<i>Mycobacterium avium</i>subspecies<i>paratuberculosis</i>infects and multiplies in enteric glial cells

Sechi, Leonardo Antonio; Ruehl, Anne; Ahmed, Niyaz; Usai, Donatella; Paccagnini, Daniela; Felis, Giovanna E.; Zanetti, Stefania Anna Lucia

doi:10.3748/wjg.v13.i43.5731

Cited by 11 publications

(6 citation statements)

References 31 publications

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“…A number of gastrointestinal hormones appear to affect intestinal motility [65]. Interestingly, it was shown earlier that the enteric nervous system is involved in inflammatory bowel disease in which MAP is associated [66], [67]. In cattle and sheep with Johne's disease, myenteric ganglionitis with cellular infiltration occurs [68].…”

Section: Discussionmentioning

confidence: 99%

Systems Biology Analysis of Gene Expression during In Vivo Mycobacterium avium paratuberculosis Enteric Colonization Reveals Role for Immune Tolerance

et al. 2012

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Survival and persistence of Mycobacterium avium subsp. paratuberculosis (MAP) in the intestinal mucosa is associated with host immune tolerance. However, the initial events during MAP interaction with its host that lead to pathogen survival, granulomatous inflammation, and clinical disease progression are poorly defined. We hypothesize that immune tolerance is initiated upon initial contact of MAP with the intestinal Peyer's patch. To test our hypothesis, ligated ileal loops in neonatal calves were infected with MAP. Intestinal tissue RNAs were collected (0.5, 1, 2, 4, 8 and 12 hrs post-infection), processed, and hybridized to bovine gene expression microarrays. By comparing the gene transcription responses of calves infected with the MAP, informative complex patterns of expression were clearly visible. To interpret these complex data, changes in the gene expression were further analyzed by dynamic Bayesian analysis, and genes were grouped into the specific pathways and gene ontology categories to create a holistic model. This model revealed three different phases of responses: i) early (30 min and 1 hr post-infection), ii) intermediate (2, 4 and 8 hrs post-infection), and iii) late (12 hrs post-infection). We describe here the data that include expression profiles for perturbed pathways, as well as, mechanistic genes (genes predicted to have regulatory influence) that are associated with immune tolerance. In the Early Phase of MAP infection, multiple pathways were initiated in response to MAP invasion via receptor mediated endocytosis and changes in intestinal permeability. During the Intermediate Phase, perturbed pathways involved the inflammatory responses, cytokine-cytokine receptor interaction, and cell-cell signaling. During the Late Phase of infection, gene responses associated with immune tolerance were initiated at the level of T-cell signaling. Our study provides evidence that MAP infection resulted in differentially regulated genes, perturbed pathways and specifically modified mechanistic genes contributing to the colonization of Peyer's patch.

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Section: Discussionmentioning

confidence: 99%

Systems Biology Analysis of Gene Expression during In Vivo Mycobacterium avium paratuberculosis Enteric Colonization Reveals Role for Immune Tolerance

et al. 2012

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“…This loss of EGC remains at present unexplained. Selective loss of these cells in experimental animal models has been attributed to specific gliotoxins, 56 to infectious causes, 57–60 and by alterations of the enteric environment, 61 but these causes are difficult to document in patients. Moreover, there is the possibility of a loss due to congenital abnormalities, and in this respect the increase in ICC (that develops in the gut at approximately the same time 62 ) could represent a compensatory mechanism for enteric neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

An assessment of enteric nervous system and estroprogestinic receptors in obstructed defecation associated with rectal intussusception

Bassotti

Villanacci

Bellomi

et al. 2011

Neurogastroenterology Motil

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“…Associations have been found with leprosy [42], tuberculosis [43], rheumatoid arthritis [44], visceral leishmaniasis [45], multiple sclerosis [46,47], inflammatory bowel disease [48][49][50], and type 1 diabetes mellitus [51,52]. (type 1) patients but not non-autoimmune (type 2) diabetics [54][55][56]. Sechi also found an association of polymorphisms of the SLC11a1 gene and MAP in T1DM patients [51].…”

Section: Slc11a1 In Infectious and Autoimmune Diseasementioning

confidence: 99%

Mycobacterium avium subspecies paratuberculosis—An environmental trigger of type 1 diabetes mellitus

Dow¹

2012

JDM

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Type 1 diabetes mellitus (T1DM) is an autoimmune disease. The etiology of T1DM is incompletely understood but environmental agent(s) are thought to trigger T1DM in the genetically at-risk. Humans are widely exposed to Mycobacterium avium subspecies paratuberculosis (MAP), a proven multi-host chronic enteric pathogen that is mostly studied in ruminant animals and causes the inflammatory disease paratuberculosis or Johne's disease. In humans, MAP is the putative cause of Crohn's disease and has been linked to sarcoidosis, autoimmune thyroiditis, multiple sclerosis and autoimmune diabetes. The role of MAP as a trigger for T1DM was first postulated in 2005; subsequent studies suggest a link. This article discusses MAP, human exposure to MAP, genetic susceptibility to MAP and MAP in human disease including T1DM.

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Mycobacterium aviumsubspeciesparatuberculosisinfects and multiplies in enteric glial cells

Cited by 11 publications

References 31 publications

Systems Biology Analysis of Gene Expression during In Vivo Mycobacterium avium paratuberculosis Enteric Colonization Reveals Role for Immune Tolerance

Systems Biology Analysis of Gene Expression during In Vivo Mycobacterium avium paratuberculosis Enteric Colonization Reveals Role for Immune Tolerance

An assessment of enteric nervous system and estroprogestinic receptors in obstructed defecation associated with rectal intussusception

Mycobacterium avium subspecies paratuberculosis—An environmental trigger of type 1 diabetes mellitus

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