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A common immunopathogenesis mechanism for infectious diseases: the protein-homeostasis-system hypothesis.

Lee KY - Infect Chemother (2015)

Bottom Line: All biological phenomena in living organisms, including biochemical, physiological and pathological processes, are performed by the proteins that have various sizes and shapes, which in turn are controlled by an interacting network within the living organisms.The author proposes that this network is controlled by the protein homeostasis system (PHS), and that the immune system is one part of the PHS of the host.Every infectious disease has its own set of toxic substances, including PPs, associated with disease onset, and the PPs and the corresponding immune cells may be responsible for the inflammatory processes that develop in those infectious diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Korea. ; Department of Pediatrics, The Catholic University of Korea, Daejeon St. Mary's Hospital, Daejeon, Korea.

ABSTRACT
It was once believed that host cell injury in various infectious diseases is caused solely by pathogens themselves; however, it is now known that host immune reactions to the substances from the infectious agents and/or from the injured host cells by infectious insults are also involved. All biological phenomena in living organisms, including biochemical, physiological and pathological processes, are performed by the proteins that have various sizes and shapes, which in turn are controlled by an interacting network within the living organisms. The author proposes that this network is controlled by the protein homeostasis system (PHS), and that the immune system is one part of the PHS of the host. Each immune cell in the host may recognize and respond to substances, including pathogenic proteins (PPs) that are toxic to target cells of the host, in ways that depend on the size and property of the PPs. Every infectious disease has its own set of toxic substances, including PPs, associated with disease onset, and the PPs and the corresponding immune cells may be responsible for the inflammatory processes that develop in those infectious diseases.

No MeSH data available.


Related in: MedlinePlus

Immunopathogenesis of infectious diseases and infection-related immune diseases.The hosts have an initial focus in which pathogens encounter and replicate in infectious diseases or infection-related immune diseases. Various substances, including pathogens and fragments of pathogen-origin, cytokines from immune cells and materials from destructed host cells are preformed in the initial focus and/or secondary immune organs around the focus (A). These substances spread and reach various tissues via systemic circulation, and some of these bind to receptors on specific organ cells. Immune cells start to control these substances, and clinical symptoms and signs begin to appear. The pathogenic proteins (PPs) bind to receptors of target cells of the host, and this process signals cell injury and/or other protein production from target cells (B). Immune cells are recruited to the lesions for control of substances, including PPs through MHCs and cytokine networks. Initially, immune cells, including non-specific T cells and non-specific antibodies, are involved in this reaction. During this process, hyperactivated immune cells produce various inflammatory cytokines and counter-inflammatory cytokines, and the cytokine imbalances may be associated with further target cell injury (C). After appearance of specific T cell clones and B cell clones (specific antibodies) for PPs, tissue injury ceases and repair begins with immune cells (D). While the hosts that have a defect on the appearance of specific immune cells (lack of the repertoire of specific immune cells) against PPs may ensue autoimmune diseases.
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Figure 2: Immunopathogenesis of infectious diseases and infection-related immune diseases.The hosts have an initial focus in which pathogens encounter and replicate in infectious diseases or infection-related immune diseases. Various substances, including pathogens and fragments of pathogen-origin, cytokines from immune cells and materials from destructed host cells are preformed in the initial focus and/or secondary immune organs around the focus (A). These substances spread and reach various tissues via systemic circulation, and some of these bind to receptors on specific organ cells. Immune cells start to control these substances, and clinical symptoms and signs begin to appear. The pathogenic proteins (PPs) bind to receptors of target cells of the host, and this process signals cell injury and/or other protein production from target cells (B). Immune cells are recruited to the lesions for control of substances, including PPs through MHCs and cytokine networks. Initially, immune cells, including non-specific T cells and non-specific antibodies, are involved in this reaction. During this process, hyperactivated immune cells produce various inflammatory cytokines and counter-inflammatory cytokines, and the cytokine imbalances may be associated with further target cell injury (C). After appearance of specific T cell clones and B cell clones (specific antibodies) for PPs, tissue injury ceases and repair begins with immune cells (D). While the hosts that have a defect on the appearance of specific immune cells (lack of the repertoire of specific immune cells) against PPs may ensue autoimmune diseases.

Mentions: Specific antibodies (IgM and IgG) against pathogens, including viruses, mycoplasmas and legionellas, are not detected for at least 3-4 days after the onset of clinical symptoms. Since each pathogen, especially viruses, is known to attach only to specific receptors on host cells, viruses that spread by systemic circulation (viremia) may not bind other organ-specific host cells that lack these receptors. If the virus-receptor binding and subsequent tissue cell destruction by intracellular replication needed to happen, then a period of incubation following virus infection would be required. Furthermore, in experimental animal studies of mycoplasma or influenza virus infections, animals with depressed immune functions, including those with T cell deprivation or IL-17 deficiency, show milder or fewer pneumonia lesions, compared with immune-competent animals, although duration of survival of the pathogens is longer [25, 55, 56, 57]. Therefore, the immunological reaction of host immune cells against the substances produced from the foci of pathogen replication may be responsible for lung injury, and the substances may have a similar mode of binding to lung tissue cells and recruiting the corresponding immune cells [1, 2, 3, 4] (Fig. 2).


