Sheep anti Human Neutrophil Elastase polyclonal antibody [HRP]

Neutrophil elastase (NE) is the main protease from neutrophil primary granules involved in microbicidal activities. It is a serine protease that breaks down a variety of substances such as elastin, collagen and fibronectin. NE is an important factor that promotes inflammation, is bactericidal and shortens the inflammatory process, and it also regulates tumor growth by promoting tumor metastasis and tumor microenvironment remodeling. However, under certain conditions NE has a tumor-killing effect and promotes other diseases such as pulmonary ventilation dysfunction. The level and activity of NE reflects the state and severity of the disease.

Following the onset of inflammation, neutrophils rapidly accumulate toward the site of inflammation through a multistep adhesion cascade, and upon arrival at the site of inflammation, they fight pathogens through a series of processes, including participation in the phagocytosis of microorganisms, production of ROS, secretion of NE, and formation of neutrophil extracellular traps (NETs). NE is a weapon for neutrophils to destroy pathogenic microorganisms and synergizes with neutrophils to digest microorganisms. NE also prevents the degradation of toxic substances released by bacteria, and exposure to cytokines, chemokines, or bacterial products can lead to the accumulation of NE and anti-infective factors at the site of infection. Damaged basement membranes release laminin fragments that promote neutrophil migration and antioxidant factor recruitment, thereby accelerating the inflammatory process.

Figure 1. The specific process of the anti-infection effect of NE
(Source: Zeng W, et al. 2023)

NE is also recognized as a positive promoter of inflammation and is present in the airways of patients with various lung diseases. NE exposure induces airway remodeling and interrupts epithelial repair, which amplifies protease activity and inflammation within the airways by directly activating inflammation through increased cytokine expression and release, and indirectly activating inflammation by triggering extracellular traps and exosome release. CXCL8 increases neutrophil release of NE, which degrades some proteases such as secretory leukocyte protease inhibitor (SLPI) and tissue inhibitor of metalloproteinases-1 (TIMP-1) and activates some proteases such as the neutrophil metalloproteinase gelatinase, which further sustains large-scale proteolytic inflammation.

Figure 2. NE mediates pulmonary ventilation dysfunction
(Source: Zeng W, et al. 2023)

anti Human NE polyclonal antibody