Article Information, PDF download for Basal Autophagy Is Altered in . succeptibility and maintains podpcyte homeostasis in aging mice. Our lab developed a bioluminescent reporter of ER calcium homeostasis, known as a secreted ER calcium monitoring protein (SERCaMP). with homeostasis model assessment insulin resistance Epub. Nov 9. PubMed PMID: ; PubMed Central PMCID: 1) tvnovellas.info yazilarim/TESE-nedir-Kimlere-önerilebilir-Sonuçları-nasıl-.
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e-ISBN (EPUB) .. domains, which is why a homeostatic dynamics that operates in terms of Naci, Fethi (c): “Emperyalizm Nedir?. AMPK maintains energy homeostasis and survival in cancer cells via regulating p38/PGC-1α-mediated mitochondrial biogenesis. . [Epub ahead of print]. In addition, SIgA functions in mucosal immunity and intestinal homeostasis through mechanisms that have only recently been revealed. In just the past several.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Abstract Inflamm-aging is a challenging and promising new branch of aging-related research fields that includes areas such as immunosenescence. Increasing evidence indicates that inflamm-aging is intensively associated with many aging diseases, such as Alzheimer's disease, atherosclerosis, heart disease, type II diabetes, and cancer. Mounting studies have focused on the role of inflamm-aging in disease progression and many advances have been made in the last decade.
With respect to intestinal homeostasis, we make the case that SIgA's multifaceted roles in controlling inflammation and regulating immune responses to certain dietary antigens, commensal microflora, and enteric pathogens it is only beginning to be understood. The past several years has seen an emergence of evidence that indicates that SIgA influences the composition of the intestinal microbiota, promotes the uptake and delivery of antigens from the intestinal lumen to dendritic cell DC subsets located in GALT, and, influences inflammatory responses normally associated with the uptake of highly pathogenic bacteria and potentially allergenic antigens.
Due to space limitations, this review will be restricted to SIgA's activities within the intestinal lumen; we will not discuss the capacity of polymeric IgA pIgA to neutralize pathogens intracellularly during transepithelial transport, or to promote excretion of antigens present in the lamina propria.
Multiple neutralizing properties of SIgA at gut mucosal surfaces Blocking attachment to epithelial cells by steric hindrance and binding to receptor recognition domains SIgA is capable of interfering with the earliest steps in the infection process by virtue of its ability to block toxins and pathogens from adhering to the intestinal epithelium 4 - 9.
One of the best examples of this mode of protection involves cholera toxin CT , the toxin responsible for the severe secretory diarrhea associated with Vibrio cholerae infection.
In mouse models, it has been demonstrated that SIgA is essential in protecting the intestinal epithelium from the effects of luminal CT exposure 9 , Not surprisingly, mouse monoclonal IgA antibodies mAbs against the toxin's B subunit CTB , a homopentameric molecule that binds to ganglioside GM1 on the apical surfaces of enterocytes, were sufficient to prevent CT attachment to polarized intestinal epithelial cell monolayers in vitro.
These same mAbs protected neonatal mice from CT-induced secretory diarrhea, weight loss and death Therefore, it was suggested that they likely interfere with CT binding to epithelial cells through a mechanism involving steric hindrance.
SIgA has also been shown to be capable of blocking pathogens from attaching to intestinal epithelial cells by direct recognition of receptor-binding domains, as demonstrated in the case reovirus type 1 Lang T1L. SIgA is required for full protection against intestinal reovirus T1L infection, as revealed through the use of IgA knockout mice To investigate the molecular mechanism underlying SIgA-mediated immunity to reovirus, a panel of reovirus-specific monoclonal IgA antibodies was screened for those that protected mice against an oral T1L challenge.
Monoclonal IgA antibodies against the other viral surface antigens, including the capsid protein, were not protective in the T1L peroral challenge model, underscoring the importance of epitope specificity in SIgA-mediated immunity 6. Although immune exclusion has been recognized as a function of SIgA for nearly four decades 17 , and often attributed as being an important component of protective immunity 18 , very little known about the specific details of the process. Agglutination, for example, is simply the formation of macroscopic clumps of bacteria or viruses as the result of antibody-mediated cross-linking via polyvalent surface antigens.
There are no reports in the literature to suggest that agglutination per se has any detrimental effect on microbial physiology or virulence.
Research in this area has attracted attention of scholars in many fields and significant progress has been made in the last decade.
Here, we review the concept of inflamm-aging and describe various research strategies that have led to insights into its inflammatory characteristics and mechanisms of action. We also discuss the relationship of inflamm-aging with diseases and novel interventions to delay or prevent inflamm-aging-related diseases.
Inflamm-aging is the expansion of the network theory of aging [ 5 ] and the remodeling theory of aging [ 6 , 7 ]. The network theory of aging posits that aging is indirectly controlled by the network of cellular and molecular defense mechanisms.
The remodeling theory, which was put forward to explain immunosenescence, is the gradually adaptive net result of the process of the body fighting malignant damage and is a dynamic process of optimization of the trade-off in immunity [ 6 , 7 ]. In the process of aging, some researchers pointed out that the phenomenon where adaptive immunity declines is called immunosenescence, while the phenomenon where innate immunity is activated, coupled with the rise of proinflammation, is called inflamm-aging [ 8 ].
Some regard the chronic inflammatory process with age as inflamm-aging [ 9 ], while others proposed the oxidation-inflammation theory of aging [ 10 ]. Despite the lack of agreement on definitions and terminology, there is consensus that the primary feature of inflamm-aging is an increase in the body's proinflammatory status with advancing age.
In the next section the characteristics of inflamm-aging are described in more detail. The Inflammatory Characteristics of Inflamm-Aging The five states of inflamm-aging are as follows [ 12 ]: low-grade, controlled, asymptomatic, chronic, and systemic.
However, the inflammation during inflamm-aging is not in a controlled inflammatory state.
We propose that inflammation in the process of inflamm-aging belongs to nonresolving inflammation [ 13 ]. Inflammation is a series of complex response events which are caused by the host system facing a pathogen infection or various types of tissue injury.
These response events are characterized by interactions between the cells and factors in the microenvironment and by regulation of the balance between physiological and pathological signaling networks. In common conditions, inflammatory responses disappear when proinflammatory factors in infection and tissue injuries are eliminated and then change into a highly active and well regulated balanced state, which is called resolving inflammation [ 13 ].
However, in the presence of some as yet uncertain factors, such as persistent and low intensity stimulation and long-term and excessive response in target tissues, inflammation fails to move into a steady state of anti-infection and tissue injury repair; instead the inflammation continues and moves to a nonresolving inflammation state [ 13 ].
Given this background, inflammation in the process of inflamm-aging belongs to the state of nonresolving inflammation. The Relationship between Inflamm-Aging and Diseases Like the immune response, inflammation has a physiological function in the normal body.
Moderate inflammatory response is beneficial to the body but when excessive, the response becomes harmful. Changes in the inflammatory cytokine network control the direction of the development of inflammation.