How inflammation influences psychiatric disease

Recent studies highlight the strong correlation between infectious diseases and the development of neuropsychiatric disorders.In this editorial,we comment on the article“Anti-infective therapy durations predict psychological stress and laparoscopic surgery quality in pelvic abscess patients”by Zhang et al,published in the recent issue of the World Journal of Psychiatry 2023;13(11):903-911.Our discussion highlighted the potential consequences of anxiety,depression,and psychosis,which are all linked to bacterial,fungal,and viral infections,which are relevant to the impact of inflammation on the sequelae in mental health as those we are observing after the coronavirus disease 2019 pandemic.We focus specifically on the immune mechanisms triggered by inflammation,the primary contributor to psychiatric complications.Importantly,pathophysiological mechanisms such as organ damage,post-injury inflammation,and infectioninduced endocrine alterations,including hypocortisolism or autoantibody formation,significantly contribute to the development of chronic low-grade inflammation,promoting the emergence or development of psychiatric alterations in susceptible individuals.As inflammation can have long-term effects on patients,a multidisciplinary treatment plan can avoid complications and debilitating health issues,and it is crucial to recognize and address the mental health implications.

Expression of triggering receptor on myeloid cell 1 and histocompatibility complex molecules in sepsis and major abdominal surgery

AIM: To evaluate the surface expression of triggering receptor on myeloid cell 1 (TREM-1), class Ⅱ major histocompatibility complex molecules (HLA-DR), andthe expression of the splicing variant (svTREM-1) ofTREM-1 in septic patients and those subjected to major abdominal surgery.METHODS: Using flow cytometry, we examined the surface expression of TREM-1 and HLA-DR in peripheral blood monocytes from 11 septic patients, 7 elective gastrointestinal surgical patients, and 10 healthy volunteers. svTREM-1 levels were analyzed by RT-PCR. RESULTS: Basal expression of TREM-1 and HLA-DR in healthy volunteers was 35.91±14.75 MFI and75.8±18.3%, respectively. In septic patients, TREM-1 expression was 59.9±23.9 MFI and HLA-DR expression was 44.39±20.25%, with a significant differencebetween healthy and septic groups (P＜0.05) for bothmolecules. In the surgical patients, TREM-1 and HLA-DR expressions were 56.8±20.85 MFI and 71±13.8% before surgery and 72.65±29.92 MlFI and 72.82±22.55% after surgery. TREM-1 expression was significantly different(P = 0.0087) between the samples before and aftersurgery and svTREM-1 expression was 0.8590±0.1451 MF1, 0.8820±0.1460 MF1, and 2.210±0.7873MF1 in the healthy, surgical (after surgery) and septic groups, respectively. There was a significant difference (P = 0.048) in svTREM-1 expression between the healthy and surgical groups and the septic group.CONCLUSION: TREM-1 expression is increased during systemic inflammatory conditions such as sepsis and the postoperative phase. Simultaneous low expression of HLA-DR molecules correlates with the severity of illness and increases susceptibility to infection. Additionally, TREM-1 expression is distinctly different in surgical patients at different stages of the inflammatory response before and after surgery. Thus, surface TREM-1 appears to be an endogenous signal during the course of the inflammatory response. svTREM-1 expression is significantly increased during sepsis, appearing to be an indicator of severity of illness. Together, these data indicate that TREM-1 may play an important role in establishing and amplifying the systemic inflammatory response. TREM-1, HLA-DR, and svTREM-1 expression analysis can provide useful diagnostic and prognostic indicators during SIRS, CARS, and sepsis.