Local shwartzman reaction in the rectal mucosa in acute diarrhoea

Mathan, M.; Mathan, V. I.

doi:10.1002/path.1711460304

Cited by 13 publications

(7 citation statements)

References 24 publications

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“…The response to parenteral C5LPS was dose related and dependent on the presence of gram negative intestinal flora. 885SR preconditioned SPF mice challenged 7 (Fig. 4).…”

Section: Resultsmentioning

confidence: 93%

“…The outer membrane protein preparations contain LPS and it was likely that LPS mediated vascular endothelial damage, of lamina propria blood vessels sensitized by LPS of Salmonellae, may have been responsible for the fluid exudation. This animal model appeared to be relevant to studies on the pathogenesis of acute diarrhea, in view of the finding of an LPS-induced vascular lesion in patients in southern India (6,7). A detailed study of this animal model is reported here and its possible clinical implications are discussed.…”

Section: Introductionmentioning

confidence: 95%

“…The prevalence of these lesions correlated with the clinical severity of diarrhea, but not with the presence or type of enteric pathogen (6). Although it was not clear whether this vascular lesion was causal or secondary to diarrhea, it appeared likely to be the result of vascular injury by bacterial LPS (7). The capillaries and venules of the intestine would normally be sensitized to LPS, as it is absorbed in minute quantities from the gram negative flora that colonizes the gut lumen (8,9) and further exposure to LPS could lead to vascular damage (10).…”

Section: Introductionmentioning

confidence: 97%

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Bacterial lipopolysaccharide-induced intestinal microvascular lesions leading to acute diarrhea.

Mathan

Penny²,

Mathan³

et al. 1988

J. Clin. Invest.

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Subcutaneous challenge of mice with lipopolysaccharide (LPS) from gram negative bacteria, produced an intestinal microvascular lesion causing fluid exudation into the lumen of the intestine and diarrhea. The microvascular lesion was characterized by endothelial cell damage and microthrombi in the venules and capillaries of the intestinal lamina propria. Marker organisms, given orally to challenged mice, grew in the exuded fluid and could invade the mucosa. Intravenous transfer of postchallenge plasma produced the lesion in normal mice and absorption of such plasma by Sepharose coupled to LPS-antibody abolished this effect. Instillation of large quantities of LPS into the lumen of the intestine produced scattered microvascular lesions, although none of these animals developed diarrhea. Since a similar microvascular lesion has been described in the rectal mucosal lamina propria of adults with acute diarrhea, it is suggested that LPS-induced vascular damage may be a novel mechanism in the pathogenesis of acute diarrhea.

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“…The response to parenteral C5LPS was dose related and dependent on the presence of gram negative intestinal flora. 885SR preconditioned SPF mice challenged 7 (Fig. 4).…”

Section: Resultsmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Bacterial lipopolysaccharide-induced intestinal microvascular lesions leading to acute diarrhea.

Mathan

Penny²,

Mathan³

et al. 1988

J. Clin. Invest.

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“…Our previous studies of rectal mucosal biopsies from healthy South Indians, prone to repeated enteric infections, have shown evidence of vascular injury with reduplication of the basal lamina and occlusive thrombi (Mathan and Mathan, 1985b). This indicates damage to endothelial cells that probably occurred during previous episodes of diarrhea.…”

Section: Introductionmentioning

confidence: 96%

Vascular changes in duodenal mucosa in shigellosis and cholera

et al. 2003

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Vascular endothelial cells are highly specialized cells with numerous sensory and modulator functions. Our previous studies show extensive microvascular changes in rectal mucosal vasculature of patients with acute infective diarrhea (Mathan and Mathan 1985a, Gut 26:710-717). We looked for changes in the duodenal mucosal vasculature in two naturally occurring diarrheal infections: shigellosis and cholera. Duodenal mucosal biopsies from 14 patients with shigellosis, 12 patients with cholera, and 10 healthy volunteers were examined under the electron microscope. There were extensive microvascular changes in the duodenum in shigellosis and cholera. Congestion and dilatation of capillaries and venules, stagnation of blood, thinning of the endothelial lining, and platelet clumping were commonly seen in both conditions. Endothelial damage was also common to both conditions but was mild to moderate in cholera and severe in shigellosis with frank hemorrhage, frequent formation of stress fibers, widening of intercellular spaces, cytoplasmic blebbing, cell fragmentation, and intravascular thrombosis. Erythrocyte aggregates, platelet aggregates, and leucocyte plugging lead to capillary obstruction. The arterioles were severely constricted. These changes in the endothelial lining of the microvasculature could contribute to the pathogenesis of the disease resulting in peripheral vascular insufficiency, inadequate oxygen delivery to intestine, and organ dysfunction. The factors influencing these changes, their implications, and possible therapeutic interventions are discussed.

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“…injections of LPS 24 h apart, and individual LPS injection is not lethal per se [11]. Many clinical case reports have suggested the occurrence of the GSR/LSR following gram-negative septicemia in humans [12][13][14][15][16][17][18][19][20][21][22]. In addition, a univisceral LSR is suggested to be involved in acute/early graft rejection [21,22], and this remains a serious problem in transplantation [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

An in vitro Shwartzman reaction-like response is augmented age-dependently in human peripheral blood mononuclear cells

Motegi

Kinoshita

Sato

et al. 2005

Journal of Leukocyte Biology

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A lethal human septic shock model, mouse generalized Shwartzman reaction (GSR), was elicited by two consecutive lippolysaccharide (LPS) injections (24 h apart) in which interferon-gamma (IFN-gamma) induced by interleukin (IL)-12 played a critical role in the priming phase, and tumor necrosis factor (TNF) was an important effector molecule in the second phase. We recently reported IL-12/LPS-induced mouse GSR age-dependently enhanced. We herein demonstrate that human peripheral blood mononuclear cells (PBMC) from healthy adults/elderly, cultured with IL-12 for 24 h and with LPS for an additional 24 h, produced a much larger amount of TNF (which increased age-dependently) than did PBMC without IL-12 priming. Whereas macrophages mainly produced TNF following LPS stimulation, macrophages and lymphocytes were necessary for a sufficient TNF production. IL-12-induced IFN-gamma up-regulated Toll-like receptor 4 (TLR-4) on macrophages of adults. Although the PBMC from children produced a substantial amount of IFN-gamma after IL-12 priming, the GSR response, with augmented TNF production and an up-regulated TLR-4 expression of macrophages, was not elicited by LPS stimulation. CD56+natural killer cells, CD56+T cells, and CD57+T cells (NK-T cells), which age-dependently increased in PBMC, produced much larger amounts of IFN-gamma after IL-12 priming than that of conventional CD56-CD57-T cells and also induced cocultured macrophages to produce TNF by subsequent LPS stimulation. The elder septic patients were consistently more susceptible to lethal shock with enhanced serum TNF levels than the adult patients. The NK cells, NK-T cells, and macrophages, which change proportionally or functionally with aging, might be involved in the enhanced GSR response/septic shock observed in elderly patients.

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Local shwartzman reaction in the rectal mucosa in acute diarrhoea

Cited by 13 publications

References 24 publications

Bacterial lipopolysaccharide-induced intestinal microvascular lesions leading to acute diarrhea.

Bacterial lipopolysaccharide-induced intestinal microvascular lesions leading to acute diarrhea.

Vascular changes in duodenal mucosa in shigellosis and cholera

An in vitro Shwartzman reaction-like response is augmented age-dependently in human peripheral blood mononuclear cells

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