51 research outputs found
Phthalate Exposure During the Prenatal and Lactational Period Increases the Susceptibility to Rheumatoid Arthritis in Mice
The prenatal and early postnatal period is highly sensitive to environmental exposures
that may interfere with the developmental programming of the immune system leading
to an altered disease risk in later life. To clarify the role of early influences in activation
or exacerbation of autoimmune diseases like rheumatoid arthritis (RA) we investigated
the effect of maternal exposure during the prenatal and lactational period of DBA/1
mice to the plasticizer benzyl butyl phthalate (BBP) on the development of RA in the
offspring. Using a mild collagen-induced arthritis (CIA) model, maternal BBP-exposure
increased both the prevalence and the severity of RA in the progeny compared to
un-exposed dams. Additionally, maternal BBP exposure led to elevated serum IgG1
and IgG2a level in the offspring and increased the IFN-g and IL-17 release from
collagen-re-stimulated spleen cells. Transcriptome analysis of splenocytes isolated from
3-week-old pups before RA-induction revealed considerable changes in gene expression
in the offspring from BBP-exposed dams. Among them were regulator of G-protein
signaling 1 (rgs1), interleukin-7 receptor (il-7r) and CXC chemokine 4 (cxcr4), all genes
that have previously been described as associated with RA pathology. In summary, our
results demonstrate that perinatal exposure to BBP increases the susceptibility of the
offspring to RA, probably via a phthalate-induced disturbed regulation of RA-relevant
genes or signaling pathway
Environment‐induced epigenetic reprogramming in genomic regulatory elements in smoking mothers and their children
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Mold, Mycotoxins and a Dysregulated Immune System: A Combination of Concern?
Fungi represent one of the most diverse and abundant eukaryotes on earth. The interplay
between mold exposure and the host immune system is still not fully elucidated. Literature research
focusing on up-to-date publications is providing a heterogenous picture of evidence and opinions
regarding the role of mold and mycotoxins in the development of immune diseases. While the
induction of allergic immune responses by molds is generally acknowledged, other direct health
effects like the toxic mold syndrome are controversially discussed. However, recent observations
indicate a particular importance of mold/mycotoxin exposure in individuals with pre-existing
dysregulation of the immune system, due to exacerbation of underlying pathophysiology including
allergic and non-allergic chronic inflammatory diseases, autoimmune disorders, and even human
immunodeficiency virus (HIV) disease progression. In this review, we focus on the impact of
mycotoxins regarding their impact on disease progression in pre-existing immune dysregulation.
This is complemented by experimental in vivo and in vitro findings to present cellular and molecular
modes of action. Furthermore, we discuss hypothetical mechanisms of action, where evidence is
missing since much remains to be discovered
Mold, Mycotoxins and a Dysregulated Immune System: A Combination of Concern?
Fungi represent one of the most diverse and abundant eukaryotes on earth. The interplay between mold exposure and the host immune system is still not fully elucidated. Literature research focusing on up-to-date publications is providing a heterogenous picture of evidence and opinions regarding the role of mold and mycotoxins in the development of immune diseases. While the induction of allergic immune responses by molds is generally acknowledged, other direct health effects like the toxic mold syndrome are controversially discussed. However, recent observations indicate a particular importance of mold/mycotoxin exposure in individuals with pre-existing dysregulation of the immune system, due to exacerbation of underlying pathophysiology including allergic and non-allergic chronic inflammatory diseases, autoimmune disorders, and even human immunodeficiency virus (HIV) disease progression. In this review, we focus on the impact of mycotoxins regarding their impact on disease progression in pre-existing immune dysregulation. This is complemented by experimental in vivo and in vitro findings to present cellular and molecular modes of action. Furthermore, we discuss hypothetical mechanisms of action, where evidence is missing since much remains to be discovered
Mold, Mycotoxins and a Dysregulated Immune System: A Combination of Concern?
