HMGB1 and Metabolic Pathways in Acinetobacter baumannii Severe Pneumonia: An Associative Study

Severe pneumonia, often caused by Acinetobacter baumannii, leads to lung injury and multisystem dysfunction. High Mobility Group Box 1 (HMGB1) is a key player in severe pneumonia progression. We studied 63 patients with Acinetobacter baumannii severe pneumonia, categorizing them into severe pneumonia (n=44), severe pneumonia with multi-organ failure (n=19), and healthy individuals (n=29). We assessed clinical parameters, measured HMGB1, and conducted metabolomic analysis. SD rats were used for validation. Patients with Acinetobacter baumannii severe pneumonia showed significantly elevated HMGB1 levels. In the multi-organ failure group, neutrophils, monocytes, and HMGB1 were higher, while lymphocytes were lower. Metabolomic analysis identified 335 metabolites, with 28 linked to HMGB1. Four key metabolites—12-HPETE, Asparagine, Lactic acid, and Carbamyl-aspartate—were found. 12-HPETE, Asparagine, and Lactic acid were elevated in severe pneumonia and organ failure patients, whereas Carbamylaspartate decreased specifically in organ failure (P<0.05). HMGB1 elevation was confirmed in SD rats, and HMGB1 blockade reduced lung inflammation. Our study suggests HMGB1 as a marker for risk assessment, especially in patients with multiple organ dysfunction syndromes, and its role in initiating pro-inflammatory and glycolytic pathways.