cefoxitin and Acute-Lung-Injury

Prolonged hyperoxia exposure leads to inflammation and acute lung injury. Since hyperoxia activates nuclear factor kappa B (NF-κB) and proinflammatory mediators in lung fibroblasts and murine lungs, and proinflammatory cytokines upregulate Tn (N-acetyl-d-galactosamine-O-serine/threonine) expression in human gingival fibroblasts. We hypothesized connections exist between Tn expression and inflammation regulation. Thus, we immunized adult mice with Tn antigen to examine whether Tn vaccine can protect against hyperoxia-induced lung injury by inhibiting NF-κB activity and cytokine expression through the action of anti-Tn antibodies. Five-week-old female C57BL/6NCrlBltw mice were subcutaneously immunized with Tn antigen four times at biweekly intervals, and one additional immunization was performed at 1 week after the fourth immunization. Four days after the last immunization, mice were exposed to room air (RA) or hyperoxia (100% O

Topics: Acute Lung Injury; Animals; Antibodies; Antigens, Tumor-Associated, Carbohydrate; Bronchoalveolar Lavage Fluid; Cytokines; Female; Hyperoxia; Immunization; Interleukin-6; Lung; Macrophages, Alveolar; Mice; Mice, Inbred C57BL; NF-kappa B; Tumor Necrosis Factor-alpha