Biology subjects

Ketley, J. M.

Publications and source records attributed to Ketley, J. M..

3 recordsLinked to original sources

bioRxiv2023

Air pollution modifies key colonization factors of the beneficial bee gut symbiont Snodgrassella alvi and disrupts the bumblebee (Bombus terrestris) gut microbiome.

Air pollution is the worlds largest environmental health risk. Particulate pollutants, a major component of air pollution, are detrimental to human health and a significant risk to wildlife and ecosystems globally. Black carbon, a by-product of fossil fuel and biomass burning, is a key constituent of air pollution with levels continuing to increase worldwide. Here we describe the effects of black carbon on the beneficial gut microbiome of an important global insect pollinator, the buff-tailed bumblebee (Bombus terrestris). Our data shows that exposure to black carbon particulates alters the biofilm structure, gene expression and initial adhesion of beneficial bee gut coloniser, Snodgrassella alvi in vitro. Additionally, our results show that black carbon disrupts adult Bombus terrestris gut microbiome composition, a vital component to bee health. Exposure to black carbon increased bees viable gut bacteria and significantly altered the abundance of beneficial core bacteria Gilliamella and Bombilactobacillus in the microbiome. These findings demonstrate that exposure to black carbon air pollution has direct, measurable effects on bees beneficial gut commensal bacteria and microbiome. Together these data highlight that particulate pollutants are an underexplored risk for the health of insect pollinators.

microbiology↗

bioRxiv2023

A CheZ orthologue in Campylobacter jejuni plays a role in chemotaxis through conserved phosphatase activity

The major food-borne pathogen Campylobacter jejuni employs chemotactic motility to colonise the avian gut, and also as a virulence mechanism in human diarrhoeal disease. In Escherichia coli CheY activity is modulated by CheZ, a phosphatase originally thought to be absent in C. jejuni. The Hp0170 protein of Helicobacter pylori is a distant homologue of CheZ and, as C. jejuni Cj0700 is homologous to HP0170, Cj0700 could also act as a CheZ orthologue in Campylobacter. Both the C. jejuni CheV and CheA proteins also contain a response regulator (RR) domain that may be phosphorylated. Cj0700 would therefore be predicted to dephosphorylate C. jejuni CheY and possibly also the CheV and CheA RR domains. A mutant ({Delta}cj0700) and complement ({Delta}cj0700, cj0046::cj0700) were constructed in C.jejuni strains NCTC11168, NCTC11828 and 81-176. On semisolid agar the {Delta}cj0700 mutant strain showed reduced motility relative to wild-type and this phenotype was reversed in the complemented strain. In pull down and bacterial two hybrid assays, expressed Cj0700 was able to interact with CheY, CheA-RR and CheV. Cj0700 is able to dephosphorylate the RR domain of CheY and CheA-RR, but less efficiently, CheV. These findings verify that Cj0700 plays a role in C. jejuni chemotaxis through phosphatase activity with respect to CheY, and is hence likely to be a CheZ orthologue. Cj0700 also partially modulates the phosphorylation level of the RR domain on CheA and CheV, although the functional consequences of this interaction require further investigation.

microbiology↗

bioRxiv2022

Air pollution induces Staphylococcus aureus USA300 respiratory tract colonisation mediated by specific bacterial genetic responses dependent on the global virulence gene regulators Agr and Sae

Exposure to particulate matter (PM), a major component of air pollution, is associated with exacerbation of chronic respiratory disease, and infectious diseases such as community acquired pneumonia. Although PM can cause adverse health effects through direct damage to host cells, our previous study showed that PM can also impact bacterial behaviour by promoting in vivo colonisation. In this study we describe the genetic mechanisms involved in the bacterial response to exposure to black carbon (BC), a constituent of PM found in most sources of air pollution. We show that Staphylococcus aureus strain USA300 LAC grown in BC prior to inoculation showed increased murine respiratory tract colonisation and pulmonary invasion in vivo, as well as adhesion and invasion of human epithelial cells in vitro. Global transcriptional analysis showed that BC has a widespread effect on S. aureus transcriptional responses, altering the regulation of the major virulence gene regulators Sae and Agr and causing increased expression of genes encoding toxins, proteases, and immune evasion factors. Together these data describe a previously unrecognised causative mechanism of air pollution-associated infection, in that exposure to BC can increase bacterial colonisation and virulence factor expression by acting directly on the bacterium rather than via the host. Originality-Significance StatementThis study shows that exposure to air pollution results in a global change in gene expression in bacteria. Specifically, our data show that in the important human pathogen Staphylococcus aureus, exposure to a major constituent of air pollution, black carbon (BC) results in widespread changes in global gene expression, altering the expression of key virulence determinants. Furthermore, S. aureus that are exposed to BC prior to inoculation show increased colonisation of the murine nasopharynx and lungs in vivo, and increased adhesion and invasion in lung epithelial cells in vitro. These findings indicate that air pollution has a significant and direct impact on bacteria, altering their behaviour and their potential to colonise and invade during infection. While many studies have taken a host-focussed approach to studying the impact of air pollution on human health, this study takes a pathogen-focussed approach to further the understanding of these fundamental interactions to identify new causative mechanisms of the detrimental effects of air pollution. This is critical for understanding the adverse health effects caused by exposure to air pollution, the single largest environmental risk to human health in the world.

microbiology↗