Tissue Microenvironments Define and Get Reinforced by Macrophage Phenotypes in Homeostasis or during Inflammation, Repair and Fibrosis

Current macrophage phenotype classifications are based on distinct in vitro culture conditions that do not adequately mirror complex tissue environments. In vivo monocyte progenitors populate all tissues for immune surveillance which supports the maintenance of homeostasis as well as regaining homeostasis after injury. Here we propose to classify macrophage phenotypes according to prototypical tissue environments, e.g. as they occur during homeostasis as well as during the different phases of (dermal) wound healing. In tissue necrosis and/or infection, damage- and/or pathogen-associated molecular patterns induce proinflammatory macrophages by Toll-like receptors or inflammasomes. Such classically activated macrophages contribute to further tissue inflammation and damage. Apoptotic cells and antiinflammatory cytokines dominate in postinflammatory tissues which induce macrophages to produce more antiinflammatory mediators. Similarly, tumor-associated macrophages also confer immunosuppression in tumor stroma. Insufficient parenchymal healing despite abundant growth factors pushes macrophages to gain a profibrotic phenotype and promote fibrocyte recruitment which both enforce tissue scarring. Ischemic scars are largely devoid of cytokines and growth factors so that fibrolytic macrophages that predominantly secrete proteases digest the excess extracellular matrix. Together, macrophages stabilize their surrounding tissue microenvironments by adapting different phenotypes as feed-forward mechanisms to maintain tissue homeostasis or regain it following injury. Furthermore, macrophage heterogeneity in healthy or injured tissues mirrors spatial and temporal differences in microenvironments during the various stages of tissue injury and repair. Copyright (C) 2012 S. Karger AG, Base

Spatial and temporal variations in turbidity on two inshore turbid reefs on the Great Barrier Reef, Australia

This study describes the natural turbidity regimes at two inshore turbid reefs on the central Great Barrier Reef where wind-driven waves are the main agent of sediment resuspension. Many corals on inshore turbid reefs have adapted to high and fluctuating turbidity, however, anthropogenic activities such as dredging are speculated to produce larger and more prolonged turbidity events that may exceed the environmental tolerance and adaptive capacity of corals on these reefs. Natural turbidity regimes must be described and understood to determine whether and when coral communities on inshore turbid reefs are at risk from anthropogenically elevated turbidity, but at present few baseline studies exist. Here, we present turbidity data from (a) Middle Reef, a semi-protected reef located between Magnetic Island and Townsville and (b) Paluma Shoals, a reef exposed to higher energy wind and waves located in Halifax Bay. Instruments were deployed on both reefs for 16 days to measure spatial and temporal variations in turbidity and its driving forces (waves, currents, tides). Locally driven wind waves were the key driver of turbidity, but the strength of the relationship was dependent on wave exposure. Turbidity regimes thus vary markedly over individual reefs and this is reflected in community assemblage distributions, with a high abundance of heterotrophic corals (e.g. Goniopora) in reef habitats subjected to large fluctuations in turbidity (> 100 NTU). A turbidity model developed using local wind speed data explained up to 75 % and up to 46 % of the variance in turbidity at Paluma Shoals and Middle Reef, respectively. Although the model was based on a brief two-week observational period, it reliably predicted variations in 24-h averaged turbidity and identified periods when turbidity rose above ambient baseline levels, offering reef managers insights into turbidity responses to modified climate and coastal sediment delivery regimes