Possible involvement of the interleukin-15 and interleukin-15 receptor system in a heightened state of lamina propria B cell activation and differentiation in patients with inflammatory bowel disease

Ina, Kenji; Goto, Hidemi; Watanabe, Osamu; Tsuzuki, Tomoyuki; Furuta, Ryuichi; Ando, Takafumi; Hibi, Kenji; Kusugami, Kazuo

doi:10.1007/s00535-004-1510-y

Cited by 32 publications

(35 citation statements)

References 41 publications

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“…This postulation needs to be investigated in future studies. Although IL-15 was initially thought to be upregulated in predominantly Th1 cell diseases, such as rheumatoid arthritis 46 and inflammatory bowel disease, 47 results of studies demonstrated a role of IL-15 in asthma 48,49 which has long been considered a Th2-predominant disease. Studies by Meresse et al 50 and Tang et al 51 found that IL-15 plays a key role in amplifying this cytolysis reaction, which is mediated by cysteinyl leukotrienes, which are involved in asthma.…”

Section: Discussionmentioning

confidence: 99%

Heterogeneity of asthma and the risk of celiac disease in children

Patel¹,

Wi²,

Hasassri³

et al. 2018

allergy asthma proc

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Section: Discussionmentioning

confidence: 99%

Heterogeneity of asthma and the risk of celiac disease in children

Patel¹,

Wi²,

Hasassri³

et al. 2018

allergy asthma proc

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“…Regardless of whether genetic or acquired factors are responsible for the increased permeability, therapies in each are equally possible and should be considered. 34 …”

Section: Inflamm Bowel Dismentioning

confidence: 97%

“…Research indicates that disruption of tight junctions, which normally seal epithelial cells and thereby control gut barrier function, is a characteristic of UC, with increased gut permeability reported in several studies of UC patients (Table 1). 20 -22 Cytokine production is also altered in UC (Table 2), with a large number of studies [23][24][25][26][27][28][29][30][31][32][33][34] finding that increased levels of proinflammatory and anti-inflammatory cytokines are associated with 1BD and its severity. Consequently, some researchers have suggested that this altered cytokine profile is responsible for modulating epithelial gut permeability (Table 3).…”

Section: Differences Between Uc and CD In Gut Permeabilitymentioning

confidence: 99%

Hypothesis about mechanisms through which nicotine might exert its effect on the interdependence of inflammation and gut barrier function in ulcerative colitis

McGilligan

Wallace

Heavey

et al. 2007

Inflammatory Bowel Diseases

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Ulcerative colitis (UC) is characterized by impairment of the epithelial barrier and the formation of ulcer-type lesions, which result in local leaks and generalized alterations of mucosal tight junctions. Ultimately, this results in increased basal permeability. Although disruption of the epithelial barrier in the gut is a hallmark of inflammatory bowel disease and intestinal infections, it remains unclear whether barrier breakdown is an initiating event of UC or rather a consequence of an underlying inflammation, evidenced by increased production of proinflammatory cytokines. UC is less common in smokers, suggesting that the nicotine in cigarettes may ameliorate disease severity. The mechanism behind this therapeutic effect is still not fully understood, and indeed it remains unclear if nicotine is the true protective agent in cigarettes. Nicotine is metabolized in the body into a variety of metabolites and can also be degraded to form various breakdown products. It is possible these metabolites or degradation products may be the true protective or curative agents. A greater understanding of the pharmacodynamics and kinetics of nicotine in relation to the immune system and enhanced knowledge of gut permeability defects in UC are required to establish the exact protective nature of nicotine and its metabolites in UC. This review suggests possible hypotheses for the protective mechanism of nicotine in UC, highlighting the relationship between gut permeability and inflammation, and indicates where in the pathogenesis of the disease nicotine may mediate its effect.

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“…Pro-inflammatory cytokines within this group, such as IL-2, IL-6, IL-15, IL-21, IL-23, IL-17 and IL-18, have been demonstrated to be detrimental in mice models of IBD [93,97,110,111,112,113,114,115,116,117,118]. While anti-inflammatory cytokines within this group, such as IFNα/β, IL-10, IL-11 and IL-22, were shown to be beneficial in animal models of IBD, their administration did not show any significant beneficial effects in patients with IBD [119,120,121,122,123,124,125,126].…”

Section: Stat3 and Inflammatory Bowel Diseasementioning

confidence: 99%

Contribution of STAT3 to Inflammatory and Fibrotic Diseases and Prospects for its Targeting for Treatment

Kasembeli

Bharadwaj

Robinson

et al. 2018

IJMS

146

119

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Signal transducer and activator of transcription (STAT) 3 plays a central role in the host response to injury. It is activated rapidly within cells by many cytokines, most notably those in the IL-6 family, leading to pro-proliferative and pro-survival programs that assist the host in regaining homeostasis. With persistent activation, however, chronic inflammation and fibrosis ensue, leading to a number of debilitating diseases. This review summarizes advances in our understanding of the role of STAT3 and its targeting in diseases marked by chronic inflammation and/or fibrosis with a focus on those with the largest unmet medical need.

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Possible involvement of the interleukin-15 and interleukin-15 receptor system in a heightened state of lamina propria B cell activation and differentiation in patients with inflammatory bowel disease

Abstract: These data suggest that the IL-15 and IL-15R system may play important roles in the activation and differentiation of lamina propria B cells in patients with IBD, especially in those with UC.

Cited by 32 publications

References 41 publications

Heterogeneity of asthma and the risk of celiac disease in children

Heterogeneity of asthma and the risk of celiac disease in children

Hypothesis about mechanisms through which nicotine might exert its effect on the interdependence of inflammation and gut barrier function in ulcerative colitis

Contribution of STAT3 to Inflammatory and Fibrotic Diseases and Prospects for its Targeting for Treatment

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