Tissue homeostasis and inflammation - historical

You might be forgiven for believing that "tissue homeostasis" and "inflammation" have been linked for ever. However, an Ovid search reveals just 7 articles that mention the two together prior to 1995 when "Morphostasis and Immunity" appeared in Medical Hypotheses. If my articles have influenced that change, then this is so suppressed as to be invisible. Perhaps the change was just inevitable and my contribution has had no influence. Whatever, by the end of 2016 there were over 460 of them (excluding my articles).

Bischoff SC.
[Human basophilic granulocytes and mast cells: mediators between allergic inflammation and the specific immune system]. [Review; German]
Immunitat und Infektion. 22(3):93-103, 1994 Jun.
Abstract: Basophils and mast cells represent important effector cells in allergic inflammation. Furthermore, these cell types are suggested to play a role in the pathogenesis of other forms of chronic inflammation and in the maintenance of tissue homeostasis. Recent studies provided new information on the morphology, development, distribution and effector function of the histamine-containing cells. Particularly the identification of new surface membrane molecules such as CD40 ligand on basophils or c-kit on mast cells, and of new triggering agents and modulators of mediator release such as IL-3, IL-5, GM-CSF and nerve growth factor (for basophils) or c-kit ligand (for mast cells) allows a better understanding of the regulation of these cell types. The regulating cytokines are produced by lymphocytes and tissue cells. On the same time, membrane proteins and soluble mediators of basophils and mast cells regulate tissue and immune functions. Thus, basophils and mast cells are not only effectors but also regulators of inflammation. It is, therefore, tempting to speculate that both cell types play an important role as mediator cells between the unspecific effector level and the specific antigen-recognizing cells of the host immune defense system. This review is mostly restricted to the human system.

Tanneberger S; Pannuti F.
Disillusionments and hopes in the field of biological response modifiers. [Review]
Anticancer Research. 13(1):185-92, 1993 Jan-Feb.
Abstract: A number of new approaches are currently being investigated throughout the world which aim at the better simulation of immunoregulation by different BRM's. However it must be accepted that a remarkable difference exists between the positive results obtained with BRM's in experimental tumor systems and current clinical experiences. It is suggested that the treatment of preneoplastic lesions and immunoprevention of cancer could be a more rational aim for the application of BRM's than the treatment of advanced neoplastic diseases. This hypothesis is based primarily on the theoretical understanding of the immune system as a biological mechanism whose "natural" function is to eliminate "minimal deviation" cells when they occur as regular biological events during cell multiplication. BRM's should be considered first of all as bioregulators for the maintenance and restoration of cellular and tissue homeostasis.

Marks F; Furstenberger G.
Proliferative responses of the skin to external stimuli. [Review]
Environmental Health Perspectives. 101 Suppl 5:95-101, 1993 Dec.
Abstract: The skin, in particular the epidermis, offers unique opportunities to investigate the induction and control of cellular proliferation and tissue homeostasis both under in vivo and in vitro conditions. Moreover, it represents one of the most feasible model systems for experimental cancer research. As the primary border of the body, the skin has important protective and defensive functions. A general response to external injury consists of a thickening of the epithelial layer (epidermal hyperplasia) combined with an inflammatory reaction. This hyperplastic transformation of the skin is a critical condition of skin tumor development (i.e., conversion and promotion) and of the wound response. It is believed to be due to a transformation of keratinocytes into an activated state characterized by an increased rate of proliferation and the ability to release a series of growth factors and other cytokines that coordinate the defense reaction (e.g., hyperproliferation, recruitment of leukocytes, activation of the immune system) along auto- and paracrine feedback loops. The initial and probably later phases of this response depend critically on a local release of eicosanoids such as prostaglandins and lipoxygenase-generated factors. A unique reaction seen upon phorbol ester treatment of mouse skin is a strong induction of the enzyme 8-lipoxygenase, which might be involved in skin tumor development by catalyzing the generation of clastogenic metabolites thought to play a role in the conversion stage. Hyperplasia may be considered to be the result of an imbalance between the rates of cell gain and cell loss.(ABSTRACT TRUNCATED)

