PTX3 is an acute phase glycoprotein and forms the N-pentamerin family together with C-reactive protein (CRP) and serum amyloid P. PTX3 is produced by dendritic cells, epithelial cells, endothelial cells and macrophages, and is concentrated in the site of inflammation or injury[6]. PTX3 is an essential liquid phase pattern recognition molecule in the innate immune system and a functional ancestor of antibodies. The interaction with defense collagen and fibrinogen can amplify the effect function of the innate immune system[7]. Previous studies have found that PTX3 was associated with TB, and some scholars pointed out that PTX3 in peripheral blood can be used as a diagnostic marker or prognostic indicator of TB. The GSE34608 dataset in this study also showed that PTX3 in peripheral blood was significantly increased in TB. However, the control groups of these studies were all healthy physical examination subjects or sarcoidosis, which were inconsistent with the complicated clinical situation. Therefore, we included all hospitalized patients with CAP and lung tumor in the respiratory department into the control group, and found that the plasma PTX3 level was not statistically significant among TB, CAP and lung tumor, and AUC was only 0.544, which was difficult to meet clinical needs. Differently, BALF PTX3 level in TB was significantly higher than that in CAP and lung tumor, and AUC was 0.783. After selecting the optimal cut-off value, the sensitivity and specificity was both 0.765, which seemed to be a qualified diagnostic marker for TB.
But in fact, PTX3 was initially found to be elevated in small vasculitis and may be a diagnostic marker for it[8]. Besides, PTX3 was confirmed to be associated with pulmonary aspergillosis[9–13]. During my postgraduate study, we found plasma and BALF PTX3 could be used to diagnose invasive pulmonary aspergillosis in immunocompetent patients[14]. After then, PTX3 has been found to be elevated in many diseases. For example, PTX3 level in peripheral blood was positively correlated with the severity of airflow obstruction, emphasema and mortality in chronic obstructive pulmonary disease[15]. PTX3 would increase when acute lung injury occurred, and endogenous expression of PTX3 may play a protective role in acute lung injury by enhancing pulmonary neutrophils recruitment, coagulation cascade and inflammation[16, 17]. PTX3 level also increased in mice with allergic asthma, suggesting PTX3 played a regulatory role in the development of allergic inflammation[18]. Low-grade chronic inflammation is characteristic of obesity and metabolic syndrome, PTX3 played a key role in the development of obesity by promoting inflammation and limiting the vascularization of adipose tissue[19]. PTX3 was increased in lung cancer[20] and prostate cancer[21]. Tumor-promoting inflammation is now considered to be important in tumor microenvironment. Studies have shown that PTX3 deficiency can trigger complement-dependent tumor promoting inflammation, so that enhance tumor load, macrophage infiltration, cytokine generation, angiogenesis and genetic instability, which revealing PTX3, as an innate immune medium, played an exogenous tumor suppression role by inhibiting tumor-induced inflammation[22, 23]. In addition, PTX3 can elevate in subarachnoid hemorrhage[24], atherosclerotic plaque in thin cap[25], acute kidney injury[26] and heart failure with normal ejection fraction[27]. To sum up, PTX3 can participate in the pathogenesis of acute or chronic bacterial, fungal and aseptic inflammation, and may elevate in respiratory, cardiovascular, urinary and immune system diseases. Current studies have shown PTX3, same as CRP, is a non-specific inflammatory marker which will elevate in response to infection or injury. However, based on our results, it can be concluded that in respiratory diseases, PTX3 may increase higher in atypical pathogen infection, such as Aspergillus and Mycobacterium tuberculosis. Therefore, BALF PTX3 still has a supporting role in diagnosing TB.