<i>Cryptosporidium parvum</i>increases intestinal permeability through interaction with epithelial cells and IL-1β and TNFα released by inflammatory monocytes

Sablet, Thibaut de; Potiron, Laurent; Marquis, Mathilde; Bussière, Françoise; Lacroix‐Lamandé, Sonia; Laurent, Fabrice

doi:10.1111/cmi.12632

Cited by 35 publications

(33 citation statements)

References 45 publications

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“…In p66Shc 2/2 mice, expression of Il-1b and of the antimicrobial peptideencoding gene Reg3g was increased on SD and was demodulated after HFD. IL-1b is a major determinant of intestinal inflammation and permeability (23), and lectins encoded by the Reg3g gene determine bacterial adherence to the mucosa, translocation, and gut inflammation (24). Although we found no overt sign of colitis or a significant increase in permeability, we cannot exclude the notion that proinflammatory gene expression accompanies dysbiosis in the gut of p66Shc 2/2 vs. WT mice.…”

Section: Discussioncontrasting

confidence: 60%

Interplay between gut microbiota and p66Shc affects obesity‐associated insulin resistance

et al. 2018

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The 66 kDa isoform of the mammalian Shc gene promotes adipogenesis, and p66Shc mice accumulate less body weight than wild-type (WT) mice. As the metabolic consequences of the leaner phenotype of p66Shc mice is debated, we hypothesized that gut microbiota may be involved. We confirmed that p66Shc mice gained less weight than WT mice when on a high-fat diet (HFD), but they were not protected from insulin resistance and glucose intolerance. p66Shc deletion significantly modified the composition of gut microbiota and their modification after an HFD. This was associated with changes in gene expression of Il-1b and regenerating islet-derived protein 3 γ ( Reg3g) in the gut and in systemic trimethylamine N-oxide and branched chain amino acid levels, despite there being no difference in intestinal structure and permeability. Depleting gut microbiota at the end of HFD rendered both strains more glucose tolerant but improved insulin sensitivity only in p66Shc mice. Microbiota-depleted WT mice cohoused with microbiota-competent p66Shc mice became significantly more insulin resistant than WT mice cohoused with WT mice, despite no difference in weight gain. These findings reconcile previous inconsistent observations on the metabolic phenotype of p66Shc mice and illustrate the complex microbiome-host-genotype interplay under metabolic stress.-Ciciliot, S., Albiero, M., Campanaro, S., Poncina, N., Tedesco, S., Scattolini, V., Dalla Costa, F., Cignarella, A., Vettore, M., Di Gangi, I. M., Bogialli, S., Avogaro, A., Fadini, G. P. Interplay between gut microbiota and p66Shc affects obesity-associated insulin resistance.

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Section: Discussioncontrasting

confidence: 60%

Interplay between gut microbiota and p66Shc affects obesity‐associated insulin resistance

et al. 2018

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“…Parasitic enteric pathogens can disrupt the intestinal barrier directly, by binding to cell surface molecules, causing cell damage and apoptosis, or by disrupting tight junctions and cell cytoskeleton [9,10] as described in Cryptosporidium spp. [11,12], G. duodenalis [13,14] and STH infections [15,16]. The severity of the intestinal inflammatory response is variable and dependent on the immune status of the host, parasite invasive potential, and ecological niche [17].…”

Section: Introductionmentioning

confidence: 99%

“…In this cohort study, follow-up was scheduled for anthropometric measurements, neurodevelopment assessment, and intestinal parasites examination, approximately at 3,6,9,12,16,18, and 24 months of age. To assess the cumulative exposure to enteric parasitic infections, a minimum of four points of assessment (at 6, 12, 18 and 24 months) were required, which coincided with semestral appointments for feeding advice and scheduled immunizations.…”

Section: Introductionmentioning

confidence: 99%

Association of enteric parasitic infections with intestinal inflammation and permeability in asymptomatic infants of São Tomé Island

