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NEONATAL SOCIETY ABSTRACTS

The WXG100 protein secretion system of Streptococcus agalactiae

Presented at the Neonatal Society 2007 Summer Meeting (programme).

Attwood N1,2, Whitehead R1,2, Shukla A1,2, Parikh R1, Pallen M2, Anthony M1,2 (introduced by Anoo Jain)

1 Birmingham Women’s Hospital, B15 2TG, UK
2 The Bacterial Pathogenesis & Genomics Unit, University of Birmingham, B15 2TT, UK

Purpose of the Study: Mycobacterium tuberculosis secretes WXG100 proteins (100 amino acids long containing a WXG motif) through a WXG100 secretion system (Wss) into the external environment (1). WXG100 proteins signal to macrophages, for instance reducing cytokine release and causing granuloma formation (2). The Wss is essential for the virulence of TB (3,4). A Wss has also recently been described in Staphylococcus aureus, where it is also vital for full virulence of the organism (5). We sought to determine whether Streptococcus agalactiae (Group B streptococcus; GBS) also encodes Wss and WXG100 proteins.

Experimental design: We BLAST searched each of the eight genes (SA0271-0278) encoding the S. aureus Wss against the eight available GBS genomes. GBS genes were aligned to determine conservation of a putative Wss across the GBS sequenced strains, and the wider region was compared to define the genomic context.

Results: A putative Wss does exist in GBS (see Figure), and is conserved across the sequenced strains. esxAB are WXG100 homologs, essA-C and esaA-C encode homologs of proteins that are essential or accessory, respectively, to the function of the Wss in S. aureus. GBS genomes contain three WXG100 homologs, only one of which is associated with the Wss. The Wss is located within the genome on a mobile segment of DNA, termed ‘Putative Pathogenicity Island-IX’, implying that the Wss has been acquired by horizontal transfer. Similarly, the two WXG100 genes that are not associated with the Wss are also located in Putative Pathogenicity Islands -I and –XIII.

Conclusions and discussion: A Wss has not previously been recognised in GBS, but is identified in this study. This finding enhances our knowledge of the potential mechanisms by which GBS causes disease. It is now plausible that GBS also attenuates macrophages through the action of a WXG100 homolog. In TB, the absence of the Wss is the main determinant of the attenuation of BCG (4). Our finding of a putative Wss in GBS thus has implications for attenuated GBS vaccine development.

References
1. Pallen MJ: Trends in microbiology 2002, 10:209-212.
2. Stanley SA, et al. PNAS 2003, 100:13001-13006.
3. Pym AS, et al. Nature medicine 2003, 9:533-539.
4. Hsu T, et al. PNAS 2003, 100:12420-12425.
5. Burts ML, et al. PNAS 2005, 102:1169-1174.

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