Abstract
Background Basil polysaccharide (BPS) represents a main active ingredient extracted from basil (Ocimum basilicum L.), which can regulate secondary bacterial pneumonia development in the process of sepsis-mediated immunosuppression. Methods In this study, a dual model of sepsis-induced secondary pneumonia with cecal ligation and puncture and intratracheal instillation of Staphylococcus aureus or Pseudomonas aeruginosa was constructed. Results The results indicated that BPS-treated mice undergoing CLP showed resistance to secondary S. aureus pneumonia. Compared with the IgG-treated group, BPS-treated mice exhibited better survival rate along with a higher bacterial clearance rate. Additionally, BPS treatment attenuated cell apoptosis, enhanced lymphocyte and macrophage recruitment to the lung, promoted pulmonary cytokine production, and significantly enhanced CC receptor ligand 4 (CCL4). Notably, recombinant CCL4 protein could enhance the protective effect on S. aureus-induced secondary pulmonary infection of septic mice, which indicated that BPS-induced CCL4 partially mediated resistance to secondary bacterial pneumonia. In addition, BPS priming markedly promoted the phagocytosis of alveolar macrophages while killing S. aureus in vitro, which was related to the enhanced p38MAPK signal transduction pathway activation. Moreover, BPS also played a protective role in sepsis-induced secondary S. aureus pneumonia by inducing Treg cell differentiation. Conclusions Collectively, these results shed novel lights on the BPS treatment mechanism in sepsis-induced secondary S. aureus pneumonia in mice.
Highlights
Sepsis is a complex immunopathological syndrome characterized by life-threatening organ dysfunction caused by a deregulated host response to systemic infection [1]
We found that basil polysaccharide administration can improve the survival rate of S. aureus pneumonia or cecal ligation and puncture (CLP)-induced secondary S. aureus pneumonia mouse model
Our study revealed that basil polysaccharide can significantly increase the level of CC receptor ligand 4 (CCL4) in the lungs of sepsis-induced secondary S. aureus pneumonia mice (Figure 3(f))
Summary
Sepsis is a complex immunopathological syndrome characterized by life-threatening organ dysfunction caused by a deregulated host response to systemic infection [1]. A study reported that the pooled incidence of hospital-treated sepsis patients was 189/100,000 person-years, whereas the estimated mortality rate was 26.7%. Great inflammatory response is previously reported to induce sepsis-related deaths early, whereas compensatory anti-inflammatory response is suggested to cause deaths following organ failure via the dominant congenital immunity, affecting endothelial function, blood flow, and parenchymal cell metabolism [6]. The results indicated that BPS-treated mice undergoing CLP showed resistance to secondary S. aureus pneumonia. Recombinant CCL4 protein could enhance the protective effect on S. aureusinduced secondary pulmonary infection of septic mice, which indicated that BPS-induced CCL4 partially mediated resistance to secondary bacterial pneumonia. These results shed novel lights on the BPS treatment mechanism in sepsis-induced secondary S. aureus pneumonia in mice
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