Effects of Water Acidification on Senegalese Sole Solea senegalensis Health Status and Metabolic Rate: Implications for Immune Responses and Energy Use

Abstract

Increasing water CO 2 , aquatic hypercapnia, leads to higher physiological pCO 2 levels in fish, resulting in an acidosis and compensatory acid-base regulatory response. Senegalese sole is currently farmed in super-intensive recirculating water systems where significant accumulation of CO 2 in the water may occur. Moreover, anthropogenic releases of CO 2 into the atmosphere are linked to ocean acidification. The present study was designed to assess the effects of acute (4 and 24 h) and prolonged exposure (4 weeks) to CO 2 driven acidification (i.e., pH 7.9, 7.6, and 7.3) from normocapnic seawater (pH 8.1) on the innate immune status, gill acid-base ion transporter expression and metabolic rate of juvenile Senegalese sole. The acute exposure to severe hypercapnia clearly affected gill physiology as observed by an increase of NHE3b positive ionocytes and a decrease of cell shape factor. Nonetheless only small physiological adjustments were observed at the systemic level with (1) a modulation of both plasma and skin humoral parameters and (2) an increased expression of HIF-1 expression pointing to an adjustment to the acidic environment even after a short period (i.e., hours). On the other hand, upon prolonged exposure, the expression of several pro-inflammatory and stress related genes was amplified and gill cell shape factor was aggravated with the continued increase of NHE3b positive ionocytes, ultimately impacting fish growth. While these findings indicate limited effects on energy use, deteriorating immune system conditions suggest that Senegalese sole is vulnerable to changes in CO 2 and may be affected in aquaculture where a pH drop is more prominent. Further studies are required to investigate how larval and adult Senegalese sole are affected by changes in CO 2 .

Implications of microscale lung damage for COVID-19 pulmonary ventilation dynamics: A narrative review

“…Much of the damage that occurs in acute and organizing DAD, as seen in CARDS as well as typical ARDS, directly affects the function of the alveolar space through dysfunction of surfactant, alveolar edema, and atelectatic regions. As surfactant functions to regulate surface tension in alveoli, the loss or dysfunction of surfactant can increase surface tension, altering the compliance and increasing stress in the surrounding alveoli [ 6 ]. The loss of type II alveolar epithelial cells in COVID-19 leads to loss of surfactant regulation and production [ 80 ].…”

“…Although due to limited studies on the early pathogenesis of COVID-19, it is difficult to determine the cause of surfactant disruption. Loss of type I and type II epithelial cells allow the alveoli to become flooded with edema, blood, and cellular debris as ion channels regulating fluid in the alveoli are lost or impaired leading to further degradation of the surfactant layer and epithelial cells [ 6 , 80 , 81 ]. The surfactant can also be degraded by reactive oxygen species from the interstitial side.…”

“…With increase in surface tension in the alveolus, edema, hemorrhage, and atelectatic regions act as stiff regions that show little to no expansion with breathing which increases stress in surrounding alveoli [ 6 , 82 ]. Any occlusion of airspace, such as the fibrin balls in AFOP or neutrophil extracellular traps (NETs), can block airflow and act as stiff regions in otherwise homogenous lung.…”

“…The linear portion of the curve displays the elastic properties, mostly in the range of normal breathing, while the upper curve is indicative of increased lung stiffness and thus increased resistance [ 5 ]. As lung properties arise from micromechanical properties, it is seen that tissue properties are highly dependent on the surface tension, as well as the stress bearing elements of the tissues [ 6 , 7 ]. In the context of mechanics, stress refers to the forces acting on an area of tissue and is related to the stiffness of the tissue, defined as the amount of stress due to a unit change in strain.…”

“…In this way, expansion of alveolar walls is modulated by the surfactant maintaining optimal surface area without overstretching the axial fibers and smoothing the alveolar epithelial surface for efficient gas exchange [ 17 ]. Dysfunction or compromise of the surfactant layer can arise from damage to the type II epithelial cells and edematous fluid or other cellular components filling the alveolar space [ 6 , 11 ].…”