L48H37

HL-60 cells are a human promyelocytic leukemia cell model that can be induced toward granulocytic/neutrophil-like differentiation by DMSO, ATRA, or combined ATRA+DMSO treatment; differentiation is evaluated by morphology, reduced proliferation, CD11b gain, CD71 loss, phagocytosis, oxidative burst/NBT reduction, ROS formation, and, where relevant, NET-related assays. A literature-supported default protocol is 5 days of combined 1 µM ATRA plus 1% DMSO, because this condition produced neutrophil-like morphology, cell-cycle arrest, high CD11b positivity, low CD71 positivity, and increased phagocytic capacity compared with ATRA or DMSO alone in the cited study.

Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.

Inhalation toxicity studies expose rodents to a controlled aerosol, vapor, gas, or smoke atmosphere and assess respiratory and systemic toxicity using exposure-atmosphere characterization, clinical observations, body and organ weights, bronchoalveolar lavage fluid, histopathology, blood chemistry, hematology, and, when included, molecular endpoints such as transcriptomics, proteomics, lipidomics, or tissue burden analysis. The primary biological readouts are airway irritation, pulmonary inflammation, cytotoxicity, altered surfactant or lipid homeostasis, impaired particle clearance, and tissue remodeling, reflected by BALF cell differentials, BALF protein, LDH, phosphatase activities, cytokines, lung weight, microscopic respiratory-tract lesions, and retained lung burden.