pneumonia

pneumoniajourn

Vol7SpecialIssueforweb

EuroPneumo Special Issue / pneumonia 2015 Oct 21;7:I–72

to establish a productive infection and cause meningitis in the model, resulting in significant mortality. Brain damage

(cortical damage, hippocampal apoptosis) and leukocyte pleocytosis were evident from histomorphological analysis. The

non-encapsulated mutant failed to establish an infection or cause any detectable pathology. The presence of capsule

is essential for establishing meningitis in this model. The modified model is appropriate for studying the meningitisinducing

potential of non-passaged clinical isolates.

P1.04

An investigation of the impact of air pollutants on Streptococcus

pneumoniae

Shane Hussey 1, 2 , Peter Andrew 2 , Paul Monks 3 , Julian Ketley 1 , Julie Morrissey 1

1

Department of Genetics, University of Leicester, Leicester, UK; 2 Department of Infection, Immunity and Inflammation, University of Leicester,

Leicester, UK; 3 Department of Chemistry, University of Leicester, Leicester, UK

Despite legislation to reduce air pollution, it is the largest global environmental and health problem we are faced with

in current times and was responsible for 1 in 8 deaths worldwide in 2012. One of its most toxic components, particulate

matter (PM) is responsible for increases in cardiovascular and respiratory diseases and infections. To date this has been

attributed to deleterious and immunomodulatory effects on the human host, including tissue damage, inflammatory

responses, and oxidative stress. However, there has been a major oversight in this field as no studies have investigated the

direct impact of air pollution on bacteria of the human respiratory tract. This may be a serious omission because bacteria

play an essential role in maintaining the health of a host. We have investigated the effect of a specific component of PM

and black carbon (BC), which is a by-product of fossil fuel combustion, on the behaviour of Streptococcus pneumoniae.

S. pneumoniae was chosen as it asymptomatically colonises much of the population whilst retaining the ability to cause

severe disease. Our data show, for the first time, that there is an interaction between air pollutants and bacteria, with

BC inducing species-specific alterations in biofilm formation and structure. Biofilms are vital in both host colonisation

and infection, providing protection from the environment and the host immune system. Biofilm alterations will have

a significant impact on bacterial survival in vivo as well as on the potential for disease progression and transmission.

Therefore our data suggests a major effect of air pollution has been overlooked.

P1.05

Studies on pneumococcal esterases

Hasan Kahya, Peter Andrew, Hasan Yesilkaya

Infection, Immunity and Inflammation/University of Leicester, Leicester, UK

The genome of pneumococcal strain contains 4 putative esterase genes (SPD_0534 (estA), SPD_0932, SPD_1239, and

SPD_1506 (axe); however, their importance in pneumococcal biology is very sparse. In this study, we determined

the contribution of each esterase gene to total esterase activity, evaluated the substrate specificity of pneumococcal

esterases, and investigated their role in potentiation of neuraminidase activity and glycoprotein utilisation. The results

showed that all mutants displayed significantly less esterase activity than the parental strain EstA, which is responsible

for the main esterase activity, and the pneumococcal esterases are specific for short acyl chains. In addition, EstA, but not

Axe, was found to catalyse tributyrin, and both EstA and Axe could use acetylated xylan as substrate. It was also found

that EstA and Axe use bovine submaxillary mucin (BSM), which is highly acetylated, as substrate to release acetate, and

pre-treatment of BSM by either EstA or Axe increases sialic acid release by neuraminidase. Esterases’ role in potentiation

of neuraminidase activity was further supported by decrease the ability of sialic acid release and growth of esteraseneuraminidase

mutants (ΔestAnanA and ΔaxenanA) in medium containing BSM as sole carbon source compared to

each of the respective single mutants. The replacement of S 121 in EstA and S 181 in Axe to alanine abolished the catalytic

activity of esterases. In addition, the mutation of estA alone or in combination with nanA reduced the pneumococcal

colonisation and virulence significantly after intranasal infection. qRT-PCR results showed that the expression level of

estA and axe were significantly up-regulated when exposed to BSM.

pneumonia 2015 Volume 7

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