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1.
Cancer Metastasis Rev ; 30(2): 211-23, 2011 Jun.
Article in English | MEDLINE | ID: mdl-21253828

ABSTRACT

Dysregulated immune function is involved in the pathogenesis of many common human diseases. Living in urban, microbe-poor environment may have a profound influence on the immune function and eventually also on carcinogenesis. Unfortunately, few studies have thus far addressed the role of exposure to the environmental microbiota on the risk of cancer. Which mechanisms are broken in individuals prone to develop chronic inflammation in response to exposure that does not cause harm in others? Recent work in immunology has revealed that Th17 cells, a third subset of Th cells, and inflammatory cytokines, particularly IL-23, are closely linked with tumour-associated inflammation. Albeit the precise role of Th17 cells in cancer is still unclear and a matter of debate, accumulating evidence shows that Th17 cells are enriched in a wide range of human tumours, and that these tumour-derived Th17 cells may promote angiogenesis, tumour growth and inflammation. Regulatory T cells, in turn, appear to have counter-regulatory effects on Th17 cells and can inhibit their function. Thus, the regulatory network, induced and strengthened by continuous exposure to environmental microbiota, may play an important role in tumour immunobiology in preventing the establishment of chronic inflammation in its early phases. In addition, the discovery of the Toll-like receptor (TLR) system has brought micro-organisms to new light; continuous signalling via these TLRs and other receptors that sense microbial components is necessary for epithelial cell integrity, tissue repair, and recovery from injury. In this communication, we summarise the epidemiological data of living in environments with diverse microbial exposures and the risk of cancer, and discuss the related immunological mechanisms, focusing on the links between environmental microbiota, the Th17/IL-23 axis and cancer-associated inflammation.


Subject(s)
Environmental Microbiology , Inflammation/immunology , Neoplasms/immunology , Th17 Cells/immunology , Cytokines/immunology , Cytokines/metabolism , Host-Pathogen Interactions/immunology , Humans , Inflammation/metabolism , Inflammation/microbiology , Inflammation Mediators/immunology , Inflammation Mediators/metabolism , Models, Immunological , Neoplasms/metabolism , Neoplasms/microbiology , T-Lymphocytes, Regulatory/immunology , T-Lymphocytes, Regulatory/metabolism , Th17 Cells/metabolism
2.
Int Arch Allergy Immunol ; 140(2): 89-95, 2006.
Article in English | MEDLINE | ID: mdl-16554659

ABSTRACT

BACKGROUND: Evidence of the influence of pathogen exposure on the development of atopy and atopic disease is not unequivocal. We investigated the association between markers of infections and occurrence of atopy among adults in eastern Finland and western Russia, two adjacent areas with profound differences in living conditions and lifestyles. METHODS: Randomly selected adults aged 25-54 years from Finland (n = 790) and from Russia (n = 387) participated in the study. Skin prick tests were performed to 11 common airborne allergens, and at least one positive prick reaction was considered to indicate atopy. Antibodies to different pathogens including hepatitis A virus (HAV), Helicobacter pylori, Toxoplasma gondii, herpes simplex virus (HSV), Chlamydia pneumoniae and the periodontal pathogens Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans were measured. RESULTS: In Finland 34.3% and in Russia 23.3% of the study population was atopic (p < 0.001). Seroprevalences to all these pathogens were significantly higher among the Russians. In multivariate logistic regression analysis, only H. pylori was inversely associated with atopy in Russia. A further stepwise analysis revealed that H. pylori alone can explain 32% of the difference in atopy between the countries, and T. gondii, A. actinomycetemcomitans, HSV and C. pneumoniae had a slightly additive effect, whereas, unexpectedly, seropositivity to HAV and, to a lesser extent, P. gingivalis had an opposite effect. The net result of the stepwise analysis showed that 44% of the difference in atopy between the countries could be explained by seropositivity to these seven pathogens. CONCLUSIONS: Seropositivity to select pathogens, particularly to H. pylori, could explain a substantial part of the difference in atopy prevalence between Finland and Russia. Exposure to HAV was not associated with protection against atopy in this adult population.


Subject(s)
Bacterial Infections/immunology , Hypersensitivity/microbiology , Hypersensitivity/parasitology , Parasitic Diseases/immunology , Virus Diseases/immunology , Adult , Antibodies, Bacterial/blood , Antibodies, Protozoan/blood , Antibodies, Viral/blood , Bacterial Infections/blood , Bacterial Infections/microbiology , Female , Finland , Humans , Hypersensitivity/immunology , Hypersensitivity/virology , Logistic Models , Male , Middle Aged , Multivariate Analysis , Parasitic Diseases/blood , Parasitic Diseases/parasitology , Russia , Skin Tests , Virus Diseases/blood , Virus Diseases/virology
3.
J Allergy Clin Immunol ; 113(3): 401-6, 2004 Mar.
Article in English | MEDLINE | ID: mdl-15007336

ABSTRACT

The possible effects of immunization on subsequent development of asthma and atopy remains a matter of controversy. Although some studies have suggested that immunization might increase the risk for atopic disease, a number of studies have found no association or have even reported a protective effect for immunization against atopy. Recent studies have provided evidence that ethnicity might affect the susceptibility to the immunomodulatory effects of vaccination. In this review the association between immunization and atopy and the effect of ethnicity on this association are briefly outlined. The focus will be particularly on BCG vaccination.


Subject(s)
Ethnicity , Hypersensitivity, Immediate/etiology , Immunization/adverse effects , Adjuvants, Immunologic/pharmacology , BCG Vaccine/adverse effects , BCG Vaccine/pharmacology , Humans , Hypersensitivity, Immediate/prevention & control , Measles Vaccine/adverse effects , Pertussis Vaccine/adverse effects
4.
J Allergy Clin Immunol ; 109(6): 923-8, 2002 Jun.
Article in English | MEDLINE | ID: mdl-12063519

ABSTRACT

The constant increase in asthma and atopy prevalences--despite improved treatment and knowledge of many aspects of the diseases--has raised growing concern. Accumulating evidence suggests that these increases in atopic diseases are largely attributable to environmental and lifestyle factors, and the lack of systemic childhood infections has in many studies emerged as a major factor. In addition to current high standards of hygiene and the lack or scarcity of such infections, another factor characteristic of our present-day lives could be involved. This review briefly outlines the possibility that prolonged maternal stress associated with sustained excessive cortisol secretion could affect the developing immune system--especially T(H)1/T(H)2 cell differentiation--and further increase the susceptibility to asthma and atopy in genetically predisposed individuals. This hypothesis is critically evaluated in the light of current knowledge.


Subject(s)
Antigens, Differentiation, T-Lymphocyte/physiology , Asthma/etiology , Hypersensitivity/etiology , Immune System/growth & development , Prenatal Exposure Delayed Effects , Stress, Physiological/immunology , T-Lymphocytes/immunology , Asthma/immunology , Cell Differentiation , Female , Humans , Hydrocortisone/metabolism , Hypersensitivity/immunology , Pregnancy , Th1 Cells/cytology , Th2 Cells/cytology
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