Geology, Geochemistry and U-Pb SHRIMP Age of the Tacloban Ophiolite Complex, Leyte Island (Central Philippines): Implications for the Existence and Extent of the Proto-Philippine Sea Plate

The oceanic basement of the Central Philippines is exposed in ophiolitic massifs the age and origin of which remain debated. The Tacloban Ophiolite Complex (TOC) outcrops as a NW-SE trending massif in the northeastern portion of Leyte Island, Central Philippines. It is unconformably overlain by sedimentary sequences dated to Late Miocene-Pliocene and Pleistocene volcaniclastic deposits on its eastern and western flanks, respectively. Field, petrographic and trace element data suggest a subduction-related origin for this ophiolite. Sensitive High Resolution Ion Microprobe (SHRIMP) U-Pb dating of zircons from a gabbro yielded Early Cretaceous magmatic age for the TOC, which is very much older than a previously reported whole rock K-Ar derived Eocene age. The Early Cretaceous age of the TOC limits its possible progenitor to the proto-Philippine Sea Plate. Correlation with other Cretaceous ophiolites in Central Philippines reveals the possible extent of the proto-Philippine Sea Plate remnants now exposed onland

Macrophages disseminate pathogen associated molecular patterns through the direct extracellular release of the soluble content of their phagolysosomes

Recognition of pathogen-or-damage-associated molecular patterns is critical to inflammation. However, most pathogen-or-damage-associated molecular patterns exist within intact microbes/cells and are typically part of non-diffusible, stable macromolecules that are not optimally immunostimulatory or available for immune detection. Partial digestion of microbes/cells following phagocytosis potentially generates new diffusible pathogen-or-damage-associated molecular patterns, however, our current understanding of phagosomal biology would have these molecules sequestered and destroyed within phagolysosomes. Here, we show the controlled release of partially-digested, soluble material from phagolysosomes of macrophages through transient, iterative fusion-fission events between mature phagolysosomes and the plasma membrane, a process we term eructophagy. Eructophagy is most active in proinflammatory macrophages and further induced by toll like receptor engagement. Eructophagy is mediated by genes encoding proteins required for autophagy and can activate vicinal cells by release of phagolysosomally-processed, partially-digested pathogen associated molecular patterns. We propose that eructophagy allows macrophages to amplify local inflammation through the processing and dissemination of pathogen-or-damage-associated molecular patterns