As a result of pancreatic enzyme activation, acute pancreatitis (AP) causes inflammation localized to the pancreas, which ultimately causes systemic inflammation [1,2]. The majority of patients with AP are clinically mild and have a self-limiting course; however, approximately 20 % of patients progress to severe acute pancreatitis (SAP) [2]. Several studies have found that various metabolites produced by gut microbiota play a key role in SAP development, and that dysbiosis of the gut microbiota during SAP is characterized by a decrease in microbial diversity and a change in the balance between commensal and pathogenic microbiota, which is composed of Escherichia coli, Shigella flexneri, Enterobacteriaceae bacterium, Acinetobacter lwoffii, Bacillus coagulans, and Enterococcus faecium [3,4]. In SAP, the most common and earliest critical complication is acute lung injury (ALI). ALI is primarily caused by a response to inflammation [5]. Pathophysiological features of this condition include inflammation and an imbalance between proinflammatory and anti-inflammatory responses. ALI may ultimately progress to respiratory failure, with mortality and morbidity remaining relatively high and without approved effective drugs or treatments [6]. New biological targets for acute pancreatitis-associated lung damage (PALI) have been discovered as a result of limited therapy choices. A steadily increasing understanding of the role of intestinal bacteria and metabolites in mediating SAP has encouraged interest in the "gut–lung axis" in PALI [7,8].

Approximately 20 % of adults have the anaerobic bacterium Clostridium butyricum in their gut. Numerous investigations have demonstrated the ability of C. butyricum to modify the gut microecology and lessen inflammatory damage [9,10]. Our team discovered that by preserving the intestinal mucosal barrier function and controlling the intestinal microbiota, C. butyricum might lessen inflammatory damage after being pre-applied to reverse acute pancreatitis injury [11]. Moreover, by preventing the production of inflammatory pathways, C. butyricum can lessen lung inflammation [12]. Several studies have been conducted to adjust the balance between the host and microbiota using probiotics and dietary changes to maintain immune and metabolic homeostasis in the body in order to address lung conditions [13]. Cait et al. found that lung inflammation caused by dysbiosis could be effectively ameliorated by feeding short chain fatty acids [14]. In addition to lowering in-hospital mortality for patients with SAP, the implementation of methods mediated by controlling intestinal microecology or related functions also somewhat lowers the risk of combined lung injury [15]. So we propose that C. butyricum can reduce the potential for PALI by interfering with intestinal microbiota and related metabolic pathways.

Monocyte chemotactic protein-1 (MCP-1) is an important marker of lung injury, and the receptors CCR2 and MCP-1 are crucial for macrophage movement [16]. Acute respiratory distress syndrome (ALI) and its pathophysiology are mostly mediated by macrophages, and a crucial step in the development of inflammatory injury is mobilization into injured tissues [17]. The MCP-1 protein is the most powerful inducer of signaling pathways that cause monocyte migration, and it is often released by macrophages in response to pathogen infection [18]. Based on the gut–lung axis theory, this research explored the impact of C. butyricum on AP combined with lung injury from the perspective of intestinal microbiota and metabolomics, using MCP-1 as a marker of lung injury. It is speculated that C. butyricum may regulate lung injury by influencing the microbiota and metabolism, thus affecting the expression of MCP-1.