Microarray analysis of Streptococcus pneumoniae gene expression changes to human lung epithelial cells

Song, Xin-Ming; Connor, Wayne; Jalal, Shakiba; Hokamp, Karsten; Potter, Andrew

doi:10.1139/w07-133

Cited by 21 publications

(24 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Given the abundance of complex glycan structures in the airway and the ability of S. pneumoniae to modify host sugars, it seems likely that sugars released from human glycans by pneumococcal glycosidases support the growth of the bacteria during colonization. Although it is unknown how S. pneumoniae grows in the airway, transcription of nanA and a putative sialic acid transporter is increased in the presence of human airway epithelial cells (Song et al. , 2008b).…”

Section: Growthmentioning

confidence: 99%

Pneumococcal modification of host sugars: a major contributor to colonization of the human airway?

King

2010

Molecular Oral Microbiology

105

126

View full text Add to dashboard Cite

Streptococcus pneumoniae colonization of the human airway is an essential precursor for disease; however, the mechanisms by which the bacterium establishes and maintains colonization are poorly understood. It is becoming increasingly clear that S. pneumoniae expresses glycosidases that can modify many glycan structures present in the human airway, including N-linked glycans, O-linked glycans, and glycosaminoglycans. Many of these glycosidases have been shown to contribute to in vivo colonization. Although the precise role of these glycosidases during colonization remains to be elucidated, in vitro assays suggest that pneumococcal modification of host sugars may contribute to colonization in a variety of ways. Experimental evidence supports a role for pneumococcal glycosidases in providing a carbon source for growth, biofilm formation, competition with other bacteria within the airway, and exposing receptors for adherence. Herein we review the ability of S. pneumoniae to modify host sugars and the functional effects of these modifications.

show abstract

Section: Growthmentioning

confidence: 99%

Pneumococcal modification of host sugars: a major contributor to colonization of the human airway?

King

2010

Molecular Oral Microbiology

105

126

View full text Add to dashboard Cite

show abstract

“…Antibodies raised against a number of solute binding components from ABC transporters found in the Gram-negative pathogen Yersina pestis and other bacterial pathogens are also protective against bacterial infection 16,17. An adcB mutant S. pneumoniae strain shows attenuated binding to human epithelial cells in vitro 18 and AdcB is a documented virulence factor in a signature-tagged mutagenesis screen 19. In Streptococcus gordonii , an oral plaque pathogen, AdcR is reported to play an essential role in biofilm formation 20,21…”

Section: Introductionmentioning

confidence: 99%

The Metalloregulatory Zinc Site in Streptococcus pneumoniae AdcR, a Zinc-activated MarR Family Repressor

Reyes-Caballero

Guerra

Jacobsen

et al. 2010

Journal of Molecular Biology

158

View full text Add to dashboard Cite

Streptococcus pneumoniae D39 AdcR (adhesin competence repressor) is the first metal-sensing member of the MarR (multiple antibiotic resistance repressor) family to be characterized. Expression profiling with a ΔadcR strain grown in liquid culture (brain heart infusion; BHI) under microaerobic conditions reveals upregulation of 13 genes including adcR and adcCBA, encoding a high affinity ABC uptake system for zinc, and genes encoding cell-surface zinc-binding pneumococcal histidine triad (Pht) proteins and AdcAII (Lmb, laminin binding). The ΔadcR, H108Q and H112Q adcR mutant allelic strains grown in 0.2 mM Zn(II) exhibit a slow-growth phenotype and a ≈2-fold increase in cell-associated Zn(II). Apo-and Zn(II)-bound AdcR are homodimers in solution and binding to a 28-mer DNA containing an adc operator is strongly stimulated by Zn(II) with K DNA-Zn = 2.4 ×10 8 M −1 (pH 6.0, 0.2 M NaCl, 25 °C). AdcR binds two Zn(II) per dimer, with step-wise Zn(II) affinities K Zn1 and K Zn2 of ≥10 9 M −1 at pH 6.0 and ≥10 12 M −1 at pH 8.0. X-ray absorption spectroscopy (XAS) of the high affinity site reveals a pentacoordinate N/O complex and no cysteine coordination, the latter finding corroborated by wild-type-like functional properties of C30A AdcR. Alanine substitution of conserved residues His42 in the DNA binding domain, and His108 and His112 in the C-terminal regulatory domain, abolish high affinity Zn(II) binding and greatly reduce Zn(II)-activated binding to DNA. NMR studies reveal that these mutants adopt the same folded conformation as dimeric wild-type apo AdcR, but fail to conformationally switch upon Zn(II) binding. These studies clearly identify His42, His108 and H112 as metalloregulatory zinc ligands in S. pneumoniae AdcR.

show abstract

“…The intracellular Brucella cells were collected from the infected RAW264.7 cells. Briefly, the infected cells were washed three times with PBS, then immediately combined with 1 mL of RLT lysis buffer (Qiagen, Hilden, Germany), 1% β-mercaptoethanol, 1% (v/v) phenol, and 10% (v/v) ethanol per well [45]. Following incubation at 37°C for 10 min, the RAW264.7 cells were lysed and bacteria were collected by centrifugation at 14000×g for 10 min for RNA extraction.…”

Section: Methodsmentioning

confidence: 99%

Microarray-Based Identification of Differentially Expressed Genes in Intracellular Brucella abortus within RAW264.7 Cells

Tian

Han

et al. 2013

PLoS ONE

View full text Add to dashboard Cite

Brucella spp. is a species of facultative intracellular Gram-negative bacteria that induces abortion and causes sterility in domesticated mammals and chronic undulant fever in humans. Important determinants of Brucella’s virulence and potential for chronic infection include the ability to circumvent the host cell’s internal surveillance system and the capability to proliferate within dedicated and non-dedicated phagocytes. Hence, identifying genes necessary for intracellular survival may hold the key to understanding Brucella infection. In the present study, microarray analysis reveals that 7.82% (244/3334) of all Brucella abortus genes were up-regulated and 5.4% (180/3334) were down-regulated in RAW264.7 cells, compared to free-living cells in TSB. qRT-PCR verification further confirmed a >5-fold up-regulation for fourteen genes. Functional analysis classified araC, ddp, and eryD as to partake in information storage and processing, alp, flgF and virB9 to be involved in cellular processes, hpcd and aldh to play a role in metabolism, mfs and nikC to be involved in both cellular processes and metabolism, and four hypothetical genes (bruAb1_1814, bruAb1_0475, bruAb1_1926, and bruAb1_0292) had unknown functions. Furthermore, we constructed a B. abortus 2308 mutant Δddp where the ddp gene is deleted in order to evaluate the role of ddp in intracellular survival. Infection assay indicated significantly higher adherence and invasion abilities of the Δddp mutant, however it does not survive well in RAW264.7 cells. Brucella may survive in hostile intracellular environment by modulating gene expression.

show abstract

Microarray analysis of Streptococcus pneumoniae gene expression changes to human lung epithelial cells

Cited by 21 publications

References 36 publications

Pneumococcal modification of host sugars: a major contributor to colonization of the human airway?

Pneumococcal modification of host sugars: a major contributor to colonization of the human airway?

The Metalloregulatory Zinc Site in Streptococcus pneumoniae AdcR, a Zinc-activated MarR Family Repressor

Microarray-Based Identification of Differentially Expressed Genes in Intracellular Brucella abortus within RAW264.7 Cells

Contact Info

Product

Resources

About