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Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus, Severe Acute Respiratory Syndrome-Coronavi- rus-2 (SARS-CoV-2), led to the ongoing global public health crisis. Existing clinical data suggest that COVID-19 patients with acute respiratory distress syndrome (ARDS) have worse outcomes and increased risk of intensive care unit (ICU) admission. The rapid increase in the numbers of patients requiring ICU care may imply a sudden and major challenge for affected health care systems. In this narrative review, we aim to summarize current knowledge of pathophysiology, clinical and morphological characteristics of COVID-19-associated ARDS and ARDS caused by other factors (classical ARDS) as defined by Berlin criteria, and therefore to elucidate the differences, which can affect clinical management of COVID-19-as- sociated ARDS. Fully understanding the characteristics of COVID-19-associated ARDS will help identify its early progres- sion and tailor the treatment, leading to improved prognosis in severe cases and reduced mortality. The notable mechanisms of COVID-19-associated ARDS include severe pulmonary infiltration/edema and inflammation, leading to impaired alveolar homeostasis, alteration of pulmonary physiology resulting in pulmonary fibrosis, endothelial inflammation and vascular thrombosis. Despite some distinct differences between COVID-19-associated ARDS and classical ARDS as defined by Ber- lin criteria, general treatment principles, such as lung-protective ventilation and rehabilitation concepts should be applied whenever possible. At the same time, ventilatory settings for COVID-19-associated ARDS require to be adapted in individ- ual cases, depending on respiratory mechanics, recruitability and presentation timing.

The combined lactic acid, monolaurin, and nisin effects on time-to-detection (optical density at 600 nm) extension were greater (P < 0.05) than any single or paired combination effect, which demonstrates a synergistic interaction among the antimicrobials. Monolaurin exposure caused C12:0 cell membrane incorporation. Lactic acid caused increased monolaurin C12:0 membrane incorporation, while nisin had no influence. We postulate that lactic acid-enhanced monolaurin C12:0 incorporation into the cell membrane increased membrane fluidity resulting in increased nisin activity.Listeria monocytogenes is a well-known food-borne human pathogen associated with the consumption of ready-to-eat foods that is ubiquitous in the natural environment (15). One method to control L. monocytogenes in ready-to-eat foods is through the use of antimicrobial interventions. Kabara and Marshall (6) suggested that future antimicrobial applications in foods would be more likely to be not through the invention of novel antimicrobials but rather through effective combinations of existing ones by using the multiple-hurdle concept to achieve additive or synergistic effects. The effectiveness of fatty acid monoesters (such as monolaurin [ML]) against grampositive bacteria, especially L. monocytogenes, is well documented (6, 13). Low-molecular-weight organic acids (such as lactic acid [LA]) have a long history of being used to control microbial growth (3), and their synergistic interaction with ML has been previously shown (14). Bacteriocins (such as nisin [NI]) derived from LA bacteria have been investigated for use as potential antimicrobial treatments (1,11,16). Synergistic interactions of NI-LA (12) and NI-ML (8) combinations have been reported.The ability of bacteria to multiply under suboptimal conditions (low pH or in the presence of toxic chemicals) requires membrane fluidity modification, a phenomenon known as homeoviscous adaptation (15). Membrane fluidity can be altered through membrane fatty acid profile modification (18). Several reports have described fatty acid profile changes in L. monocytogenes that were caused by growth temperature (7, 9), NI (7, 9), and individual fatty acids (5). To our knowledge, no one has described the combined effects of LA, ML, and NI on growth inhibition of L. monocytogenes. In addition, we are unaware of reports demonstrating how these agents may act together to alter membrane fluidity of the bacterium. Therefore, the present study was designed to define the interaction between these agents and to elucidate how they may influence the cell membrane fluidity of L. monocytogenes. MATERIALS AND METHODSCulture preparation. NI-sensitive Listeria monocytogenes ATCC 7644 was maintained at 4°C on Trypticase soy agar plus 0.6% yeast extract (BD Diagnostic Systems, Sparks, MD) slants with biweekly transfers. Working culture preparation involved streaking slant cultures onto Trypticase soy agar plates (35°C, 24 h), followed by individual colony inoculation into 30 ml Trypticase soy broth plus 0.6% yeast extract (TSB...