Mucin isolated from rabbit colon inhibits in vitro binding of Escherichia coli RDEC-1

Mack, David R.; Sherman, Philip M.

doi:10.1128/iai.59.3.1015-1023.1991

Cited by 30 publications

(17 citation statements)

References 36 publications

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“…Interestingly, MUC2 protein expression is mediated through PGE 1 and PGE 2 (Willemsen et al, 2003), and moreover, PGE 2 was shown to enhance mucin release via a cAMP-dependent mechanism (Belley and Chadee, 1999). Bacteria were also shown to induce MUC2 transcription mainly via production of NF-kappaB and various cytokines (Deplancke and Gaskins, 2001;Dohrman et al, 1998;Mack and Sherman, 1991). Among the many (pro-inflammatory) cytokines that stimulate mucin gene expression are IL-1, IL-4, IL-6, IL-9, and tumor necrosis factor alpha (TNF-alpha) (Deplancke and Gaskins, 2001;Van Seuningen et al, 2001 and references therein).…”

Section: Discussionmentioning

confidence: 99%

Homeostasis and function of goblet cells during rotavirus infection in mice

et al. 2005

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Rotaviruses are the leading cause of severe viral gastroenteritis in young children. To gain insight in goblet cell homeostasis and intestinal mucin expression during rotavirus infection, 6-day-old mice were inoculated with murine rotavirus. To determine epithelial cell migration, mice were injected with BrdU just before inoculation. Small intestines were isolated at different days postinfection (dpi) and evaluated for rotavirus and goblet cell-specific gene expression. Small intestinal mucins of control and infected animals at 1, 2, and 4 dpi were isolated and tested for their capability to neutralize rotavirus infection in vitro. After inoculation, two peaks of viral replication were observed at 1 and 4 dpi. During infection, the number of goblet cells in infected mice was decreased in duodenum and jejunum, but was unaffected in the ileum. Goblet cells in infected animals accumulated at the tips of the villi. Muc2 mRNA levels were increased during the peak of viral replication at 1 dpi, whereas at other time points Muc2 and Tff3 mRNA levels were maintained at control levels. Muc2 protein levels in the tissue were also maintained, however Tff3 protein levels were strongly decreased. The number of goblet cells containing sulfated mucins was reduced during the two peaks of infection. Mucins isolated at 1 and 2 dpi from control and infected mice efficiently neutralized rotavirus infection in vitro. Moreover, mucins isolated from infected mice at 4 dpi were more potent in inhibiting rotavirus infection than mucins from control mice at 4 dpi. In conclusion, these data show that during rotavirus infection, goblet cells, in contrast to enterocytes, are relatively spared from apoptosis especially in the ileum. Goblet cell-specific Muc2 expression is increased and mucin structure is modified in the course of infection. This suggests that goblet cells and mucins play a role in the active defense against rotavirus infection and that age-dependent differences in mucin quantities, composition, and/or structure alter the anti-viral capabilities of small intestinal mucins.

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Section: Discussionmentioning

confidence: 99%

Homeostasis and function of goblet cells during rotavirus infection in mice

et al. 2005

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“…Organisms colonizing mucosal epithelia in vivo are immersed in mucosal fluids. In this milieu, they are surrounded by high concentrations of nucleic acids, lipids and soluble glycoproteins, including both proteoglycans and CD66 family members (Moghissi, 1973; Krause, 1980; Asseo et al ., 1986; Neutra and Forstner, 1987; Fujii et al ., 1988; Nanbu et al ., 1988; Briese et al ., 1989; Mack and Sherman, 1991; Tabak, 1995; Widdicombe, 1995). In addition, the female reproductive tract is periodically washed with menstrual blood and tissue debris.…”

Section: Discussionmentioning

confidence: 99%

“…Because numerous such components are present at high concentrations, they would be expected to compete with, and therefore inhibit, Opa‐mediated binding to receptors on host cells (van Putten et al ., 1997). Indeed, a major function attributed to mucus is inhibition of microbial adhesion by soluble decoys that compete with or block adhesin–receptor interactions (Neutra and Forstner, 1987; Mack and Sherman, 1991; Tabak, 1995; Widdicombe, 1995). For example, low concentrations (1–10 μg ml −1 ) of DNA or heparin substantially inhibit adhesion or invasion by P − GC (Swanson, 1992b; Chen et al ., 1995; van Putten and Paul, 1995; van Putten et al ., 1997).…”

Section: Discussionmentioning

confidence: 99%

Type IV pili of pathogenic Neisseriae elicit cortical plaque formation in epithelial cells

