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Devlin, R.

Publications and source records attributed to Devlin, R..

4 recordsLinked to original sources

Macrophage chemotaxis steered by complex self-generated gradients of complement C5a

Macrophages rely on efficient chemotaxis to locate sites of infection and tissue damage. One general strategy that enhances chemotactic accuracy is the use of self-generated gradients, where cells locally deplete attractants to create or sharpen guidance cues. Here we show that mouse bone marrow-derived macrophages (BMDMs) migrate toward the complement component C5a using this strategy. Cells actively deplete C5a from their surroundings, establishing local gradients as fresh attractant diffuses inward. We visualized this process in real time with fluorescent C5a and reproduced its dynamics using computational models. C5a depletion is mediated primarily by C5aR1-dependent endocytosis. This mechanism produces complex responses, with different C5a concentrations inducing temporally distinct waves of migration, and maximal chemotaxis occurring below 10 nM C5a. As expected, increasing C5a concentrations recruit more cells. In contrast, human macrophages inactivate C5a mainly through carboxypeptidase-mediated enzymatic degradation, yielding a higher optimal concentration ([~]30 nM) and distinct migratory dynamics. Both species also deplete externally imposed C5a gradients, sharpening them and enhancing guidance. These findings identify C5a degradation as a critical mechanism by which macrophages extract directional information from their environment. Self-generated gradient formation, despite different mechanisms across species, emerges as a conserved and versatile strategy for immune navigation.

immunology↗

POLYGENIC DETERMINANTS OF H5N1 ADAPTATION TO BOVINE CELLS

Avian influenza H5N1 clade 2.3.4.4b viruses caused a global panzootic and, unexpectedly, widespread outbreaks in dairy cattle, therefore representing a pandemic threat. To inform effective control strategies, it is critical to determine whether the potential to adapt to bovine cells is a generalised feature of H5N1 viruses, or is specific to clade 2.3.4.4b, or even more restricted to specific genotypes within this clade (e.g., B3.13 and D1.1). Using a large panel of H5N1 viruses representing >60 years of their natural history and other IAV for comparative purposes, we demonstrate that virus adaptation to bovine cells is: (i) highly variable across 2.3.4.4b genotypes, (ii) limited in viruses predating the global expansion of this clade, (iii) determined by the viral internal gene cassette, and (iv) not restricted to udder epithelial cells. Mutations in the PB2 polymerase subunit, particularly M631L, emerge as key determinants of adaptation, although their phenotypic effects are context dependent and have limited enhanced viral polymerase activity in human cells. Bovine B3.13 and some avian genotypes also exhibit enhanced modulation of bovine interferon-induced antiviral responses, determined by at least the viral PB2, nucleoprotein, and the non-structural protein NS1. Our results highlight the polygenic nature of IAV host range and reveal that the potential to cross the species barrier varies during the evolutionary trajectory of H5N1, with some avian viruses more predisposed to spillover than others.

microbiology↗

Superinfection exclusion creates spatially distinct influenza virus populations

Influenza viruses can interact during coinfections, allowing viral fitness to be altered by genome complementation and competition, and increasing population diversity through reassortment. However, opportunities for these interactions are limited, as coinfection is blocked shortly after primary infection by a process known as superinfection exclusion (SIE). We asked whether SIE, which occurs at the level of individual cells, could limit within-host interactions between populations of influenza viruses as they spread across regions of cells. We first created a simplified model of within-host spread by infecting monolayers of cells with two isogenic influenza A viruses, each encoding a different fluorophore, and measuring the proportion of coinfected cells. In this system SIE begins within 2-4 hours of primary infection, with the kinetics of onset defined by the dose of primary virus. We then asked how SIE controls opportunities for coinfection as viruses spread across a monolayer of cells. We observed that viruses spreading from a single coinfected focus continued to coinfect cells as they spread, as all new infections were of cells that had not yet established SIE. In contrast, viruses spreading towards each other from separately infected foci could only establish minimal regions of coinfection before SIE blocked further coinfection. This patterning was recapitulated in the lungs of infected mice and is likely to apply to other viruses that exhibit SIE. It suggests that the kinetics of SIE onset separate a spreading infection into discrete regions, within which interactions between virus populations can occur freely, and between which they are blocked. ImportanceViral fitness and diversity are altered by genome interactions, which occur when multiple viruses coinfect a cell. This has been extensively studied for influenza A viruses (IAV), which use genome reassortment to adapt to new hosts and create pandemic strains, and whose replication can be compromised by the acquisition of defective-interfering RNAs. Coinfection of an individual cell by IAV is restricted by the gradual onset of superinfection exclusion (SIE). Replication of IAVs within host organisms involve the asynchronous replication of viruses as they spread to infect multiple cells. We found that under these circumstances, SIE creates spatially separated sub-populations of IAV, between which there are limited opportunities for genome interactions. Our work suggests SIE will cause many viruses to segregate into distinct subpopulations within their hosts, constraining the effects of genome interactions on their fitness and evolution.

microbiology↗

Growth hormone transgenesis disrupts immune function in muscle of coho salmon (Oncorhynchus kisutch) impacting cross-talk with growth systems

The suppression of growth during infection should facilitate resource allocation towards effective immune function. Work supporting this hypothesis has been recently reported in teleosts, demonstrating immune-responsive regulation of the insulin-like growth factor (IGF) system - a key endocrine growth pathway that acts downstream of growth hormone (GH). Skeletal muscle is the main target for growth and energetic storage in fish, yet little is known about how growth is regulated in this tissue during an immune response. We addressed this knowledge gap by characterizing muscle immune responses in size-matched coho salmon (Oncorhynchus kisutch) achieving different growth rates. We compared a wild-type strain with two GH transgenic groups achieving either maximal or highly-suppressed growth - an experimental design that separates GHs direct effects from its influence on growth rate. Fish were sampled 30h post-injection with PBS (control) or mimics of bacterial (peptidoglycan) or viral (Poly:IC) infection. We quantified the mRNA level expression of genes from the GH, GH receptor (GHR), IGF hormone, IGF1 receptor (IGF-1R) and IGF binding protein (IGFBP) families, along with marker genes for muscle growth and host defence genes involved in inflammatory or antiviral responses. We provide strong evidence for dampened immunity in the GH transgenics compared to wild-type animals. Strikingly, the muscle of GH transgenics achieving rapid growth showed no detectable antiviral response, coupled with evidence of a constitutive inflammatory state. GH and IGF system gene expression was also strongly altered by GH transgenesis and fast growth, both for baseline expression levels and responses to immune stimulation. Overall, our findings demonstrate that GH transgenesis disrupts normal immune function and growth-immune cross-talk in muscle, with implications for the health and welfare of farmed salmon.

physiology↗