Fungi represent one of the most diverse and abundant eukaryotes on earth. The interplay
between mold exposure and the host immune system is still not fully elucidated. Literature research
focusing on up-to-date publications is providing a heterogenous picture of evidence and opinions
regarding the role of mold and mycotoxins in the development of immune diseases. While the
induction of allergic immune responses by molds is generally acknowledged, other direct health
effects like the toxic mold syndrome are controversially discussed. However, recent observations
indicate a particular importance of mold/mycotoxin exposure in individuals with pre-existing
dysregulation of the immune system, due to exacerbation of underlying pathophysiology including
allergic and non-allergic chronic inflammatory diseases, autoimmune disorders, and even human
immunodeficiency virus (HIV) disease progression. In this review, we focus on the impact of
mycotoxins regarding their impact on disease progression in pre-existing immune dysregulation.
This is complemented by experimental in vivo and in vitro findings to present cellular and molecular
modes of action. Furthermore, we discuss hypothetical mechanisms of action, where evidence is
missing since much remains to be discovered
Phthalate Exposure During the Prenatal and Lactational Period Increases the Susceptibility to Rheumatoid Arthritis in Mice
The prenatal and early postnatal period is highly sensitive to environmental exposures
that may interfere with the developmental programming of the immune system leading
to an altered disease risk in later life. To clarify the role of early influences in activation
or exacerbation of autoimmune diseases like rheumatoid arthritis (RA) we investigated
the effect of maternal exposure during the prenatal and lactational period of DBA/1
mice to the plasticizer benzyl butyl phthalate (BBP) on the development of RA in the
offspring. Using a mild collagen-induced arthritis (CIA) model, maternal BBP-exposure
increased both the prevalence and the severity of RA in the progeny compared to
un-exposed dams. Additionally, maternal BBP exposure led to elevated serum IgG1
and IgG2a level in the offspring and increased the IFN-g and IL-17 release from
collagen-re-stimulated spleen cells. Transcriptome analysis of splenocytes isolated from
3-week-old pups before RA-induction revealed considerable changes in gene expression
in the offspring from BBP-exposed dams. Among them were regulator of G-protein
signaling 1 (rgs1), interleukin-7 receptor (il-7r) and CXC chemokine 4 (cxcr4), all genes
that have previously been described as associated with RA pathology. In summary, our
results demonstrate that perinatal exposure to BBP increases the susceptibility of the
offspring to RA, probably via a phthalate-induced disturbed regulation of RA-relevant
genes or signaling pathway
Phthalate Exposure During the Prenatal and Lactational Period Increases the Susceptibility to Rheumatoid Arthritis in Mice
The prenatal and early postnatal period is highly sensitive to environmental exposures
that may interfere with the developmental programming of the immune system leading
to an altered disease risk in later life. To clarify the role of early influences in activation
or exacerbation of autoimmune diseases like rheumatoid arthritis (RA) we investigated
the effect of maternal exposure during the prenatal and lactational period of DBA/1
mice to the plasticizer benzyl butyl phthalate (BBP) on the development of RA in the
offspring. Using a mild collagen-induced arthritis (CIA) model, maternal BBP-exposure
increased both the prevalence and the severity of RA in the progeny compared to
un-exposed dams. Additionally, maternal BBP exposure led to elevated serum IgG1
and IgG2a level in the offspring and increased the IFN-g and IL-17 release from
collagen-re-stimulated spleen cells. Transcriptome analysis of splenocytes isolated from
3-week-old pups before RA-induction revealed considerable changes in gene expression
in the offspring from BBP-exposed dams. Among them were regulator of G-protein
signaling 1 (rgs1), interleukin-7 receptor (il-7r) and CXC chemokine 4 (cxcr4), all genes
that have previously been described as associated with RA pathology. In summary, our
results demonstrate that perinatal exposure to BBP increases the susceptibility of the
offspring to RA, probably via a phthalate-induced disturbed regulation of RA-relevant
genes or signaling pathway
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