionmentioning

confidence: 73%

Role of Serotype-Specific Polysaccharide in the Resistance ofStreptococcus mutansto Phagocytosis by Human Polymorphonuclear Leukocytes

et al. 2000

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To clarify the role of cell surface components of Streptococcus mutans in resistance to phagocytosis by human polymorphonuclear leukocytes (PMNs), several isogenic mutants of S. mutans defective in cell surface components were studied with a luminol-enhanced chemiluminescence (CL) assay, a killing assay, and a transmission electron microscope. The CL responses of human PMNs to mutant Xc11 defective in a major cell surface antigen, PAc, and mutant Xc16 defective in two surface glucosyltransferases (GTF-I and GTF-SI) were the same as the response to the wild-type strain, Xc. In contrast, mutant Xc24R, which was defective in serotype c-specific polysaccharide, induced a markedly higher CL response than the other strains. The killing assay showed that human PMNs killed more Xc24R than the parent strain and the other mutants. The transmission electron microscopic observation indicated that Xc24R cells were more internalized by human PMNs than the parental strain Xc. These results may be reflected by the fact that strain Xc24R was more phagocytosed than strain Xc. The CL response of human PMNs to a mutant defective in polysaccharide serotype e or f was similar to the response to Xc24R. Furthermore, mutants defective in serotype-specific polysaccharide were markedly more hydrophobic than the wild-type strains and the other mutants, suggesting that the hydrophilic nature of polysaccharides may protect the bacterium from phagocytosis. We conclude that the serotype-specific polysaccharide, but not the cell surface proteins on the cell surface of S. mutans, may play an important role in the resistance to phagocytosis.

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The influence of the O and K antigens of Klebsiella aerogenes on surface hydrophobicity and susceptibility to phagocytosis and antimicrobial agents

Cited by 58 publications

References 31 publications

Nonopsonic Binding of Type III Group B Streptococci to Human Neutrophils Induces Interleukin-8 Release Mediated by the p38 Mitogen-Activated Protein Kinase Pathway

Nonopsonic Binding of Type III Group B Streptococci to Human Neutrophils Induces Interleukin-8 Release Mediated by the p38 Mitogen-Activated Protein Kinase Pathway

Genomic organization of the Klebsiella pneumoniae cps region responsible for serotype K2 capsular polysaccharide synthesis in the virulent strain Chedid

Role of Serotype-Specific Polysaccharide in the Resistance ofStreptococcus mutansto Phagocytosis by Human Polymorphonuclear Leukocytes

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