[Mechanism of immune suppression after surgical stress and host defense against infection]. 2003

Satoshi Ono, and Hidetaka Mochizuki
Department of Surgery I, National Defense Medical College, Tokorozawa, Japan.

Suppression of cellular immunity secondary to decreased immunocyte function is one of the surgical stress-induced biological responses. Monocytes/macrophages, natural killer (NK) cells, lymphocytes, and neutrophils play an important role in this immune system. These immunity charge cells are expressed through various surface antigens, such as major histocompatibility complex (MHC) class antigens, T cell receptors, and the cytokines interferon-gamma, interleukin (IL)-2, and IL-12. MHC class II antigen expression of monocytes and the cytokine production of CD4+ T cells are decreased after surgical stress. In this immune-suppressed condition, patients after surgical stress can easily experience infectious complications, and therefore the up-regulation of the immune system is necessary to avoid those complications. Recently, the role of natural immunity as a defense system against infection has received attention. The discovery of Toll-like receptor families revealed how the macrophage system cells recognize microorganisms. Furthermore, liver natural killer(NK) cells and NK T cells are important to induce the Th1 immune response in bacterial peritonitis. In this manuscript, we explain the mechanism of immune suppression after surgical stress and the host defense against infection by analyzing cytokine production and surface membrane molecules in mononuclear cells.

UI MeSH Term Description Entries
D007108 Immune Tolerance The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc. Immunosuppression (Physiology),Immunosuppressions (Physiology),Tolerance, Immune
D007239 Infections Invasion of the host organism by microorganisms or their toxins or by parasites that can cause pathological conditions or diseases. Infection,Infection and Infestation,Infections and Infestations,Infestation and Infection,Infestations and Infections
D008562 Membrane Glycoproteins Glycoproteins found on the membrane or surface of cells. Cell Surface Glycoproteins,Surface Glycoproteins,Cell Surface Glycoprotein,Membrane Glycoprotein,Surface Glycoprotein,Glycoprotein, Cell Surface,Glycoprotein, Membrane,Glycoprotein, Surface,Glycoproteins, Cell Surface,Glycoproteins, Membrane,Glycoproteins, Surface,Surface Glycoprotein, Cell,Surface Glycoproteins, Cell
D011956 Receptors, Cell Surface Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands. Cell Surface Receptor,Cell Surface Receptors,Hormone Receptors, Cell Surface,Receptors, Endogenous Substances,Cell Surface Hormone Receptors,Endogenous Substances Receptors,Receptor, Cell Surface,Surface Receptor, Cell
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D013312 Stress, Physiological The unfavorable effect of environmental factors (stressors) on the physiological functions of an organism. Prolonged unresolved physiological stress can affect HOMEOSTASIS of the organism, and may lead to damaging or pathological conditions. Biotic Stress,Metabolic Stress,Physiological Stress,Abiotic Stress,Abiotic Stress Reaction,Abiotic Stress Response,Biological Stress,Metabolic Stress Response,Physiological Stress Reaction,Physiological Stress Reactivity,Physiological Stress Response,Abiotic Stress Reactions,Abiotic Stress Responses,Abiotic Stresses,Biological Stresses,Biotic Stresses,Metabolic Stress Responses,Metabolic Stresses,Physiological Stress Reactions,Physiological Stress Responses,Physiological Stresses,Reaction, Abiotic Stress,Reactions, Abiotic Stress,Response, Abiotic Stress,Response, Metabolic Stress,Stress Reaction, Physiological,Stress Response, Metabolic,Stress Response, Physiological,Stress, Abiotic,Stress, Biological,Stress, Biotic,Stress, Metabolic
D013514 Surgical Procedures, Operative Operations carried out for the correction of deformities and defects, repair of injuries, and diagnosis and cure of certain diseases. (Taber, 18th ed.). Surgical Procedures,Ghost Surgery,Operative Procedures,Operative Surgical Procedure,Operative Surgical Procedures,Procedure, Operative Surgical,Procedures, Operative Surgical,Surgery, Ghost,Surgical Procedure, Operative,Operative Procedure,Procedure, Operative,Procedure, Surgical,Procedures, Operative,Procedures, Surgical,Surgical Procedure
D051193 Toll-Like Receptors A family of pattern recognition receptors characterized by an extracellular leucine-rich domain and a cytoplasmic domain that share homology with the INTERLEUKIN 1 RECEPTOR and the DROSOPHILA toll protein. Following pathogen recognition, toll-like receptors recruit and activate a variety of SIGNAL TRANSDUCING ADAPTOR PROTEINS. Receptors, Toll-Like,Toll-Like Receptor,Receptor, Toll-Like,Receptors, Toll Like,Toll Like Receptor,Toll Like Receptors

Related Publications

Satoshi Ono, and Hidetaka Mochizuki
November 2009, Expert review of anti-infective therapy,
Satoshi Ono, and Hidetaka Mochizuki
January 2019, Infection and immunity,
Satoshi Ono, and Hidetaka Mochizuki
December 1972, The Surgical clinics of North America,
Satoshi Ono, and Hidetaka Mochizuki
February 2007, Nihon rinsho. Japanese journal of clinical medicine,
Satoshi Ono, and Hidetaka Mochizuki
February 1977, The Journal of pediatrics,
Satoshi Ono, and Hidetaka Mochizuki
October 2006, Nihon rinsho. Japanese journal of clinical medicine,
Satoshi Ono, and Hidetaka Mochizuki
December 2004, Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology,
Satoshi Ono, and Hidetaka Mochizuki
June 1980, Current problems in surgery,
Satoshi Ono, and Hidetaka Mochizuki
May 1980, Current problems in surgery,
Satoshi Ono, and Hidetaka Mochizuki
June 2003, The Journal of infectious diseases,
Copied contents to your clipboard!