Systemic Dissemination by Intrarectal Infection with <i>Listeria monocytogenes</i> in Mice

Nishikawa, S.; Hirasue, Mayuko; Miura, Tomisato; Yamada, Kyogo; Sasaki, Sanae; Nakane, Akio

doi:10.1111/j.1348-0421.1998.tb02290.x

Cited by 15 publications

(19 citation statements)

References 15 publications

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“…This range is comparable to previously reported doses used in animal models of oral listeria infection (17,24,26). Viability and the exact number of L. monocytogenes cells in the inocula were determined by plating on PALCAM.…”

Section: Methodssupporting

confidence: 74%

“…To study the efficacy of food components, an animal model of food-derived listeriosis with a quantitative, reliable, and accurate biomarker for translocation is required. Translocation of L. monocytogenes is observed in rats (24,28) and mice (26), making them suitable models. Classically, translocation of listeria in animal models is determined by microbiological culturing of lymphoid organs (24,26,28).…”

mentioning

confidence: 99%

“…Our laboratory has previously shown that urinary nitrate and nitrite (summed as NO x ), which reflects the production of nitric oxide (NO) by phagocytic cells (15), is a quantitative biomarker of salmonella translocation and is useful in studying the efficacy of functional food components on salmonella infection (5,6,27). Upon translocation, L. monocytogenes infects mesenteric lymph nodes (MLNs), spleen, and liver (24,26,28), resulting in infiltration of neutrophils and monocytes (7). These leukocytes, together with hepatocytes, Kupffer cells, and splenic macrophages, are able to induce NO synthase (12,22,23,25,33).…”

mentioning

confidence: 99%

“…Translocation of L. monocytogenes is observed in rats (24, 28) and mice (26), making them suitable models. Classically, translocation of listeria in animal models is determined by microbiological culturing of lymphoid organs (24,26,28). This approach has some disadvantages.…”

mentioning

confidence: 99%

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Quantifying Translocation ofListeria monocytogenesin Rats by Using Urinary Nitric Oxide-Derived Metabolites

Sprong

Hulstein

Meer

2000

Appl Environ Microbiol

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The urinary nitric oxide metabolites NO 2 ؊ and NO 3 ؊ (summed as NO x ) are a noninvasive, quantitative biomarker of translocation of salmonella from the intestinal lumen to systemic organs. Listeria monocytogenes is a food-borne gram-positive pathogen that can also cross the intestinal epithelium. In this study, we tested the efficacy of urinary NO x as a marker of listeria translocation. Rats (eight per group) were orally infected with increasing doses of L. monocytogenes; control rats received heat-killed listeria. The kinetics of urinary NO x and population levels of listeria in feces were determined for 7 days. Another group of rats was killed 1 day after infection to verify translocation by culturing viable listeria from systemic organs. Oral administration of increasing doses of L. monocytogenes resulted in a time-and dose-dependent increase in urinary NO x excretion. Translocation was a prerequisite for inducing a NO x response, since heat-killed L. monocytogenes did not elevate NO x excretion in urine. Fecal counts of listeria also showed dose and time dependency. Moreover, the number of viable L. monocytogenes cells in mesenteric lymph nodes also increased in a dose-dependent manner and correlated with urinary NO x . In conclusion, urinary NO x is a quantitative, noninvasive biomarker of listeria translocation.Listeria monocytogenes is a food-borne gram-positive pathogen that is able to translocate across the gut epithelium, resulting in listeriosis, i.e., systemic infection. Most healthy adults experience a limited infection, with at most mild influenza-like symptoms or, in some cases, gastroenteritis (2, 13, 30). However, listeriosis is extremely dangerous for pregnant women, causing abortions and stillbirths, and for newborn, elderly, and immunocompromised individuals, causing meningitis, meningoencephalitis, or sepsis (13,14,18,21,30). In Europe, the incidence of listeriosis is increasing (2, 14). The rate of mortality caused by listeriosis, excluding abortions, is one of the highest among bacterial infections. Overall fatality rates of 24 to 44% have been reported (2,14,18,21). Because of the property of pathogens to acquire resistance to antibiotics, new approaches to prevent listeriosis deserve attention. Luminal factors such as gastric acidity, antimicrobial bile salts and fatty acids, and pancreatic enzymes contribute to the intestinal nonspecific defenses by killing pathogens. Therefore, changing the composition of the diet and thus changing the composition of gastrointestinal contents may affect colonization and translocation of L. monocytogenes. To study the efficacy of food components, an animal model of food-derived listeriosis with a quantitative, reliable, and accurate biomarker for translocation is required. Translocation of L. monocytogenes is observed in rats (24, 28) and mice (26), making them suitable models. Classically, translocation of listeria in animal models is determined by microbiological culturing of lymphoid organs (24,26,28). This approach has some disadvantages. First,...

