Prostanoids inhibit intestinal NaCl absorption in experimental porcine cryptosporidiosis

Argenzio, Robert A.; Lecce, James G.; Powell, Don W.

doi:10.1016/0016-5085(93)90412-6

Cited by 116 publications

(82 citation statements)

References 20 publications

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“…12 In contrast, expression of TNF-␣ and IL-1 in adult volunteers did not correlate with enteric symptoms. 13 This study demonstrated that compared with control and pre-challenge levels of fecal IL-8 in children and human volunteers, respectively, three of 11 children with diarrhea and one of 11 adults who developed diarrhea post-challenge had detectable IL-8. Although this difference was not statistically significant, 40% of the control children were noted to have elevated levels of IL-8 compared with only 23% of the infected children.…”

Section: Discussionmentioning

confidence: 66%

INTERLEUKIN-8, TUMOR NECROSIS FACTOR-α, AND LACTOFERRIN IN IMMUNOCOMPETENT HOSTS WITH EXPERIMENTAL AND BRAZILIAN CHILDREN WITH ACQUIRED CRYPTOSPORIDIOSIS

ALCANTARA¹,

White²,

Okhuysen³

et al. 2003

The American Journal of Tropical Medicine and Hygiene

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Section: Discussionmentioning

confidence: 66%

INTERLEUKIN-8, TUMOR NECROSIS FACTOR-α, AND LACTOFERRIN IN IMMUNOCOMPETENT HOSTS WITH EXPERIMENTAL AND BRAZILIAN CHILDREN WITH ACQUIRED CRYPTOSPORIDIOSIS

ALCANTARA¹,

White²,

Okhuysen³

et al. 2003

The American Journal of Tropical Medicine and Hygiene

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“…8 The diarrhea is often profuse and has been shown to be both malabsorptive and secretory, with some studies suggesting that a hostderived factor, such as prostaglandin E 2 or a proinflammatory cytokine, may be responsible for the secretory diarrhea. 25 Biliary cryptosporidiosis is also associated with a nonspecific inflammatory response. Histologically, there is a periductal inflammatory response with interstitial edema, mixed inflammatory cell infiltrates, and hyperplasia and dilatation of the periductal glands.…”

Section: Discussionmentioning

confidence: 99%

Cryptosporidium parvum is cytopathic for cultured human biliary epithelia via an apoptotic mechanism

Chen¹,

Levine²,

Tietz³

et al. 1998

Hepatology

101

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While the clinical features of sclerosing cholangitis secondary to opportunistic infections of the biliary tree in patients with acquired immunodeficiency syndrome (AIDS) are well known, the mechanisms by which microbial pathogens such as Cryptosporidium parvum associated with this syndrome actually cause disease are obscure. We established an in vitro model of biliary cryptosporidiosis employing a human biliary epithelial cell line. Using morphological and biochemical techniques, we examined the interaction of C. parvum with cultured human cholangiocytes. When the apical plasma membrane of polarized, confluent monolayers of human biliary epithelial cells was exposed to C. parvum oocysts that had been excysted in vitro, sporozoites attached to and invaded the cells in a time-, dose-, temperature-, and pH-dependent manner. The infectious process was both plasma membrane domain-and cell-specific, because no attachment or invasion occurred when the basolateral membrane of cholangiocytes was exposed to the parasite, or when a human hepatocyte cell line (HepG2) was used. Time-lapse video microscopy and scanning electron microscopy (SEM) showed that sporozoite attachment was rapid, involved extensive cholangiocyte membrane ruffling, and culminated in parasite penetration into a tight-fitting vacuole formed by invagination of the plasma membrane similar to those found in naturally occurring infection in vivo. Transmission electron microscopy (TEM) showed that C. parvum organisms formed parasitophorus vacuoles and were able to undergo a complete reproductive cycle, forming both asexual and sexual reproductive stages. Unexpectedly, direct cytopathic effects were noted in infected monolayers, with widespread programmed cell death (i.e., apoptosis) of biliary epithelial cells as assessed both morphologically and biochemically beginning within hours after exposure to the organism. The novel finding of specific cytopathic invasion of biliary epithelia by C. parvum may be relevant to the pathogenesis and possible therapy of the secondary sclerosing cholangitis seen in AIDS patients with biliary cryptosporidiosis. (HEPATOLOGY 1998;28:906-913.)