Camussi G; Albano E; Tetta C; Bussolino F.
The molecular action of tumor necrosis factor-alpha. [Review]
European Journal of Biochemistry. 202(1):3-14, 1991 Nov 15.
Abstract: Tumor necrosis factor-alpha (TNF-alpha) is a polypeptide hormone newly synthesized by different cell types upon stimulation with endotoxin, inflammatory mediators (C5a anaphylatoxin), or cytokines such as interleukin-1 and, in an autocrine manner, TNF itself. The net biological effect of TNF-alpha may vary depending on relative concentration, duration of cell exposure and presence of other mediators which may act in synergism with this cytokine. TNF-alpha may be relevant either in pathological events occurring in cachexia and endotoxic shock and inflammation or in beneficial processes such as host defense, immunity and tissue homeostasis. The biological effects of TNF-alpha are triggered by the binding to specific cell surface receptors. The formation of TNF-alpha-receptor complex activates a variety of biochemical pathways that include the transduction of the signal at least in part controlled by guanine-nucleotide-binding regulatory proteins (G proteins), its amplification through activation of adenyl cyclase, phospholipases and protein kinases with the generation of second messenger pathways. The transduction of selected genes in different cell types determines the characteristics of the cell response to TNF-alpha. The full understanding of the molecular mechanisms of TNF-alpha will provide the basis for a pharmacological approach intended to inhibit or potentiate selected biological actions of this cytokine.

Pettingale KW.
Towards a psychobiological model of cancer: biological considerations.
Social Science & Medicine. 20(8):779-87, 1985.
Abstract: The control of tissue homeostasis is extremely complex and many factors contribute to the growth and development of tumours. Although the immune system has been regarded as an essential intermediary between putative psychological factors and the development or restraint of malignant tumours, this review indicates that many other possible mechanisms also exist. Current aspects of tumour biology, immunology and hormonal control systems are reviewed, and detailed psychobiological mediating mechanisms are considered at each stage of tumour development. An approach to the future investigation of this difficult field is proposed.

Mikhailov VP; Katinas GS.
[Tissue homeostasis and its mechanisms]. [Review; Russian]
Arkhiv Anatomii, Gistologii i Embriologii. 87(9):5-13, 1984 Sep.

Olsson L.
Autoreactive cells as mediators of the natural defense against malignant tumors.
Recent Results in Cancer Research. 75:10-5, 1980.
Abstract: The present paper suggests that the natural defense mechanisms against tumors are part and a logical consequence of the natural mechanisms that maintain tissue uniformity. We further suggest that biologic errors steadily are accumulated in cells with increasing age, and that the number of cells with insufficient functional capacity (aberrant cells) increases with age. Since this increasing number of aberrant cells threatens the uniformity and function of the cell population, aberrant cells must be removed in order to maintain tissue uniformity. The aberrant cells may be removed by autonomous destruction or by cytotoxic attack by autoreactive cells. Such autoreactive cells are present in the normal organism throughout life, may be suppressed by thymus-derived cells, and may be activated by immune adjuvants. We suggest from theoretic and experimental reasons that the major function of autoreactive cells is the maintenance of tissue uniformity and tissue homeostasis within a cell population.

Similarly, the following search returned just 5 results, one of which was my article.

Ovid Search "tissue homeostasis" and "immune system"

Search for: limit 3 to yr="1902 – 1995"

Results: 5

Cunliffe J.
Morphostasis and immunity.
Medical Hypotheses – 1995 Feb
Scientists have traditionally been resistant to fundamental changes in perspective. New ideas are rejected if they challenge essential, accepted paradigms. Here I present a concept that, I believe, represents a paradigm shift in the way self/non-self discrimination is perceived. Traditional opinion has it that lymphocytes carry out this discrimination. I propose an alternative view. Self/non-self discrimination is driven by mechanisms closely related to those that lead to cell sorting in disaggregated embryos. Lymphocytes are only used to classify cells according to their mode of death (apoptosis or necrosis). The hypothesis outlines the process of morphostasis (tissue homeostasis). It fills in much detail about the gradual evolution of the mammalian immune system. Earlier versions of this hypothesis have been reflexly rejected by numerous journals. Until recently, I too was unsure of the validity of the core concept. Recent publications have dispelled this doubt from my mind. A paradigm shift is due.