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Section: Methodssupporting

confidence: 74%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Quantifying Translocation ofListeria monocytogenesin Rats by Using Urinary Nitric Oxide-Derived Metabolites

Sprong

Hulstein

Meer

2000

Appl Environ Microbiol

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“…2). Similarly, our previous study showed that bacterial growth in livers and spleens began on day 2 when L. monocytogenes infection was induced by an oral route (23,25). These results suggest that L. monocytogenes can finally result in systemic infection irrespective of routes of invasion.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Host Resistance to Primary and SecondaryListeria monocytogenesInfections in Mice by Intranasal and Intravenous Routes

et al. 2002

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There have been no studies on the susceptibility and host immune responses to an intranasal infection with Listeria monocytogenes. In this study, we compared the susceptibilities and cytokine responses between intranasal and intravenous infections with L. monocytogenes in mice. Moreover, we compared efficiency of acquisition of host resistance to L. monocytogenes infection between intranasally and intravenously immunized mice because an intranasal immunization of vaccines is reportedly available for induction of adaptive immunity against various infectious pathogens. The susceptibility to an intranasal infection with L. monocytogenes was markedly lower than that to the intravenous infection. The bacterial growth in the lungs, spleens, and livers was substantially similar between intranasally and intravenously infected mice. Titers of endogenous gamma interferon (IFN-␥) and tumor necrosis factor-␣ (TNF-␣) in the spleens, livers, and lungs were parallel to bacterial numbers in each organ of mice during intranasal infection and intravenous infection. IFN-␥-deficient mice and TNF-␣-deficient mice were highly susceptible to intranasal infection as well as intravenous infection.Susceptibilities to intranasal and intravenous L. monocytogenes infection were the same in these cytokinedeficient mice. These results suggest that both IFN-␥ and TNF-␣ play critical roles in host resistance to intranasal L. monocytogenes infection as well as the intravenous infection. Acquisition of host resistance to intravenous and intranasal L. monocytogenes infection was induced in intranasally immunized mice as well as intravenously immunized mice, suggesting that intranasal immunization is effective for prevention of a systemic infection with L. monocytogenes.

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A Listeria adhesion protein-deficient Listeria monocytogenes strain shows reduced adhesion primarily to intestinal cell lines

Jaradat

Wampler

Bhunia

2003

Med Microbiol Immunol

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Listeria monocytogenes adheres and penetrates intestinal cell linings for systemic infection. A 104-kDaListeria adhesion protein (LAP) from L. monocytogenes was previously demonstrated to be responsible for adhesion to intestinal enterocyte-like Caco-2 cells. We investigated the adhesion and invasion characteristics of a LAP-deficient mutant L. monocytogenes strain (A572) to various human intestinal and non-intestinal cell lines to assess the possible target host cells. Among the intestinal cell lines, A572 showed significantly reduced adhesion than the wild type (WT) strain to the cells of ileumcecum (HCT-8) and colon (Caco-2 and HT-29), whereas A572 and WT did not show any significant differences in adhesion to other intestinal cell lines from duodenum (HuTu-80) or jejunum (Int-407). Differences in adhesion between A572 and WT were little or none in nonintestinal cell lines from liver, kidney, bladder, ovary, cervix, breast, larynx, or skin. Invasion data showed that A572 was invasive but the invasion efficiency was proportional to its adhesion characteristics to respective cell lines. In mouse bioassay, A572 was not found in liver following oral administration, suggesting that LAP mutant was possibly unable to pass through intestinal cell linings. Immuno-electron microscopy revealed that the LAP is localized in the bacterial surface as well as the cytoplasm. In summary, this study indicated that the LAP-mediated adhesion is associated with the intestinal cells originating from the lower part of small intestine and from the upper part of large intestine, and possibly plays an important role during the intestinal phase of infection.

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Systemic Dissemination by Intrarectal Infection with Listeria monocytogenes in Mice

Cited by 15 publications

References 15 publications

Quantifying Translocation ofListeria monocytogenesin Rats by Using Urinary Nitric Oxide-Derived Metabolites

Quantifying Translocation ofListeria monocytogenesin Rats by Using Urinary Nitric Oxide-Derived Metabolites

Comparison of Host Resistance to Primary and SecondaryListeria monocytogenesInfections in Mice by Intranasal and Intravenous Routes

A Listeria adhesion protein-deficient Listeria monocytogenes strain shows reduced adhesion primarily to intestinal cell lines

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