Leptin mediates Clostridium difficile toxin A–induced enteritis in mice

Mykoniatis, Andreas; Anton, Pauline M.; Wlk, Michael; Wang, Chi Chung; Ungsunan, Linda; Blüher, Susann; Venihaki, Maria; Simeonidis, Simos; Zacks, Jeff; Zhao, Dan; Sougioultzis, Stavros; Karalis, Katia; Mantzoros, Christos S.; Pothoulakis, Charalabos

doi:10.1053/gast.2003.50101

Cited by 47 publications

(43 citation statements)

References 46 publications

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“…Histological examination of the colon, early after the induction of disease, revealed marked inflammation in mice injected with wild-type cells, whereas no inflammation was observed in mice receiving db/db cells (66). These data suggest that leptin may prove to be a pivotal mediator in intestinal inflammation (58).…”

Section: Leptin Inflammation and Enhanced Anti-self-immune Responsesmentioning

confidence: 77%

Leptin in Immunology

Matarese

Moschos

Mantzoros

2005

The Journal of Immunology

516

426

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Leptin is an adipokine which conveys information on energy availability. In humans, leptin influences energy homeostasis and regulates neuroendocrine function primarily in states of energy deficiency. As a cytokine, leptin also affects thymic homeostasis and, similar to other proinflammatory cytokines, leptin promotes Th1 cell differentiation and cytokine production. We review herein recent advances on the role of leptin in the pathophysiology of immune responses.

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Section: Leptin Inflammation and Enhanced Anti-self-immune Responsesmentioning

confidence: 77%

Leptin in Immunology

Matarese

Moschos

Mantzoros

2005

The Journal of Immunology

516

426

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“…Clostridium difficile toxin A increases plasma corticosterone levels in Wistar rats and in C57BL/6J mice (Castagliuolo et al 2001, Mykoniatis et al 2003. It is thought that this toxin activates the HPA axis through inflammatory mediators, such as tumor necrosis factor (TNF ) and prostaglandin E 2 (PGE 2 ), which are released prior to corticosterone induction following injection into rodent intestine (Castagliuolo et al 1997).…”

Section: Bacterial Hpa Axis Activationmentioning

confidence: 99%

“…Thus, removal of endogenous glucocorticoid responses by the GR antagonist RU486 or by adrenalectomy results in enhanced C. difficile toxin A-induced fluid secretion and inflammation (Castagliuolo et al 2001, Mykoniatis et al 2003. Similarly, adrenalectomy enhances time to lethality in Shiga toxin 2-injected BALB/c mice and also increases the pathologic effects of this toxin, as seen by increased serum urea levels and histopathology (Gomez et al 2003).…”

Section: Bacterial Toxinsmentioning

confidence: 99%

Role of the hypothalamic-pituitary-adrenal axis, glucocorticoids and glucocorticoid receptors in toxic sequelae of exposure to bacterial and viral products

Webster

Sternberg

2004

Journal of Endocrinology

164

124

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The hypothalamic-pituitary-adrenal (HPA) axis is activated during many bacterial and viral infections, resulting in an increase in circulating glucocorticoid levels. This HPA axis activation and glucocorticoid response are critical for the survival of the host, as demonstrated by the fact that removal of the HPA axis (by adrenalectomy or hypophysectomy) or glucocorticoid receptor (GR) blockade enhances the severity of the infection and in some cases enhances the mortality rate. Replacement with a synthetic glucocorticoid reverses these effects by reducing the severity of the infection and provides protection against lethal effects. In addition, some bacteria and viral infections have been shown to affect the GR directly. These have been described and the implications of such an effect discussed.

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“…Several reports of the in vivo effects of TcdA in animal models reflect efforts to understand the cellular mechanism leading to clinical symptoms as well as to the release of mediators that are involved in the inflammatory process (2,13,15,18,20). The inherent glucosyltransferase…”

mentioning

confidence: 99%

Application of Mutated Clostridium difficile Toxin A for Determination of Glucosyltransferase-Dependent Effects

et al. 2006

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Mutation of tryptophan-101 in Clostridium difficile toxin A, a 308-kDa glucosyltransferase, resulted in a 50-fold-reduced cytopathic activity in cell culture experiments. The mutant toxin A was characterized and applied to distinguish between glucosyltransferase-dependent and -independent effects with respect to RhoB up-regulation as a cellular stress response.Clostridium difficile toxins A and B (TcdA and TcdB, respectively) are the major pathogenicity factors that are causative for antibiotic-associated pseudomembranous colitis (19). Several reports of the in vivo effects of TcdA in animal models reflect efforts to understand the cellular mechanism leading to clinical symptoms as well as to the release of mediators that are involved in the inflammatory process (2,13,15,18,20). The inherent glucosyltransferase

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Leptin mediates Clostridium difficile toxin A–induced enteritis in mice

Cited by 47 publications

References 46 publications

Leptin in Immunology

Leptin in Immunology

Role of the hypothalamic-pituitary-adrenal axis, glucocorticoids and glucocorticoid receptors in toxic sequelae of exposure to bacterial and viral products

Application of Mutated Clostridium difficile Toxin A for Determination of Glucosyltransferase-Dependent Effects

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