Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0241981 (loss of balance)
 452 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Allergic lung diseases such as atopic asthma and extrinsic allergic alveolitis are now recognized as chronic inflammatory lung diseases promoted by dysregulation of T cell-mediated immune mechanisms. The basis of this regulation and the impact of the atopic status of these individuals on this chronic inflammatory disease have yet to be fully explained. The studies described in this paper reveal mechanisms of macrophage lymphocyte interaction in which evidence is presented that a balance of functionally distinct macrophage subsets needs to be maintained to regulate T cell reactivity in the lung. Similarly a balance within the T cell populations may influence and regulate the relative proportions of functionally distinct macrophages. Investigations of bronchoalveolar lavage and biopsy from patients with allergic lung disease have revealed a gross imbalance within the lung macrophage populations and an associated dysregulation in T cell stimulation. In vitro studies have revealed that imbalances in the macrophage populations may lead to changes in local level of cytokine production specifically TGF-beta which would then impact on the control of T cell populations. Conversely aberrant development of activated T cells with a TH2-like cytokine repertoire may influence the balance of macrophages. Our in vitro studies have revealed that macrophage phenotype and function can be modulated in vitro by contact with T cell-derived cytokines and that this change in phenotype is reflected in a change in function. These data support the hypothesis that components of the immune system normally associated with allergic reactions may be stimulated in the absence of any overt atopic reactivity in the individual concerned. Thus immediate type allergic reactions may represent a "super-imposed" burden [provocating factor] in atopic individuals but the underlying immunopathogenesis of these diseases may not be dependent on this state of immediate type hypersensitivity. It is concluded that the loss of balance within functional distinct macrophage populations within the lung may represent the fundamental problem in allergic lung disease. This possibility is discussed in the light of other work in this field.
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PMID:Macrophages and allergic lung disease. 893 58

Colon cancer remains a significant global health concern. The impact of specific dietary components on colon tissue likely depends on a host of genomic processes that influence the growth, development, and differentiation of the epithelial cells at the colon crypt surface, where the balance between proliferation and differentiation is maintained possibly through the Wnt (beta-catenin/T-cell factor) signaling pathway. A loss of balance caused by either genetic mutations or environmental factors such as dietary habits can modulate the risk for the formation of aberrant crypt foci and ultimately the development of colon cancer. Evidence exists that butyrate reduces the number and the size of aberrant crypt foci in the colon. Butyrate is a natural histone deacetylase inhibitor as well as a molecule involved with enhanced TGF-beta-induced SMAD3 phosphorylation, increased IFN-gamma-mediated apoptosis, and altered expression of the intestinal muc2 gene that is responsible for mucin synthesis. Other dietary components, such as vitamin D and (n-3) fatty acids, may regulate proliferative properties of colon progenitor cells as well as the differentiation of subcellular lineages. Although these findings are intriguing, there are uncertainties that remain to be resolved including the optimal exposure needed to bring about an effect, the appropriate timing of administration, and if nutrient-nutrient and nutrient-gene interactions determine the overall response. The expanded use of high-throughput technologies, knowledge about the expression of genes and protein fingerprints, and metabolomic profiling will assist in addressing these issues and ultimately in determining the physiological significance of bioactive food components as cancer protectants.
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PMID:Dietary modulation of colon cancer risk. 1795 6