Size Doesn't Matter: Towards a More Inclusive Philosophy of Biology

notes: As the primary author, O’Malley drafted the paper, and gathered and analysed data (scientific papers and talks). Conceptual analysis was conducted by both authors.publication-status: Publishedtypes: ArticlePhilosophers of biology, along with everyone else, generally perceive life to fall into two broad categories, the microbes and macrobes, and then pay most of their attention to the latter. ‘Macrobe’ is the word we propose for larger life forms, and we use it as part of an argument for microbial equality. We suggest that taking more notice of microbes – the dominant life form on the planet, both now and throughout evolutionary history – will transform some of the philosophy of biology’s standard ideas on ontology, evolution, taxonomy and biodiversity. We set out a number of recent developments in microbiology – including biofilm formation, chemotaxis, quorum sensing and gene transfer – that highlight microbial capacities for cooperation and communication and break down conventional thinking that microbes are solely or primarily single-celled organisms. These insights also bring new perspectives to the levels of selection debate, as well as to discussions of the evolution and nature of multicellularity, and to neo-Darwinian understandings of evolutionary mechanisms. We show how these revisions lead to further complications for microbial classification and the philosophies of systematics and biodiversity. Incorporating microbial insights into the philosophy of biology will challenge many of its assumptions, but also give greater scope and depth to its investigations

Subgingival Biofilm Communities in Health and Disease

AbstractOral biofilm-related diseases such as periodontal disease are infection processes that arise from the resident (indigenous) flora. Prior to the development of a periodontal lesion, a change in the proportion of certain species with greater pathogenic potential occurs within the biofilm. This change from a “commensal” flora to one considered pathogenic is accompanied by a disruption of the immune homeostasis and development of an inflammatory response. Chronic inflammation of the supporting periodontal structures eventually progresses to tooth loss. Although periodontal diseases have a multifactorial etiology in which environmental and host factors play an important role, polymicrobial biofilm communities with pathogenic properties are the primary etiological factor of periodontal lesions. Therefore, a thorough understanding of the events that lead to the maturation of subgingival biofilm communities is necessary in order to develop better diagnostic and treatment strategies. This review article will summerize our current understanding of the ecology of subgingival biofilms and the role of these multi-species communities as etiological agents of periodontal disease. An overview of the process of subgingival biofilm formation will be presented followed by a description of the ecological determinants of biofilm development in the subgingival environment. Finally, the concept of subgingival polymicrobial biofilm communities as the etiological agents that initiate a host-mediated inflamamtory response will be discussed

Coaggregation between Rhodococcus

In this study, coaggregation interactions between Rhodococcus and Acinetobacter strains isolated from food-processing surfaces were characterized. Rhodococcus sp. strain MF3727 formed intrageneric coaggregates with Rhodococcus sp. strain MF3803 and intergeneric coaggregates with 2 strains of Acinetobacter calcoaceticus (MF3293, MF3627). Stronger coaggregation between A. calcoaceticus MF3727 and Rhodococcus sp. MF3293 was observed after growth in batch culture at 30 °C than at 20 °C, after growth in tryptic soy broth than in liquid R2A medium, and between cells in exponential and early stationary phases than cells in late stationary phase. The coaggregation ability of Rhodococcus sp. MF3727 was maintained even after heat and Proteinase K treatment, suggesting its ability to coaggregate was protein independent whereas the coaggregation determinants of the other strains involved proteinaceous cell-surface-associated polymers. Coaggregation was stable at pH 5-9. The mechanisms of coaggregation among Acinetobacter and Rhodococcus strains bare similarity to those displayed by coaggregating bacteria of oral and freshwater origin, with respect to binding between proteinaceous and nonproteinaceous determinants and the effect of environmental factors on coaggregation. Coaggregation may contribute to biofilm formation on industrial food surfaces, protecting bacteria against cleaning and disinfection.submittedVersio