The protective role of endogenous cytokines in host resistance against an intragastric infection with Listeria monocytogenes in mice

Nishikawa, S

doi:10.1016/s0928-8244(96)00096-x

Cited by 13 publications

(16 citation statements)

References 13 publications

(21 reference statements)

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“…Hybridoma cell lines secreting mAbs against mouse IFN-Q (R4-6A2; IgG1), mouse TNF-K (MP6-XT22.11; rat IgG1), mouse IL-4 (11B11, rat IgG1), mouse IL-6 (MP5-20F3.11; rat IgG1) and mouse IL-10 (JES5-2A5, rat IgG1) were used [34]. The mAbs found in the ascites £uid were partially puri¢ed by (NH R ) P SO R precipitation.…”

Section: In Vivo Depletion Of Endogenous Cytokinesmentioning

confidence: 99%

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Nakane¹

1999

FEMS Microbiology Letters

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It has been demonstrated that endogenous cytokines including Q interferon (IFN-Q), tumour necrosis factor-K (TNF-K), and interleukin-6 (IL-6) play protective roles but that IL-4 and IL-10 play detrimental roles in nonlethal Listeria monocytogenes infection in mice. In this paper, we studied the roles of endogenous cytokines in a lethal infection with L. monocytogenes in mice. TNF-K and IL-6 titres in the bloodstreams, spleens and livers paralleled bacterial numbers in the organs, and both these cytokines and the bacterial numbers peaked just before the mice died. The high titres of TNF-K notably detected in the circulation in lethal infection were different from those in nonlethal infection. The maximum production of IFN-Q was observed before the peaks of TNF-K and IL-6, and IFN-Q almost disappeared from the bloodstreams and organs just before the mice died. No notable difference of IFN-Q titres between lethal infection and nonlethal infection in the specimens obtained from mice was observed. IL-10 was also detected in the bloodstreams earlier than the peaks of TNF-K and IL-6 during lethal infection, while IL-4 was never detected in the sera. The administration of monoclonal antibodies (mAbs) against TNF-K, IFN-Q, IL-6, IL-4 or IL-10 failed to rescue mice from lethal L. monocytogenes infection, whereas anti-TNF-K mAb and anti-IFN-Q mAb prevented mice from lethality by high-dose endotoxin shock. These results suggest that lethality in L. monocytogenes infection might not be determined solely by these cytokines. z

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Section: In Vivo Depletion Of Endogenous Cytokinesmentioning

confidence: 99%

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Nakane¹

1999

FEMS Microbiology Letters

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“…Third, cell proliferation and phorbol myristate acetate-and ionomycin-stimulated gamma interferon secretion by IELs from mdr1a Ϫ/Ϫ mice were actually greater (P Ͻ 0.05) than those by normal IELs. Because gamma interferon is essential for host response to L. monocytogenes, any cytokine changes in the present study would not be in a direction detrimental to host defense (19,20,23). Lastly, peripheral-T-cell proliferation, cytokine secretion, and cytotoxic function are unaffected by a lack of the mdr1a gene in mice (7).…”

Section: Discussionmentioning

confidence: 97%

“…Undoubtedly, there are numerous host defense mechanisms in place which interfere with the invasion of pathogenic bacteria such as L. monocytogenes (4,6,9,20). P glycoprotein appears to be one important protein at the epithelial level, most likely working in concert with these other factors to protect the host.…”

Section: Discussionmentioning

confidence: 99%

Intestinal P Glycoprotein Acts as a Natural Defense Mechanism against Listeria monocytogenes

