Immunophysiology of the gut: a research frontier for integrative studies of the common mucosal immune system

Castro, Gilbert A.; Arntzen, Charles J.

doi:10.1152/ajpgi.1993.265.4.g599

Cited by 46 publications

(37 citation statements)

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“…These cell populations share common features with other immune cell populations associated with mucosal surfaces, lending support to the concept of a common mucosa-associated immune system, whose biologic role is a dual one, i.e., immunity against potentially pathogenic organisms, but downregulation of immune responsiveness to foodstuffs or other beneficial environmental antigens (Castro and Arntzen 1993). Development of this specialized lymphoid tissue is dependent on the establishment of the normal indigenous gut flora (Umesaki et al 1993).…”

Section: The Gut-associated Lymphoid Tissues (Galt)mentioning

confidence: 82%

The gut as a potential trigger of exercise-induced inflammatory responses

Marshall¹

1998

Can. J. Physiol. Pharmacol.

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Multiple lines of evidence support the hypothesis that ischemia-induced impairment of normal gut barrier function, with loss of the normal tonic counterinflammatory influence of the gut immune system, contributes to the expression of uncontrolled inflammation in critically ill victims of trauma and overwhelming infection. The clinical syndrome known as the systemic inflammatory response syndrome (SIRS), which embodies uncontrolled inflammation in trauma and sepsis, is reproduced in its entirety by vigourous exercise, raising the possibility that the gut may also play a role in exercise-induced inflammation. Both strenuous exercise and systemic sepsis result in impairment of the normal gut barrier to luminal microorganisms, and result in elevated circulating levels of bacterial endotoxin. Under normal circumstances, the immune tissues of the gut-liver axis inhibit the expression of a host response to foodstuffs in the gut lumen, or to the indigenous microbial flora of the gut wall. This influence is an active, energy-requiring process. Both strenuous exercise and critical illness are associated with gut ischemia, providing a common biologic basis for the initiation of a dysregulated inflammatory response. Although direct evidence supporting or refuting the hypothesis that the gut can serve as a trigger for systemic inflammation following strenuous exercise is sparse, the similarities in the clinical manifestations of SIRS and exercise, and the promising results of prophylactic or therapeutic gut-directed strategies in critical illness, suggest that similar approaches may provide benefit for individuals engaged in extreme physical exercise.

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Section: The Gut-associated Lymphoid Tissues (Galt)mentioning

confidence: 82%

The gut as a potential trigger of exercise-induced inflammatory responses

Marshall¹

1998

Can. J. Physiol. Pharmacol.

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“…but fits with the notion of a role in intestinal cell differentiation. In addition, glucocorticoids are known suppressors of the immune response and inflammation (Castro and Arntzen, 1993;Janeway and Travers, 1996). CRIP has previously been shown to be upregulated late in the immune response, during a period when suppression of the immune response would occur (Hallquist et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Structural Characterization of the Rat Cysteine-Rich Intestinal Protein Gene and Overexpression of This LIM-Only Protein in Transgenic Mice

Davis¹,

Blanchard²,

Lanningham-Foster³

et al. 1998

DNA and Cell Biology

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Cysteine-rich intestinal protein (CRIP) has a double zinc-finger motif called the LIM domain. The most elementary member of the Group 2 LIM-only protein family, CRIP was initially identified as a developmentally regulated intestinal gene. Subsequently, it was found to be highly expressed in immune cells. The structural portion of the rat CRIP gene is comprised of five exons extending over i.8 kb, with the two zinc-finger motifs of the LIM domain being divided among the first three exons. In addition to transcriptional regulatory elements previously identified in the promoter, consensus sequences for AP-1, AP2, Sp-1, and a glucocorticoid response element are located within the first intron. We have developed a line of transgenic mice that overexpress the rat CRIP gene with an expression profile that mirrors that of the endogenous gene. Driven by the homologous rat CRIP promoter, expression increased threefold to sevenfold in intestine, thymus, spleen, and lung over endogenous levels. The transgenic mice had only about 50% of the white blood cell count found in nontransgenic animals. Differential leukocyte counts showed transgenic animals had proportionately fewer lymphocytes and more monocytes, eosinophils, neutrophils. Flow cytometry data suggested that mice overexpressing CRIP have more CD4+/CD8+ thymic lymphocytes. These data suggest that CRIP plays a significant role in differentiation or maturation of cells with rapid turnover such as those found in the intestine and immune system.

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“…The gut is the largest immune organ in the body (78), harboring 70-80% of the body's immune cells (79), and has been implicated as a major source of inflammation suggested to contribute to diseases such as NAFLD (80,81) and CKD (82). Several studies have shown immunomodulatory activities for a variety of DFs, including FOSs (83), arabinoxylans (84), and b-glucans (85).…”

Section: Impact Of Df On the Gut The Gatekeeper Of The Bodymentioning

confidence: 99%

Impact of Dietary Fibers on Nutrient Management and Detoxification Organs: Gut, Liver, and Kidneys

Kieffer

Martin

Adams

2016

Advances in Nutrition

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Increased dietary fiber (DF) intake elicits a wide range of physiologic effects, not just locally in the gut, but systemically. DFs can greatly alter the gut milieu by affecting the gut microbiome, which in turn influences the gut barrier, gastrointestinal immune and endocrine responses, and nitrogen cycling and microbial metabolism. These gut-associated changes can then alter the physiology and biochemistry of the body's other main nutrient management and detoxification organs, the liver and kidneys. The molecular mechanisms by which DF alters the physiology of the gut, liver, and kidneys is likely through gut-localized events (i.e., bacterial nitrogen metabolism, microbe-microbe, and microbe-host cell interactions) coupled with specific factors that emanate from the gut in response to DF, which signal to or affect the physiology of the liver and kidneys. The latter may include microbe-derived xenometabolites, peptides, or bioactive food components made available by gut microbes, inflammation signals, and gut hormones. The intent of this review is to summarize how DF alters the gut milieu to specifically affect intestinal, liver, and kidney functions and to discuss the potential local and systemic signaling networks that are involved. Adv Nutr 2016;7:1111-21.

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Immunophysiology of the gut: a research frontier for integrative studies of the common mucosal immune system

Cited by 46 publications

References 0 publications

The gut as a potential trigger of exercise-induced inflammatory responses

The gut as a potential trigger of exercise-induced inflammatory responses

Structural Characterization of the Rat Cysteine-Rich Intestinal Protein Gene and Overexpression of This LIM-Only Protein in Transgenic Mice

Impact of Dietary Fibers on Nutrient Management and Detoxification Organs: Gut, Liver, and Kidneys

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