Bovine Lactoferrin Decreases Cholera-Toxin-Induced Intestinal Fluid Accumulation in Mice by Ganglioside Interaction

Rivera, Fulton P.; Medina, Anicia M.; Bezada, Sandra; Muñiz‐Valencia, Roberto; Bernal, María Luisa Pérez del Molino; Meza, Rina; Maves, Ryan C; Ochoa, Theresa J.

doi:10.1371/journal.pone.0059253

Cited by 9 publications

(5 citation statements)

References 37 publications

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“…By binding LPS, it prevents inflammation, sepsis and gastroenteritis caused by enteric viruses, Salmonella , Shigella , or E. coli ( Ochoa and Cleary, 2009 ; Latorre et al, 2010 ). It is also able to counteract cholera toxin by decreasing binding of the toxin to GM1-ganglioside on the target cell surface ( Rivera et al, 2013 ). Cholera toxin belongs to the bacterial AB 5 toxins ( Merritt and Hol, 1995 ), which exhibit a mode of action different from the pore-forming B. cereus enterotoxins.…”

Section: Discussionmentioning

confidence: 99%

Consumed Foodstuffs Have a Crucial Impact on the Toxic Activity of Enteropathogenic Bacillus cereus

et al. 2018

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Enteropathogenic Bacillus cereus cause diarrhea due to the production of enterotoxins in the intestine. To start this process, spores have to be ingested together with contaminated food and survive the stomach passage. In this study, the influence of consumed foodstuffs on spore survival as well as on cytotoxicity toward colon epithelial cells was investigated. Spore survival of 20 enteropathogenic and apathogenic B. cereus strains during simulated stomach passage was highly strain-specific and did not correlate with the toxic potential. Survival of three tested strains was strain-specifically altered by milk products. Whereas milk, a follow-on formula and rice pudding had only little influence, spores seemed to be protected by milk products with high fat content such as whipped cream and mascarpone. Furthermore, tested milk products decreased the toxic activity of three B. cereus strains toward CaCo-2 cells. Investigating the individual components, lactoferrin, a skim milk powder and vitamins C, B5 and A showed the most inhibiting effects. On the other hand, biotin, vitamin B3 and another skim milk powder even enhanced cytotoxicity. Further studies suggested that these inhibiting effects result only partially from inhibiting cell binding, but rather from blocking the interaction between the single enterotoxin components.

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Section: Discussionmentioning

confidence: 99%

Consumed Foodstuffs Have a Crucial Impact on the Toxic Activity of Enteropathogenic Bacillus cereus

et al. 2018

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“…On the other hand, the comparatively subtle neural contribution in the murine ENS found in this present study suggests that the mouse model may be more useful for studying CT effects on the mucosal epithelium. Indeed, mice have been commonly used for testing cholera therapies which target its effects on or interaction with the mucosa (Thiagarajah et al, 2004 ; Rivera et al, 2013 ). Nevertheless, the effects of CT on the ENS were only examined following pre-incubation and its more acute effects on the circuitry remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…The mouse is a commonly-used model for screening cholera vaccines and therapies (Izzo et al, 2003 ; Thiagarajah et al, 2004 ; Rivera et al, 2013 ; Sawasvirojwong et al, 2013 ; Chatterjee et al, 2015 ). However, these studies have focused on CT effects on the mucosal epithelium.…”

Section: Introductionmentioning

confidence: 99%

Cholinergic Submucosal Neurons Display Increased Excitability Following in Vivo Cholera Toxin Exposure in Mouse Ileum

et al. 2018

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Cholera-induced hypersecretion causes dehydration and death if untreated. Cholera toxin (CT) partly acts via the enteric nervous system (ENS) and induces long-lasting changes to enteric neuronal excitability following initial exposure, but the specific circuitry involved remains unclear. We examined this by first incubating CT or saline (control) in mouse ileal loops in vivo for 3.5 h and then assessed neuronal excitability in vitro using Ca2+ imaging and immunolabeling for the activity-dependent markers cFos and pCREB. Mice from a C57BL6 background, including Wnt1-Cre;R26R-GCaMP3 mice which express the fluorescent Ca2+ indicator GCaMP3 in its ENS, were used. Ca2+-imaging using this mouse model is a robust, high-throughput method which allowed us to examine the activity of numerous enteric neurons simultaneously and post-hoc immunohistochemistry enabled the neurochemical identification of the active neurons. Together, this provided novel insight into the CT-affected circuitry that was previously impossible to attain at such an accelerated pace. Ussing chamber measurements of electrogenic ion secretion showed that CT-treated preparations had higher basal secretion than controls. Recordings of Ca2+ activity from the submucous plexus showed that increased numbers of neurons were spontaneously active in CT-incubated tissue (control: 4/149; CT: 32/160; Fisher's exact test, P < 0.0001) and that cholinergic neurons were more responsive to electrical (single pulse and train of 20 pulses) or nicotinic (1,1-dimethyl-4-phenylpiperazinium (DMPP; 10 μM) stimulation. Expression of the neuronal activity marker, pCREB, was also increased in the CT-treated submucous plexus neurons. c-Fos expression and spontaneous fast excitatory postsynaptic potentials (EPSPs), recorded by intracellular electrodes, were increased by CT exposure in a small subset of myenteric neurons. However, the effect of CT on the myenteric plexus is less clear as spontaneous Ca2+ activity and electrical- or nicotinic-evoked Ca2+ responses were reduced. Thus, in a model where CT exposure evokes hypersecretion, we observed sustained activation of cholinergic secretomotor neuron activity in the submucous plexus, pointing to involvement of these neurons in the overall response to CT.

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“…Lactoferrin protects rabbits form Shigella flexneri induced inflammatory enteritis [40] and protects against Salmonella ser. Typhimurium infection in mice, reducing the severity, mortality and the degree of inflammation [41]; it decreases cholera toxin induced fluid accumulation in the mouse ileal loop by decreasing the binding of the toxin with its receptor [42]. …”

Section: Protective Components Of Human Milkmentioning

confidence: 99%

The Role of Maternal Breast Milk in Preventing Infantile Diarrhea in the Developing World

Turin

Ochoa

2014

Curr Trop Med Rep

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Multiple interventions have been designed to decrease mortality and disability in children. Among these, breastfeeding is the most cost effective intervention for protecting children against diarrhea and all causes of mortality. Human milk is uniquely suited to the human infant, both in its nutritional composition and in the nonnutritive bioactive factors that promote survival and healthy development. Suboptimal breastfeeding has been linked with numerous adverse child health outcomes including increased incidence of diarrhea and pneumonia. This review provides an update regarding recent studies on the effect of breastfeeding on diarrhea morbidity and mortality in children in developing countries, describes major human milk components responsible for this protective effect (oligosaccharides, secretory immunoglobulins, lactoferrin, bacterial microbiota, etc.), and highlights areas for future research in this topic. Breastfeeding promotion remains an intervention of enormous public health potential to decrease global mortality and promote better growth and neurodevelopment in children.

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Bovine Lactoferrin Decreases Cholera-Toxin-Induced Intestinal Fluid Accumulation in Mice by Ganglioside Interaction

Cited by 9 publications

References 37 publications

Consumed Foodstuffs Have a Crucial Impact on the Toxic Activity of Enteropathogenic Bacillus cereus

Consumed Foodstuffs Have a Crucial Impact on the Toxic Activity of Enteropathogenic Bacillus cereus

Cholinergic Submucosal Neurons Display Increased Excitability Following in Vivo Cholera Toxin Exposure in Mouse Ileum

The Role of Maternal Breast Milk in Preventing Infantile Diarrhea in the Developing World

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