Merz¹,

Enns

So³

1999

Molecular Microbiology

174

210

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SummaryThe pathogenic Neisseriae Neisseria meningitidis and Neisseria gonorrhoeae, initiate colonization by attaching to host cells using type IV pili. Subsequent adhesive interactions are mediated through the binding of other bacterial adhesins, in particular the Opa family of outer membrane proteins. Here, we have shown that pilus-mediated adhesion to host cells by either meningococci or gonococci triggers the rapid, localized formation of dramatic cortical plaques in host epithelial cells. Cortical plaques are enriched in both components of the cortical cytoskeleton and a subset of integral membrane proteins. These include: CD44v3, a heparan sulphate proteoglycan that may serve as an Opa receptor; EGFR, a receptor tyrosine kinase; CD44 and ICAM-1, adhesion molecules known to mediate inflammatory responses; f-actin; and ezrin, a component that tethers membrane components to the actin cytoskeleton. Genetic analyses reveal that cortical plaque formation is highly adhesin specific. Both pilE and pilC null mutants fail to induce cortical plaques, indicating that neisserial type IV pili are required for cortical plaque induction. Mutations in pilT, a gene required for pilus-mediated twitching motility, confer a partial defect in cortical plaque formation. In contrast to type IV pili, many other neisserial surface structures are not involved in cortical plaque induction, including Opa, Opc, glycolipid GgO 4 -binding adhesins, polysialic acid capsule or a particular lipooligosaccharide variant. Furthermore, it is shown that type IV pili allow gonococci to overcome the inhibitory effect of heparin, a soluble receptor analogue, on gonococcal invasion of Chang and A431 epithelial cells. These and other observations strongly suggest that type IV pili play an active role in initiating neisserial infection of the mucosal surface in vivo. The functions of type IV pili and other neisserial adhesins are discussed in the specific context of the mucosal microenvironment, and a multistep model for neisserial colonization of mucosal epithelia is proposed.

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“…The mucous secreted by epithelial cells is the first layer of mucosal defense and consists of a combination of immunoglobulin A (IgA), antimicrobial peptides, and a complex mixture of glycosylated proteins that are coded for by several genes. The various glycoproteins in mucous are capable of binding pathogens, preventing them from adhering to the epithelium (Mack & Sherman, 1991), can inhibit replication of some viruses (Yolken et al 1994), and may provide a nutrient source to LAB and other commensal bacteria. It is not surprising that disruption of mucous secretion is associated with inflammatory bowel disease (Shirazi et al 2000).…”

Section: Defense Mechanisms Of the Gastrointestinal Tractmentioning

confidence: 99%

Non–digestible oligosaccharides and defense functions: lessons learned from animal models

et al. 2002

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Animals are constantly exposed to a diversity of health challenges and the gastrointestinal tract (GIT) is a major, if not the principal, site of exposure. Animal models and a limited number of human clinical studies have shown that the assemblages and metabolic activities of the resident bacteria are important determinants of the effectiveness of the various host defense mechanisms and thereby influence the ability of animals to respond to health challenges. The assemblages of bacteria resident in the GIT provide a first line of defense that can exclude invading pathogens, reduce the proliferation of opportunistic pathogens already resident in the GIT, and reduce the availability, carcinogenicity, or toxicity of noxious chemicals. The mucosa of the GIT is a second, multilayered line of defense that includes the mucous and other secretions, the epithelial cells, and immune-associated cells scattered within and under the epithelium. The final line of defense contends with pathogens or noxious chemicals that transcend the mucosal barrier and enter the host and consists of the innate and acquired components of the systemic immune system and the xenobiotic metabolizing enzymes. The lactic acid producing bacteria (LAB) are considered to be immunomodulatory and directly or indirectly influence the GIT and systemic defense functions. Corresponding with this, supplementing the diet with inulin, oligofructose, or other nondigestible oligosaccharides that increase the densities and metabolic capacities of the LAB enhances defense mechanisms of the host, increases resistance to various health challenges, and accelerates recovery of the GIT after disturbances. b-fructans: Inulin: Oligofructose: Oligosaccharides: Immune: Lactic acid bacteria:Gastrointestinal tract

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Mucin isolated from rabbit colon inhibits in vitro binding of Escherichia coli RDEC-1

Cited by 30 publications

References 36 publications

Homeostasis and function of goblet cells during rotavirus infection in mice

Homeostasis and function of goblet cells during rotavirus infection in mice

Type IV pili of pathogenic Neisseriae elicit cortical plaque formation in epithelial cells

Non–digestible oligosaccharides and defense functions: lessons learned from animal models

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