Septicism is an organ function that directly threatens the life and well-being of a patient as a result of an infection-response disorder. As clinical research on sepsis has advanced in recent years, understanding of sepsis has evolved from a purely inflammatory response in the past to diseases involving immunosuppression and immune imbalances. The immunisation status of the patient will continue to change as a result of the development of the pathology, and the different biomarkers will facilitate the effective identification of the patient ‘ s immunisation phase and the timely implementation of the enhanced immunisation treatment,
Septic immunity
Immunosuppression is a concept introduced in the field of organ transplantation and oncology research, and the hypotheses of immune mechanisms for sepsis were first discovered and introduced in 1996 and further introduced in 1997, thus filling the gap in the interpretation of sepsis as a mechanism for multi-organ functional impairment. Since 2000, clinical studies have gradually concluded that the physical response to inflammation injuries includes both a catalytic response and a surrogate response to inflammation, the latter sustainable development being chronic immunosuppression, which is a major component of current clinical research, and that several studies point to long periods of poor post-hospital planning and a marked increase in relapse and death rates for septic patients, which means that septicism continues to affect their immune function for long periods of time after the patient ‘ s clinical symptoms have recovered and has been discharged, resulting in chronic immunosuppression and subsequent poor clinical prognosis.
After the initial contact of the pathogens and the host, it is expected that the innate immunisation of the organism will take place, thus preventing the inoculation of the pathogens, causing local inflammation, inflammation and a restorative response. This is the initial defensive function of the immune function of the human body, which is designed to eliminate invasive microorganisms in order to restore the internal balance. If the infection is not eliminated by the inherent immunisation, it will activate the adaptive immune system, making B lymphocyte cells antibodies and activation of T lymphocyte cells. In the case of sepsis, sepsis itself can seriously damage the inherent immune and adaptive immune system of the patient, while at the same time it activates the remedial system as well as the condensation system, increases the release of the inflammation factor, leads to the occurrence of hyperinflammatory disorders, and eventually leads to the occurrence of multi-organ functional disorders, during which time there has been a continuous increase in the release of anti-inflammatory cytogens and immunospect molecules, a decrease in the expression of the human white cell DR antigen, an increase in the death of the immune effect cell and an increase in the number of regulated cells, resulting in immunosuppression.
Treatment of sepsis immunosuppression
In the past, sepsis was dominated by antibiotics, liquid resuscitation and organ support treatment, with immunization treatment concentrated mainly on the control of inflammatory responses, but actual research found that control of positive symptoms alone was difficult to control chronic immunosuppressions of sepsis and required more effective treatment.
Immunisation point treatment: Immunisation point is one of the specific membrane molecules in humans, located mainly on T-lymphocytes, which can identify antigen formulation cells such as mononucleic cells, megacormic cells, and conjunctivated formulations on tree spectrocellular cells, which, when combined with receptors, continue to transmit negative to T-cellular inhibition. For sepsis patients, an increase in the expression of the receptor at the point of immunization can reduce T-cytology and thus contribute to the occurrence of sepsis. Therefore, immunosuppressants can be used for treatment to effectively block the immunosuppressors.
Interferant-gamma: Interferant-gamma enhances the ability of the inherently immunosuppolymers to swallow and bacterium kill. Interferant-gamma can be found to be effective in improving sepsis mortality in mice, promoting T-cells and natural lethal cell function after clinical in vitro and exterior trials. At the same time, interferon-gamma can regulate the metabolic levels of megacorts to control inflammation. In addition, interferobin-gamma studies have found that it is possible to restore the inherent immune function of the patient, to achieve the effective clean-up of the virus and bacteria, and that the patient ‘ s response to the interferoferant-gamma has been good and no significant adverse events have been detected. Interferophorism-gamma has been found to have good tolerance in research on sepsis immunotherapy, which can effectively improve patient T-cell function, while the potential value of interferoferant-gamma in sepsis treatment is still under ongoing study.
Summary
In general, there are mechanisms in place for specific immunopathological mechanisms for sepsis, although it is important to note that the clinical use of immunotherapy for treatment of patients is premised on its compatibility with the patient ‘ s symptoms and physical condition. By observing biomarkers associated with the immunisation status of patients, patients can be more effectively screened in favour of targeted immunisation treatment. Although there are currently no gold standards for the detection of the immune function of septics, it is believed that a complete system of evaluation of the immune function of septics will be established in future studies, thus providing a reasonable direction for the immune treatment of septics.
