Intestinal mucosal injury is associated with mast cell activation and leukotriene generation duringNippostrongylus-induced inflammation in the rat

Perdue, Mary H.; Ramage, John; Burget, D. W.; Marshall, Jean S.; Masson, Stephen

doi:10.1007/bf01540344

Cited by 67 publications

(33 citation statements)

References 31 publications

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“…LTB 4 was found in high concentrations in the mucosa of IBD patients and came down to normal levels after treatment with nonsteroidal anti-inflammatory drugs (25). In Nippostrongylus sp.-infected rats, intestinal mucosal injury was associated with mast cell activation and LTB 4 generation (24). Similarly, we also found that pediatric patients with severe inflammation had higher concentrations of LTB 4 in stool in comparison to those with mild inflammation during the acute stage.…”

Section: Discussionsupporting

confidence: 63%

Innate Immune Responses in Children and Adults with Shigellosis

Raqib¹,

MIa²,

Qadri³

et al. 2000

Infect Immun

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An array of pro-and anti-inflammatory mediators of the innate immune system was analyzed in stool, urine, and rectal mucosa samples from adults and children with shigellosis to better understand their role in recovery from and in the immunopathogenesis of the disease. Increased concentrations of lactoferrin (Lf), myeloperoxidase (MPO), prostaglandin E 2 , and leukotriene B 4 (LTB 4 ) in stool during acute shigellosis in both children and adults indicated that activated cells of the innate defense system at the mucosal site were secreting the mediators. Increased concentration of MPO and 8-iso-prostaglandin F 2␣ and lower levels of superoxide dismutase (SOD) activity in stool during acute Shigella infection suggested increased formation of reactive oxygen species, free radical-catalyzed peroxidation of membrane lipids, and decreased scavenging of the reactive oxygen radicals. In children, lower expression of SOD in tissue with severe inflammation and lower levels of SOD activity in stool for longer periods compared to adults may further worsen the tissue damage and predispose the children to a lowered defense. Both adult and pediatric patients had significantly higher expression of inducible nitric oxide synthase (iNOS) in the rectum with severe inflammation, compared to that seen with mild inflammation, accompanied by persistently up-regulated iNOS mRNA, reflecting increased production of nitric oxide at the local site. However, in contrast to adults, reduced urinary nitrate levels in pediatric patients during acute shigellosis suggested lower production of nitric oxide in the renal compartment.

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Section: Discussionsupporting

confidence: 63%

Innate Immune Responses in Children and Adults with Shigellosis

Raqib¹,

MIa²,

Qadri³

et al. 2000

Infect Immun

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“…Before or around the time of worm rejection, a variety of pathological changes occur in the intestinal mucosa; these changes include edema, eosinophil infiltration, mastocytosis, and partial villus atrophy with crypt hyperplasia (9,13,25). However, the alterations resolve quickly after worm rejection, along with the occurrence of goblet cell hyperplasia with mucins that have altered sugar residues (15,19,21).…”

mentioning

confidence: 99%

Up-Regulation of Fas (CD95) and Induction of Apoptosis in Intestinal Epithelial Cells by Nematode - Derived Molecules

et al. 2002

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Infection by the intestinal nematode Nippostrongylus brasiliensis induces acceleration of apoptosis in the small intestinal villus epithelial cells in vivo. In the present study, we examined whether worm extract or excretory-secretory product induces apoptosis in the rat intestinal epithelial cell line IEC-6 in vitro. In the presence of worm extract or excretory-secretory product (>6 g/ml), IEC-6 cell growth was significantly suppressed, and there was a concomitant increase in the number of detached cells in culture dishes. Detached cells showed nuclear fragmentation, activation of caspase-3, and specific cleavage of poly(ADP-ribose) polymerase, suggesting that apoptosis was induced in these cells. Semiquantitative reverse transcription-PCR showed that expression of Fas (CD95) mRNA was up-regulated as early as 6 h after addition of excretorysecretory product, while Fas ligand expression and p53 expression were not up-regulated. Fluorescenceactivated cell sorter analyses revealed a significant increase in Fas expression and a slight increase in FasL expression in IEC-6 cells cultured in the presence of excretory-secretory product, while control IEC-6 cells expressed neither Fas or FasL. These results indicated that N. brasiliensis worms produce and secrete biologically active molecules that trigger apoptosis in intestinal epithelial cells together with up-regulation of Fas expression, although the mechanism of induction of apoptosis remains to be elucidated.

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“…Mast cells have been shown by a number of groups to modify the epithelial barrier function within the intestine and, when activated, to increase intestinal permeability and fluid loss. [53][54][55][56][57] Such processes could explain enhanced weight loss in mast cell-containing animals.…”

Section: Discussionmentioning

confidence: 99%

Tissue Eosinophilia in a Mouse Model of Colitis Is Highly Dependent on TLR2 and Independent of Mast Cells

Albert

Duplisea

Dawicki

et al. 2011

The American Journal of Pathology

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The mechanisms initiating eosinophil influx into sites of inflammation have been well studied in allergic disease but are poorly understood in other settings. This study examined the roles of TLR2 and mast cells in eosinophil accumulation during a nonallergic model of eosinophilia-associated colitis. TLR2-deficient mice (TLR2 ؊/؊ ) developed a more severe colitis than wild-type mice in the dextran sodium sulfate (DSS) model. However, they had significantly fewer eosinophils in the submucosa of the cecum (P < 0.01) and mid-colon (P < 0.01) than did wild-type mice after DSS treatment. Decreased eosinophilia in TLR2 ؊/؊ mice was associated with lower levels of cecal CCL11 (P < 0.01). Peritoneal eosinophils did not express TLR2 protein, but TLR2 ligand injection into the peritoneal cavity induced local eosinophil recruitment, indicating that TLR2 activation of other cell types can mediate eosinophil recruitment. After DSS treatment, mast celldeficient (Kit W-sh/W-sh ) mice had similar levels of intestinal tissue eosinophilia were observed as those in wild-type mice. However, mast cell-deficient mice were partially protected from DSS-induced weight loss, an effect that was reversed by mast cell reconstitution. Overall, this study indicates a critical role for indirect TLR2-dependent pathways, but not mast cells, in the generation of eosinophilia in the large intestine during experimental colitis and has important implications for the regulation of eosinophils at mucosal inflammatory sites.

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Intestinal mucosal injury is associated with mast cell activation and leukotriene generation duringNippostrongylus-induced inflammation in the rat

Cited by 67 publications

References 31 publications

Innate Immune Responses in Children and Adults with Shigellosis

Innate Immune Responses in Children and Adults with Shigellosis

Up-Regulation of Fas (CD95) and Induction of Apoptosis in Intestinal Epithelial Cells by Nematode - Derived Molecules

Tissue Eosinophilia in a Mouse Model of Colitis Is Highly Dependent on TLR2 and Independent of Mast Cells

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