et al. 2004

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Mechanisms by which the intestinal epithelium resists invasion by food-borne pathogens such as Listeria monocytogenes are an evolving area of research. Intestinal P glycoprotein is well known to limit the absorption of xenobiotics and is believed to act as a cytotoxic defense mechanism. The aim of this study was to determine if intestinal P glycoprotein is involved in host defense against L. monocytogenes. Caco-2 cells and a Pglycoprotein-overexpressing subclone (Caco-2/MDR) were employed in addition to mdr1a ؊/؊ mice and wildtype controls. In vitro invasion assays and in vivo experiments were employed to measure bacterial invasion and dissemination. In addition, L. monocytogenes proteins were labeled with [35 S]methionine, and the transepithelial transport across Caco-2 monolayers was characterized in both directions. Overexpression of P glycoprotein in Caco-2/MDR cells led to increased resistance to L. monocytogenes invasion, whereas P-glycoprotein inhibition led to increased invasion. Flux of [35 S]methionine-labeled L. monocytogenes proteins was significantly greater in the basolateral-to-apical direction than in the apical-to-basolateral direction, indicating dependence on an apically located efflux transporter. Moreover, inhibiting P glycoprotein reduced the basolateral-to-apical flux of the proteins. Early dissemination of L. monocytogenes from the gastrointestinal tract was significantly greater in the mdr1a ؊/؊ mice than in wild-type controls. Expression and function of intestinal P glycoprotein is an important determinant in resistance to early invasion of L. monocytogenes.P glycoprotein is the 170-kDa product of the human MDR1 gene and is arguably one of the most extensively studied members of the ATP-binding cassette superfamily of transport proteins (28). P glycoprotein is best known for its ability to transport drug substrates out of cells in a variety of tissues, including the intestine (1,12,27). Both the expression and the function of P glycoprotein have been linked to considerable variability in oral drug absorption; however, the precise physiological role of intestinal P glycoprotein is unknown. Because P glycoprotein is well conserved throughout evolution and has a broad substrate affinity, it is widely believed to act as a cytotoxic protection mechanism. Given its apical distribution on the enterocyte, P glycoprotein is exquisitely positioned to limit the absorption of substances that the cell perceives as harmful. Thus, it is conceivable that P glycoprotein restricts the absorption of other, nondrug substances in the intestine. Proteins facilitating invasion of pathogenic bacteria would be ideal candidates given the purported mechanism of action of P glycoprotein.Listeria monocytogenes is a food-borne pathogen responsible for considerable morbidity and mortality (11,24). Although multiple sites of invasion have been proposed, the vanguard of the body's interaction with L. monocytogenes is the intestinal epithelial barrier. Intestinal epithelial cells come in contact with not only the bacter...

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“…Some studies show that IL-10 could be detrimental to the infected host. In other studies, this cytokine has been shown to enhance resistance against infection [29][30][31]. Some strains of lactobacilli induce production of interleukin 10 (IL-10) and transforming growth factor (TGF-b) that modulate the immune responses [32,33].…”

mentioning

confidence: 99%

Monoassociation with probiotic Lactobacillus delbrueckii UFV-H2b20 stimulates the immune system and protects germfree mice against Listeria monocytogenes infection

Santos

Silva

et al. 2010

Med Microbiol Immunol

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In the present study, we investigated the protective effects of Lactobacillus delbrueckii UFV-H2b20 on the resistance to Listeria monocytogenes infection in gnotobiotic mice. Germfree mice or monoassociated mice were infected with L. monocytogenes, and the microbiological and immunological responses were evaluated after 1, 3, and 5 days of infection. Monoassociation with L. delbrueckii was capable of protecting mice against death caused by L. monocytogenes and induced a faster clearance of the bacteria in the liver, spleen, and peritoneal cavity at days 1, 3, and 5 post-infection. Also, monoassociated mice displayed less liver injury than germfree mice. The production of TNF-α in the serum, peritoneal cavity, and gut was augmented in monoassociated mice. Likewise, the levels of IFN-γ found on supernatants of spleen cells cultures were higher after the monoassociation. In addition, increased production of nitric oxide in peritoneal cell cultures supernatants and in serum was observed in mice that received L. delbrueckii. The monoassociation with L. delbrueckii induced higher production of IL-10 in the mucosal immune system. We conclude that monoassociation with L. delbrueckii UFV-H2b20 protects mice from death caused by L. monocytogenes infection by favoring effector responses while preventing their immunopathological consequences.

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The protective role of endogenous cytokines in host resistance against an intragastric infection with Listeria monocytogenes in mice

Cited by 13 publications

References 13 publications

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Intestinal P Glycoprotein Acts as a Natural Defense Mechanism against Listeria monocytogenes

Monoassociation with probiotic Lactobacillus delbrueckii UFV-H2b20 stimulates the immune system and protects germfree mice against Listeria monocytogenes infection

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