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“…Neutrophils mediate barrier function independently of effects on mucosal prostaglandin synthesis. An increase in endogenous prostaglandin synthesis has been demonstrated previously to promote paracellular barrier function in C. parvum infection (2,12). Therefore, we sought to determine whether neutrophils mediate barrier function of C. parvum-infected mucosa by serving as a source or stimulus of mucosal prostaglandin synthesis.…”

Section: Resultsmentioning

confidence: 96%

“…For assay of mucosal PGE 2 synthesis, sheets of ileal mucosae from anti-CD18 antibody-or isotype control antibody-treated piglets were mounted in Ussing chambers. After 120 min of incubation, the serosal bath was assayed for PGE 2 . No significant difference in PGE 2 synthesis between piglets receiving isotype control or anti-CD18 antibody was observed (1,216 Ϯ 442 pg/ml for C. parvum plus isotype control and 990 Ϯ 181 pg/ml for C. parvum plus anti-CD18 [n ϭ 5 each]).…”

Section: Resultsmentioning

confidence: 99%

“…Diarrhea has been attributed both to villus atrophy-associated malabsorption and to mucosal inflammation-induced alteration in intestinal water and electrolyte transport. Neutrophils are a source of mediators, including reactive oxygen metabolites (4), TNF-␣ (17), 5Ј-AMP (24), and prostaglandins (1,2,4,12), that may directly or indirectly promote epithelial secretion and diarrhea in C. parvum infection. Neutrophil depletion of C. parvum-infected piglets had no effect on clinical severity of diarrhea or epithelial Cl Ϫ secretion, suggesting that mediators derived from or stimulated by neutrophils do not play a significant role in the genesis of diarrhea in the infection.…”

Section: Discussionmentioning

confidence: 99%

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Neutrophils Do Not Mediate the Pathophysiological Sequelae of Cryptosporidium parvum Infection in Neonatal Piglets

Zadrozny¹,

Stauffer²,

Armstrong³

et al. 2006

Infect Immun

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Cryptosporidium parvum is a minimally invasive protozoal pathogen of intestinal epithelium that results in villus atrophy, mucosal lipid peroxidation, diarrhea, and diminished barrier function. Influx of neutrophils is a consistent feature of human and animal cryptosporidiosis, and yet their contribution to the pathological sequelae of infection has not been investigated. Accordingly, we used an established neonatal piglet model of C. parvum infection to examine the role of neutrophils in disease pathogenesis by inhibiting their recruitment and activation in vivo using a monoclonal anti-CD18 antibody. Infected piglets were treated daily with anti-CD18 or isotype control immunoglobulin G and euthanized at peak infection, at which time neutrophil infiltrates, lipid peroxidation, severity of infection, and intestinal barrier function were quantified. C. parvum infection resulted in a significant increase in mucosal neutrophil myeloperoxidase activity that was prevented by treatment of piglets with anti-CD18 antibody. Neutrophil recruitment was dependent on mucosal superoxide formation (prevented by treatment of infected piglets with superoxide dismutase). Neutrophils did not contribute to peroxynitrite formation or peroxidative injury of C. parvum-infected mucosa and had no impact on the severity of epithelial infection, villus atrophy, or diarrhea. The presence of neutrophils in C. parvuminfected mucosa was associated with enhanced barrier function that could not be attributed to mucosal elaboration of prostaglandins or stimulation of their synthesis. These studies are the first to demonstrate that neutrophilic inflammation arising in response to infection by a noninvasive epithelial pathogen results in physiologic rather than pathological effects in vivo.

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Prostanoids inhibit intestinal NaCl absorption in experimental porcine cryptosporidiosis

Cited by 116 publications

References 20 publications

INTERLEUKIN-8, TUMOR NECROSIS FACTOR-α, AND LACTOFERRIN IN IMMUNOCOMPETENT HOSTS WITH EXPERIMENTAL AND BRAZILIAN CHILDREN WITH ACQUIRED CRYPTOSPORIDIOSIS

INTERLEUKIN-8, TUMOR NECROSIS FACTOR-α, AND LACTOFERRIN IN IMMUNOCOMPETENT HOSTS WITH EXPERIMENTAL AND BRAZILIAN CHILDREN WITH ACQUIRED CRYPTOSPORIDIOSIS

Cryptosporidium parvum is cytopathic for cultured human biliary epithelia via an apoptotic mechanism

Neutrophils Do Not Mediate the Pathophysiological Sequelae of Cryptosporidium parvum Infection in Neonatal Piglets

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