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Multiple lines of evidences have unraveled the emerging role of ferroptosis in the pathophysiological process of acute lung injury (ALI). In this study, we aimed to decipher the role of BACH1 in the onset and progression of ALI with a focus on ferroptosis and elucidated potential molecular mechanism. We observed that BACH1 expression was drastically elevated in BEAS-2B cells upon exposure to LPS. In the functional aspect, BACH1 deletion exerted an anti-inflammatory property, featured by decreased the secretion of several cytokines including TNF-α, IL-1β and IL-6 in the face of LPS challenge. What's more important, BACH1 knockout evidently repressed LPS-triggered oxidative stress damage, as evidenced by reduced reactive oxygen species (ROS) production and malondialdehyde (MDA) generation, accompanied with the elevated the activities of superoxide dismutase (SOD), GSH-Px and CAT. Meanwhile, ablation of BACH1 restrained LPS-elicited ferroptosis, as characterized by decreased iron content and PTGS2 expression, accompanied with increased expression of SLC7A11 and GPX4. In terms of mechanism, Nrf2/HO-1 signaling inhibitor effectively abrogated the beneficial effects of BACH1 inhibition on LPS-stimulated inflammation, oxidative damage and ferroptosis. Taken together, these preceding outcomes strongly illuminated that BACH1 was a novel regulator of LPS-evoked injury through regulation of inflammation response, oxidative stress and ferroptosis via activation Nrf2/HO-1 signaling, indicating that BACH1 may represent as a promising novel therapeutic candidate for ALI treatment. • BACH1 was aberrantly expressed in LPS-induced bronchial epithelial cells. • Deficiency of BACH1 mitigated LPS-elicited inflammatory response, oxidative stress damage and ferroptosis of BEAS-2B cells. • Interference of BACH1 protected against LPS-evoked injury via the activation of Nrf2/HO-1 signaling. [ABSTRACT FROM AUTHOR]

A total of 1,050 strains of heterotrophic bacteria isolated from farming seawater and the intestines of oyster species Crassostrea hongkongensis were tested for resistance to 10 antibiotics by the Kirby–Bauer diffusion method. The resistant rates of seawater-derived bacteria to chloramphenicol, enrofloxacin, and ciprofloxacin were low (less than 20%), whereas the bacteria obtained from oysters showed low resistance to chloramphenicol and enrofloxacin. Many strains showed high resistant rates (more than 40%) to furazolidone, penicillin G, and rifampin. A total of 285 strains from farming seawater and oysters were resistant to more than three antibiotics. Several strains showed resistance to more than nine antibiotics. Furthermore, the peak resistant rates of the seawater-derived strains to multiple antibiotics overlapped in April, June, September, and November, and those of oyster-derived strains overlapped during April, July, and September. The multi-resistant rate patterns of strains from farming seawater and oyster intestines were similar. [ABSTRACT FROM AUTHOR]