Chromofungin (CHR) is a biologically active peptide derived from chromogranin A that exhibits anti-inflammatory effects. However, it remains unclear whether and how CHR protects against sepsis-induced acute lung injury (ALI). A murine model of sepsis-induced ALI was established through cecal ligation and puncture, with intraperitoneal injection of CHR. Lung inflammation and macrophage polarization were examined by measuring the levels of cytokines and markers of M1 (CD86, inducible nitric oxide synthase [iNOS]) or M2 macrophages (arginase-1 [Arg1], resistin-like molecule α1 [Fizz1] and CD206). In vitro, mouse MH-S cells pretreated with CHR was employed to explore the interplay between the lipopolysaccharide-binding protein (LBP)/toll-like receptor 4 (TLR4) signaling pathway and M1/M2 polarity. The results revealed CHR's ability to enhance the 7-day survival rate and protect lung pathological injury in sepsis-induced ALI. CHR increased the expression of interleukin-4 and interleukin-10 but decreased the expression of tumour necrosis factor-α and interleukin-1β. In addition, CHR notably facilitated M2 macrophage polarization, while significantly suppressingM1 polarization of alveolar macrophages. Mechanistic investigations delineated CHR's role in macrophage polarization by downregulating nuclear factor-κB expression through modulation of the LBP/TLR4 signaling pathway. Therefore, CHR may represent a novel strategy for the prevention of sepsis-induced ALI.

Sepsis-associated encephalopathy (SAE) is a common complication of sepsis, raise the mortality rate with an incidence of up to 71%. Pathological neuroinflammation after sepsis leads to acute brain dysfunction, survivors may remain long-term cognitive impairment. At present, the evaluation of SAE severity and prognosis mainly depends on clinical manifestations and imaging features, but lack of effectiveness and timeliness. Biomarkers of nerve injuries nowadays, have shown good application value and perspectives in the diagnosis and evaluation of SAE. This article will review the current biomarkers for accurate diagnosis and evaluation, basing on the possible pathophysiological mechanism of different stages of SAE.