A common immunopathogenesis mechanism for infectious diseases: the protein-homeostasis-system hypothesis.

Lee KY - Infect Chemother (2015)

Immunopathogenesis of infectious diseases and infection-related immune diseases.The hosts have an initial focus in which pathogens encounter and replicate in infectious diseases or infection-related immune diseases. Various substances, including pathogens and fragments of pathogen-origin, cytokines from immune cells and materials from destructed host cells are preformed in the initial focus and/or secondary immune organs around the focus (A). These substances spread and reach various tissues via systemic circulation, and some of these bind to receptors on specific organ cells. Immune cells start to control these substances, and clinical symptoms and signs begin to appear. The pathogenic proteins (PPs) bind to receptors of target cells of the host, and this process signals cell injury and/or other protein production from target cells (B). Immune cells are recruited to the lesions for control of substances, including PPs through MHCs and cytokine networks. Initially, immune cells, including non-specific T cells and non-specific antibodies, are involved in this reaction. During this process, hyperactivated immune cells produce various inflammatory cytokines and counter-inflammatory cytokines, and the cytokine imbalances may be associated with further target cell injury (C). After appearance of specific T cell clones and B cell clones (specific antibodies) for PPs, tissue injury ceases and repair begins with immune cells (D). While the hosts that have a defect on the appearance of specific immune cells (lack of the repertoire of specific immune cells) against PPs may ensue autoimmune diseases.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4384454&req=5

Figure 2: Immunopathogenesis of infectious diseases and infection-related immune diseases.The hosts have an initial focus in which pathogens encounter and replicate in infectious diseases or infection-related immune diseases. Various substances, including pathogens and fragments of pathogen-origin, cytokines from immune cells and materials from destructed host cells are preformed in the initial focus and/or secondary immune organs around the focus (A). These substances spread and reach various tissues via systemic circulation, and some of these bind to receptors on specific organ cells. Immune cells start to control these substances, and clinical symptoms and signs begin to appear. The pathogenic proteins (PPs) bind to receptors of target cells of the host, and this process signals cell injury and/or other protein production from target cells (B). Immune cells are recruited to the lesions for control of substances, including PPs through MHCs and cytokine networks. Initially, immune cells, including non-specific T cells and non-specific antibodies, are involved in this reaction. During this process, hyperactivated immune cells produce various inflammatory cytokines and counter-inflammatory cytokines, and the cytokine imbalances may be associated with further target cell injury (C). After appearance of specific T cell clones and B cell clones (specific antibodies) for PPs, tissue injury ceases and repair begins with immune cells (D). While the hosts that have a defect on the appearance of specific immune cells (lack of the repertoire of specific immune cells) against PPs may ensue autoimmune diseases.
Mentions: Specific antibodies (IgM and IgG) against pathogens, including viruses, mycoplasmas and legionellas, are not detected for at least 3-4 days after the onset of clinical symptoms. Since each pathogen, especially viruses, is known to attach only to specific receptors on host cells, viruses that spread by systemic circulation (viremia) may not bind other organ-specific host cells that lack these receptors. If the virus-receptor binding and subsequent tissue cell destruction by intracellular replication needed to happen, then a period of incubation following virus infection would be required. Furthermore, in experimental animal studies of mycoplasma or influenza virus infections, animals with depressed immune functions, including those with T cell deprivation or IL-17 deficiency, show milder or fewer pneumonia lesions, compared with immune-competent animals, although duration of survival of the pathogens is longer [25, 55, 56, 57]. Therefore, the immunological reaction of host immune cells against the substances produced from the foci of pathogen replication may be responsible for lung injury, and the substances may have a similar mode of binding to lung tissue cells and recruiting the corresponding immune cells [1, 2, 3, 4] (Fig. 2).

Bottom Line: All biological phenomena in living organisms, including biochemical, physiological and pathological processes, are performed by the proteins that have various sizes and shapes, which in turn are controlled by an interacting network within the living organisms.The author proposes that this network is controlled by the protein homeostasis system (PHS), and that the immune system is one part of the PHS of the host.Every infectious disease has its own set of toxic substances, including PPs, associated with disease onset, and the PPs and the corresponding immune cells may be responsible for the inflammatory processes that develop in those infectious diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Korea. ; Department of Pediatrics, The Catholic University of Korea, Daejeon St. Mary's Hospital, Daejeon, Korea.

ABSTRACT
It was once believed that host cell injury in various infectious diseases is caused solely by pathogens themselves; however, it is now known that host immune reactions to the substances from the infectious agents and/or from the injured host cells by infectious insults are also involved. All biological phenomena in living organisms, including biochemical, physiological and pathological processes, are performed by the proteins that have various sizes and shapes, which in turn are controlled by an interacting network within the living organisms. The author proposes that this network is controlled by the protein homeostasis system (PHS), and that the immune system is one part of the PHS of the host. Each immune cell in the host may recognize and respond to substances, including pathogenic proteins (PPs) that are toxic to target cells of the host, in ways that depend on the size and property of the PPs. Every infectious disease has its own set of toxic substances, including PPs, associated with disease onset, and the PPs and the corresponding immune cells may be responsible for the inflammatory processes that develop in those infectious diseases.

No MeSH data available.


Related in: MedlinePlus