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Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis.

Terato K, Do CT, Shionoya H - Autoimmune Dis (2015)

Bottom Line: A widely accepted hypothesis to explain the pathogenic mechanism of ADs is "molecular mimicry," which states that antibodies against an infectious agent cross-react with a self-antigen sharing an identical or similar antigenic epitope.However, this hypothesis was most likely established based on misleading antibody assay data largely influenced by intense false positive reactions involved in immunoassay systems.Thus reinvestigation of this hypothesis using an appropriate blocking agent capable of eliminating all types of nonspecific reactions and proper assay design is strongly encouraged.

View Article: PubMed Central - PubMed

Affiliation: Chondrex, Inc., 2607 151st Place NE, Redmond, WA 98052, USA.

ABSTRACT
Autoimmune diseases (ADs) are considered to be caused by the host immune system which attacks and destroys its own tissue by mistake. A widely accepted hypothesis to explain the pathogenic mechanism of ADs is "molecular mimicry," which states that antibodies against an infectious agent cross-react with a self-antigen sharing an identical or similar antigenic epitope. However, this hypothesis was most likely established based on misleading antibody assay data largely influenced by intense false positive reactions involved in immunoassay systems. Thus reinvestigation of this hypothesis using an appropriate blocking agent capable of eliminating all types of nonspecific reactions and proper assay design is strongly encouraged. In this review, we discuss the possibility that low immune function may be the fundamental, common defect in ADs, which increases the susceptibility to potential disease causative pathogens located in the gastrointestinal tract (GI), such as bacteria and their components or dietary components. In addition to these exogenous agents, aberrations in the host's physical condition may disrupt the host defense system, which is tightly orchestrated by "immune function," "mucosal barrier function," and "intestinal bacterial balance." These disturbances may initiate a downward spiral, which can lead to chronic health problems that will evolve to an autoimmune disorder.

No MeSH data available.


Related in: MedlinePlus

Age associated changes of intestinal flora composition.
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Related In: Results  -  Collection


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fig3: Age associated changes of intestinal flora composition.

Mentions: Intestinal bacterial balance is maintained under the influence of host immune function [71, 72] from childhood through adulthood but starts to change at around 50–60 years of age [73, 74] as illustrated in Figure 3. For example, the relative population of beneficial bacteria such as Bifidobacterium declines gradually with aging, whereas the relative population of hazardous bacteria such as Clostridium perfringens (C. perfringens) and E. coli increases. This shift may be attributed to immunosenescence and may increase disease risk in the elderly [45, 73]. Similarly, the imbalance of intestinal bacteria may be due to low immune function associated with stress [41–43] and GI disorders [44]. Consequently, increases in the bacterial toxin levels in the GI tract may not only trigger and exacerbate inflammatory reactions, but also further deteriorate the host's immune system.


Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis.

Terato K, Do CT, Shionoya H - Autoimmune Dis (2015)

Age associated changes of intestinal flora composition.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4377354&req=5

fig3: Age associated changes of intestinal flora composition.
Mentions: Intestinal bacterial balance is maintained under the influence of host immune function [71, 72] from childhood through adulthood but starts to change at around 50–60 years of age [73, 74] as illustrated in Figure 3. For example, the relative population of beneficial bacteria such as Bifidobacterium declines gradually with aging, whereas the relative population of hazardous bacteria such as Clostridium perfringens (C. perfringens) and E. coli increases. This shift may be attributed to immunosenescence and may increase disease risk in the elderly [45, 73]. Similarly, the imbalance of intestinal bacteria may be due to low immune function associated with stress [41–43] and GI disorders [44]. Consequently, increases in the bacterial toxin levels in the GI tract may not only trigger and exacerbate inflammatory reactions, but also further deteriorate the host's immune system.

Bottom Line: A widely accepted hypothesis to explain the pathogenic mechanism of ADs is "molecular mimicry," which states that antibodies against an infectious agent cross-react with a self-antigen sharing an identical or similar antigenic epitope.However, this hypothesis was most likely established based on misleading antibody assay data largely influenced by intense false positive reactions involved in immunoassay systems.Thus reinvestigation of this hypothesis using an appropriate blocking agent capable of eliminating all types of nonspecific reactions and proper assay design is strongly encouraged.

View Article: PubMed Central - PubMed

Affiliation: Chondrex, Inc., 2607 151st Place NE, Redmond, WA 98052, USA.

ABSTRACT
Autoimmune diseases (ADs) are considered to be caused by the host immune system which attacks and destroys its own tissue by mistake. A widely accepted hypothesis to explain the pathogenic mechanism of ADs is "molecular mimicry," which states that antibodies against an infectious agent cross-react with a self-antigen sharing an identical or similar antigenic epitope. However, this hypothesis was most likely established based on misleading antibody assay data largely influenced by intense false positive reactions involved in immunoassay systems. Thus reinvestigation of this hypothesis using an appropriate blocking agent capable of eliminating all types of nonspecific reactions and proper assay design is strongly encouraged. In this review, we discuss the possibility that low immune function may be the fundamental, common defect in ADs, which increases the susceptibility to potential disease causative pathogens located in the gastrointestinal tract (GI), such as bacteria and their components or dietary components. In addition to these exogenous agents, aberrations in the host's physical condition may disrupt the host defense system, which is tightly orchestrated by "immune function," "mucosal barrier function," and "intestinal bacterial balance." These disturbances may initiate a downward spiral, which can lead to chronic health problems that will evolve to an autoimmune disorder.

No MeSH data available.


Related in: MedlinePlus