Some Effects of Oral Administration of Oxazolone to Mice

Glaister, J. R.

doi:10.1159/000231083

Cited by 9 publications

(4 citation statements)

References 5 publications

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“…Contrary to this, systemic tolerance rather than sensitivity has been reported to occur as a result of priming at mucosal membranes (Tomasi, 1980). Thus, oral ingestion of haptens or soluble proteins resulted in a state of systemic (skin) DTH hyporesponsiveness (Chase, 1946;Glaister, 1973;Asherson et al, 1977;Richman et al, 1978). Others have reported that under certain conditions oral administration of haptens can give rise to effective contact sensitivity elicitable at skin sites (Asherson et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Contact sensitivity in the murine oral mucosa. I. An experimental model of delayed-type hypersensitivity reactions at mucosal surfaces

Ahlfors

Czerkinsky

1991

Clinical and Experimental Immunology

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Section: Discussionmentioning

confidence: 99%

Contact sensitivity in the murine oral mucosa. I. An experimental model of delayed-type hypersensitivity reactions at mucosal surfaces

Ahlfors

Czerkinsky

1991

Clinical and Experimental Immunology

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“…In comparison to conventionally housed animals, GF animals have decreased plasma cells and IgA, decreased expression of activation markers on intestinal macrophages, decreased MHCII on epithelial cells, decreased nitric oxide, and histamine levels in the small intestine (Gordon, 1959; Beaver and Wostmann, 1962; Glaister, 1973; Moreau et al, 1978; Matsumoto et al, 1992; Mikkelsen et al, 2004; Sobko et al, 2004; Smith et al, 2007). Peyer’s patch follicles are reduced in number and size and the mesenteric lymph nodes are smaller, less cellular, and do not have germinal centers in GF animals (Gordon, 1959; Glaister, 1973). However, reconstitution of GF mice with an intestinal microflora is sufficient to restore the mucosal immune system (Umesaki et al, 1995).…”

Section: Functional Relevance Of the Microbiotamentioning

confidence: 99%

Brain?Gut?Microbe Communication in Health and Disease

Grenham¹,

Clarke²,

Cryan³

et al. 2011

Front. Physio.

775

613

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Bidirectional signalling between the gastrointestinal tract and the brain is regulated at neural, hormonal, and immunological levels. This construct is known as the brain–gut axis and is vital for maintaining homeostasis. Bacterial colonization of the intestine plays a major role in the post-natal development and maturation of the immune and endocrine systems. These processes are key factors underpinning central nervous system (CNS) signaling. Recent research advances have seen a tremendous improvement in our understanding of the scale, diversity, and importance of the gut microbiome. This has been reflected in the form of a revised nomenclature to the more inclusive brain–gut–enteric microbiota axis and a sustained research effort to establish how communication along this axis contributes to both normal and pathological conditions. In this review, we will briefly discuss the critical components of this axis and the methodological challenges that have been presented in attempts to define what constitutes a normal microbiota and chart its temporal development. Emphasis is placed on the new research narrative that confirms the critical influence of the microbiota on mood and behavior. Mechanistic insights are provided with examples of both neural and humoral routes through which these effects can be mediated. The evidence supporting a role for the enteric flora in brain–gut axis disorders is explored with the spotlight on the clinical relevance for irritable bowel syndrome, a stress-related functional gastrointestinal disorder. We also critically evaluate the therapeutic opportunities arising from this research and consider in particular whether targeting the microbiome might represent a valid strategy for the management of CNS disorders and ponder the pitfalls inherent in such an approach. Despite the considerable challenges that lie ahead, this is an exciting area of research and one that is destined to remain the center of focus for some time to come.

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“…On this basis, it seemed possible that administration of other haptenating agents per rectum to mice might elicit a different type of colitis. An additional reason for exploring the colitogenic potential of a second haptenating agent arises from the fact that the feeding of a haptenating agent, as alluded to above, results in antigen nonspecific suppressor T cell responses which could potentially mediate bystander suppres-sion of a colitis induced by an unrelated haptenating reagent (6,7,(17)(18)(19)(20)(21)(22)(23). Thus, the identification of a second colitogenic haptenating reagent would allow one to test the possibility that the feeding of a haptenating agent could nonspecifically suppress (treat) colitis occurring in humans.…”

mentioning

confidence: 99%

Oxazolone Colitis: A Murine Model of T Helper Cell Type 2 Colitis Treatable with Antibodies to Interleukin 4

Boirivant

Fuss

Chu

et al. 1998

The Journal of Experimental Medicine

486

365

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In this study we describe oxazolone colitis, a new form of experimental colitis. This model is induced in SJL/J mice by the rectal instillation of the haptenating agent, oxazolone, and is characterized by a rapidly developing colitis confined to the distal half of the colon; it consists of a mixed neutrophil/lymphocyte infiltration limited to the superficial layer of the mucosa which is associated with ulceration. Oxazolone colitis is a T helper cell type 2 (Th2)-mediated process since stimulated T cells from lesional tissue produce markedly increased amounts of interleukin (IL)-4 and IL-5; in addition, anti–IL-4 administration leads to a striking amelioration of disease, whereas anti–IL-12 administration either has no effect or exacerbates disease. Finally, this proinflammatory Th2 cytokine response is counterbalanced by a massive transforming growth factor-β (TGF-β) response which limits both the extent and duration of disease: lesional (distal) T cells manifest a 20–30-fold increase in TGF-β production, whereas nonlesional (proximal) T cells manifest an even greater 40–50-fold increase. In addition, anti–TGF-β administration leads to more severe inflammation which now involves the entire colon. The histologic features and distribution of oxazolone colitis have characteristics that resemble ulcerative colitis (UC) and thus sharply distinguish this model from most other models, which usually resemble Crohn's disease. This feature of oxazolone colitis as well as its cytokine profile have important implications to the pathogenesis and treatment of UC.

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Some Effects of Oral Administration of Oxazolone to Mice

Cited by 9 publications

References 5 publications

Contact sensitivity in the murine oral mucosa. I. An experimental model of delayed-type hypersensitivity reactions at mucosal surfaces

Contact sensitivity in the murine oral mucosa. I. An experimental model of delayed-type hypersensitivity reactions at mucosal surfaces

Brain?Gut?Microbe Communication in Health and Disease

Oxazolone Colitis: A Murine Model of T Helper Cell Type 2 Colitis Treatable with Antibodies to Interleukin 4

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