Pettingale KW.
Towards a psychobiological model of cancer: biological considerations.
Social Science & Medicine – 1985
The control of tissue homeostasis is extremely complex and many factors contribute to the growth and development of tumours. Although the immune system has been regarded as an essential intermediary between putative psychological factors and the development or restraint of malignant tumours, this review indicates that many other possible mechanisms also exist. Current aspects of tumour biology, immunology and hormonal control systems are reviewed, and detailed psychobiological mediating mechanisms are considered at each stage of tumour development. An approach to the future investigation of this difficult field is proposed.

Bischoff SC.
[Human basophilic granulocytes and mast cells: mediators between allergic inflammation and the specific immune system]. [Review] [72 refs] [German] Humane basophile Granulozyten und Mastzellen: Vermittler zwischen allergischer Entzundung und spezifischem Immunsystem.
Immunitat und Infektion – 1994 Jun
Basophils and mast cells represent important effector cells in allergic inflammation. Furthermore, these cell types are suggested to play a role in the pathogenesis of other forms of chronic inflammation and in the maintenance of tissue homeostasis. Recent studies provided new information on the morphology, development, distribution and effector function of the histamine-containing cells. Particularly the identification of new surface membrane molecules such as CD40 ligand on basophils or c-kit on mast cells, and of new triggering agents and modulators of mediator release such as IL-3, IL-5, GM-CSF and nerve growth factor (for basophils) or c-kit ligand (for mast cells) allows a better understanding of the regulation of these cell types. The regulating cytokines are produced by lymphocytes and tissue cells. On the same time, membrane proteins and soluble mediators of basophils and mast cells regulate tissue and immune functions. Thus, basophils and mast cells are not only effectors but also regulators of inflammation. It is, therefore, tempting to speculate that both cell types play an important role as mediator cells between the unspecific effector level and the specific antigen-recognizing cells of the host immune defense system. This review is mostly restricted to the human system.

Tanneberger S; Pannuti F.
Disillusionments and hopes in the field of biological response modifiers. [Review] [64 refs]
Anticancer Research – 1993 Jan-Feb
A number of new approaches are currently being investigated throughout the world which aim at the better simulation of immunoregulation by different BRM's. However it must be accepted that a remarkable difference exists between the positive results obtained with BRM's in experimental tumor systems and current clinical experiences. It is suggested that the treatment of preneoplastic lesions and immunoprevention of cancer could be a more rational aim for the application of BRM's than the treatment of advanced neoplastic diseases. This hypothesis is based primarily on the theoretical understanding of the immune system as a biological mechanism whose "natural" function is to eliminate "minimal deviation" cells when they occur as regular biological events during cell multiplication. BRM's should be considered first of all as bioregulators for the maintenance and restoration of cellular and tissue homeostasis.

Marks F; Furstenberger G.
Proliferative responses of the skin to external stimuli. [Review] [36 refs]
Environmental Health Perspectives – 1993 Dec
The skin, in particular the epidermis, offers unique opportunities to investigate the induction and control of cellular proliferation and tissue homeostasis both under in vivo and in vitro conditions. Moreover, it represents one of the most feasible model systems for experimental cancer research. As the primary border of the body, the skin has important protective and defensive functions. A general response to external injury consists of a thickening of the epithelial layer (epidermal hyperplasia) combined with an inflammatory reaction. This hyperplastic transformation of the skin is a critical condition of skin tumor development (i.e., conversion and promotion) and of the wound response. It is believed to be due to a transformation of keratinocytes into an activated state characterized by an increased rate of proliferation and the ability to release a series of growth factors and other cytokines that coordinate the defense reaction (e.g., hyperproliferation, recruitment of leukocytes, activation of the immune system) along auto- and para-crine feedback loops. The initial and probably later phases of this response depend critically on a local release of eicosanoids such as prostaglandins and lipoxygenase-generated factors. A unique reaction seen upon phorbol ester treatment of mouse skin is a strong induction of the enzyme 8-lipoxygenase, which might be involved in skin tumor development by catalyzing the generation of clastogenic metabolites thought to play a role in the conversion stage. Hyperplasia may be considered to be the result of an imbalance between the rates of cell gain and cell loss (abstract truncated)

So:- all nearly all the articles from 1995 onwards that include the term "immune system" and also refer to "tissue homeostasis" have failed to acknowledge any of these as precedence papers. Should they – by rights – have identified and acknowledged at least some of them?