Correction: Lagrois et al. Low-to-Mid-Frequency Monopole Source Levels of Underwater Noise from Small Recreational Vessels in the St. Lawrence Estuary Beluga Critical Habitat. Sensors 2023, 23, 1674.

There was an error in the original publication [...].

Low-to-Mid-Frequency Monopole Source Levels of Underwater Noise from Small Recreational Vessels in the St. Lawrence Estuary Beluga Critical Habitat.

Anthropogenic noise from navigation is a major contributor to the disturbance of the acoustic soundscape in underwater environments containing noise-sensitive life forms. While previous studies mostly developed protocols for the empirical determination of noise source levels associated with the world's commercial fleet, this work explores the radiated noise emitted by small recreational vessels that thrive in many coastal waters, such as in the St. Lawrence Estuary beluga population's summer habitat. Hydrophone-based measurements in the Saguenay River (QC, Canada) were carried out during the summers of 2021 and 2022. Shore-based observations identified 45 isolated transits of small, motorized vessels and were able to track their displacement during their passage near the hydrophone. Received noise levels at the hydrophone typically fell below the hearing audiogram of the endangered St. Lawrence Estuary beluga. Monopole source levels at low frequencies (0.1-≲2 kHz) held on average twice the acoustic power compared to their mid-frequency (≳2-30 kHz) counterparts. The speed over ground of recreational vessel showed a positive correlation with the back-propagated monopole source levels. Estimations of the mid-frequency noise levels based on low-frequency measurements should be used moderately.

Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis.

The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis (MS). However, the impact of endothelial-derived factors on CNS immune responses remains unknown. Bioactive lipids, in particular oxysterols downstream of Cholesterol-25-hydroxylase (Ch25h), promote neuroinflammation but their functions in the CNS are not well-understood. Using floxed-reporter Ch25h knock-in mice, we trace Ch25h expression to CNS endothelial cells (ECs) and myeloid cells and demonstrate that Ch25h ablation specifically from ECs attenuates experimental autoimmune encephalomyelitis (EAE). Mechanistically, inflamed Ch25h-deficient CNS ECs display altered lipid metabolism favoring polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC) expansion, which suppresses encephalitogenic T lymphocyte proliferation. Additionally, endothelial Ch25h-deficiency combined with immature neutrophil mobilization into the blood circulation nearly completely protects mice from EAE. Our findings reveal a central role for CNS endothelial Ch25h in promoting neuroinflammation by inhibiting the expansion of immunosuppressive myeloid cell populations.

Avoiding sharp accelerations can mitigate the impacts of a Ferry's radiated noise on the St. Lawrence whales.

Exposure to anthropogenic noise from the commercial fleet is one of the primary constituents of the acoustic pollution perturbing the environment of aquatic life. Merchant ships (e.g. bulkers, tankers) have been the focus of numerous studies for underwater noise source level determination and modeling. This work extends pre-existing studies to the ferry ship class. Hydrophone-based measurements of the N.M. Trans-Saint-Laurent ferry near the Rivière-du-Loup harbor (Rivière-du-Loup, QC CANADA) were obtained for 186 transits between 2020 July 22th and 2020 September 5th. For each transit, monopole source levels are estimated for two (2) different modes of operation i.e., the low-speed phases of acceleration/deceleration when the ferry launches/docks at Rivière-du-Loup and the passages at quasi-operational speed at the hydrophone's closest-point-of-approach. Relative differences between the two (2) modes of operation are presented here in the low-frequency domain between 141 and 707 Hz. An average excess of 8 to 11.5 dB indicates that the ferry is likely one order of magnitude noisier, within this frequency band, during acceleration/deceleration when compared to passages at operational speed. This highlights that, in terms of marine mammal conservation, a significant reduction of the noise pollution could be achieved, for instance, by avoiding sudden speed changes in the vicinity of whales.

Macroautophagy in lymphatic endothelial cells inhibits T cell-mediated autoimmunity.

Lymphatic endothelial cells (LECs) present peripheral tissue antigens to induce T cell tolerance. In addition, LECs are the main source of sphingosine-1-phosphate (S1P), promoting naive T cell survival and effector T cell exit from lymph nodes (LNs). Autophagy is a physiological process essential for cellular homeostasis. We investigated whether autophagy in LECs modulates T cell activation in experimental arthritis. Whereas genetic abrogation of autophagy in LECs does not alter immune homeostasis, it induces alterations of the regulatory T cell (T reg cell) population in LNs from arthritic mice, which might be linked to MHCII-mediated antigen presentation by LECs. Furthermore, inflammation-induced autophagy in LECs promotes the degradation of Sphingosine kinase 1 (SphK1), resulting in decreased S1P production. Consequently, in arthritic mice lacking autophagy in LECs, pathogenic Th17 cell migration toward LEC-derived S1P gradients and egress from LNs are enhanced, as well as infiltration of inflamed joints, resulting in exacerbated arthritis. Our results highlight the autophagy pathway as an important regulator of LEC immunomodulatory functions in inflammatory conditions.

Lymph Node Stromal Cells: Mapmakers of T Cell Immunity.

Stromal cells (SCs) are strategically positioned in both lymphoid and nonlymphoid organs to provide a scaffold and orchestrate immunity by modulating immune cell maturation, migration and activation. Recent characterizations of SCs have expanded our understanding of their heterogeneity and suggested a functional specialization of distinct SC subsets, further modulated by the microenvironment. Lymph node SCs (LNSCs) have been shown to be particularly important in maintaining immune homeostasis and T cell tolerance. Under inflammation situations, such as viral infections or tumor development, SCs undergo profound changes in their numbers and phenotype and play important roles in contributing to either the activation or the control of T cell immunity. In this review, we highlight the role of SCs located in LNs in shaping peripheral T cell responses in different immune contexts, such as autoimmunity, viral and cancer immunity.