Vanessa Schipani

Ecologists and immunologists have long approached scientific inquiry in fundamentally different ways. Immunologists thrive on drilling down into molecular minutiae, but ecologists strive to uncover broad associations between organisms and their environment. One field's signal has also been the other's noise—ecology explores uncontrolled variation, whereas immunology seeks to reduce it at all costs. “When I was in graduate school 10 years ago and I tried to get immunologists to help me, they thought I was crazy,” says Amy Pedersen, a disease ecologist at the University of Edinburgh. But the tides have turned. As lab researchers make forays into immune variation with the microbiome and multiple host infections, they have increasingly sought out Pedersen's ecological expertise. Pedersen is one of a growing number of hybrid researchers—ecologists persuaded by precise tools and immunologists fascinated by variation—who have begun to bridge the two disciplines. So-called ecoimmunologists share the belief that wild animals can help explain disease and immunity in ways that lab mice cannot.

Specimens of Lamellibrachia (Annelida: Siboglinidae) were recently discovered at cold seeps in the eastern Mediterranean. In this study, we have investigated the phylogeny and function of intracellular bacterial symbionts inhabiting the trophosome of specimens of Lamellibrachia sp. from the Amon mud volcano, as well as the bacterial assemblages associated with their tube. The dominant intracellular symbiont of Lamellibrachia sp. is a gammaproteobacterium closely related to other sulfide-oxidizing tubeworm symbionts. In vivo uptake experiments show that the tubeworm relies on sulfide for its metabolism, and does not utilize methane. Bacterial communities associated with the tube form biofilms and occur from the anterior to the posterior end of the tube. The diversity of 16S rRNA gene phylotypes includes representatives from the same divisions previously identified from the tube of the vent species Riftia pachyptila, and others commonly found at seeps and vents.

Journalists are often the adult public’s central source of scientific information, which means that their reporting shapes the relationship the public has with science. Yet philosophers of science largely ignore journalistic communication in their inquiries about trust in science. This paper aims to help fill this gap in research by comparing journalistic norm conflicts that arose when reporting on COVID-19 and tobacco, among other policy-relevant scientific topics. I argue that the public’s image of scientists – as depositories of indisputable, value-free facts, trustworthy only when in consensus – makes it particularly difficult for journalists to ethically communicate policy-relevant science rife with disagreement. In doing so, I show how journalists, like scientists, face the problem of inductive risk in such cases. To overcome this problem, I sketch a model of trust in science that is grounded in an alternative image of scientists – what I call the responsiveness model of trust in science. By highlighting the process of science over its product, the responsiveness model requires scientists to respond to empirical evidence and the public’s values to warrant the public’s trust. I then show why this model requires journalists to be the public’s watchdogs by verifying and communicating whether scientists are being properly responsive both epistemically and non-epistemically.