Garzón

Pereira‐da‐Silva

Seixas

et al. 2017

Pathogens and Global Health

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The cumulative effect of repeated asymptomatic enteric infections on intestinal barrier is not fully understood in infants. We aimed to evaluate the association between previous enteric parasitic infections and intestinal inflammation and permeability at 24-months of age, in asymptomatic infants of São Tomé Island. A subset of infants from a birth cohort, with intestinal parasite evaluations in at least four points of assessment, was eligible. Intestinal inflammatory response and permeability were assessed using fecal S100A12 and alpha-1-antitrypsin (A1AT), respectively. The cutoff <-1SD for weight-for-length and length-for-age was used to define wasting and stunting. Multivariable linear regression analysis explored if cumulative enteric parasitic infections explained variability of fecal biomarkers, after adjusting for potential confounders. Eighty infants were included. Giardia duodenalis and soil-transmitted helminths (STH) were the most frequent parasites. The median (interquartile range) levels were 2.87 μg/g (2.41-3.92) for S100A12 and 165.1 μg/g (66.0-275.6) for A1AT. Weak evidence of association was found between S100A12 levels and G. duodenalis (p = 0.080) and STH infections (p = 0.089), and between A1AT levels and parasitic infection of any etiology (p = 0.089), at 24-months of age. Significant associations between A1AT levels and wasting (p = 0.006) and stunting (p = 0.044) were found. Previous parasitic infections were not associated with fecal biomarkers at 24 months of age. To summarize, previous asymptomatic parasitic infections showed no association with intestinal barrier dysfunction. Notwithstanding, a tendency toward increased levels of the inflammatory biomarker was observed for current G. duodenalis and STH infections, and increased levels of the permeability biomarker were significantly associated with stunting and wasting.

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“…Chemokines are first released by C. parvum -infected IECs to promote chemotaxis at the site of infection; chemokines induce migration of dendritic cells in the ileum and the draining lymph nodes [ 40 ] ( Figure 1 ). Inflammatory monocytes will also migrate to the subepithelial space in response to C. parvum infection and secrete TNFα and IL-1β [ 41 ]. These cytokines will increase permeability, therefore weakening the integrity of the intestinal epithelial barrier [ 41 ].…”

Section: Innate Immunitymentioning

confidence: 99%

“…Inflammatory monocytes will also migrate to the subepithelial space in response to C. parvum infection and secrete TNFα and IL-1β [ 41 ]. These cytokines will increase permeability, therefore weakening the integrity of the intestinal epithelial barrier [ 41 ]. Also, nitric oxide NO is important in C. parvum infection clearance and reduces oocyst shedding in chronically infected nude mice [ 42 ].…”

Section: Innate Immunitymentioning

confidence: 99%

Lessons Learned from Protective Immune Responses to Optimize Vaccines against Cryptosporidiosis

2017

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In developing countries, cryptosporidiosis causes moderate-to-severe diarrhea and kills thousands of infants and toddlers annually. Drinking and recreational water contaminated with Cryptosporidium spp. oocysts has led to waterborne outbreaks in developed countries. A competent immune system is necessary to clear this parasitic infection. A better understanding of the immune responses required to prevent or limit infection by this protozoan parasite is the cornerstone of development of an effective vaccine. In this light, lessons learned from previously developed vaccines against Cryptosporidium spp. are at the foundation for development of better next-generation vaccines. In this review, we summarize the immune responses elicited by naturally and experimentally-induced Cryptosporidium spp. infection and by several experimental vaccines in various animal models. Our aim is to increase awareness about the immune responses that underlie protection against cryptosporidiosis and to encourage promotion of these immune responses as a key strategy for vaccine development. Innate and mucosal immunity will be addressed as well as adaptive immunity, with an emphasis on the balance between TH1/TH2 immune responses. Development of more effective vaccines against cryptosporidiosis is needed to prevent Cryptosporidium spp.-related deaths in infants and toddlers in developing countries.

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Cryptosporidium parvumincreases intestinal permeability through interaction with epithelial cells and IL-1β and TNFα released by inflammatory monocytes

Cited by 35 publications

References 45 publications

Interplay between gut microbiota and p66Shc affects obesity‐associated insulin resistance

Interplay between gut microbiota and p66Shc affects obesity‐associated insulin resistance

Association of enteric parasitic infections with intestinal inflammation and permeability in asymptomatic infants of São Tomé Island

Lessons Learned from Protective Immune Responses to Optimize Vaccines against Cryptosporidiosis

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