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At least 91 records · Page 5Linked to original sources
PubMed1998

Nonspecific early protective immunity in Francisella and Listeria infections can be dependent on lymphocytes.

Normal mice, but not lymphocyte-deficient or B-cell-deficient mice, given a sublethal infection of Francisella tularensis LVS survive a secondary lethal challenge of more than 10,000 50% lethal doses given 3 days later. In this work, we show that similar early protection that is also strongly lymphocyte dependent operates in Listeria monocytogenes infection. Since sublethal infection with either LVS or L. monocytogenes protects against heterologous lethal challenge, this early protection is nonspecific.

Animals↗
PubMed1995

Live tularemia vaccine but not proteins purified from Francisella tularensis can confer protection against lethal Listeria infection in mice.

Immunization of Balb/c mice with Francisella tularensis vaccine strain 15/10 conferred significant protection against subsequent listerial infection. Since immunostimulatory activities could apparently be relevant to surface components of the bacterium, a technique for purification of cell wall proteins was developed. The scheme designed consisted of Triton X-100 extraction with subsequent FPLC chromatography steps, and resulted in the isolation of homogeneous proteins with molecular masses of 54 kDa (pI = 6.7) and 82 kDa (pI = 5.3), and partially purified 50, 85 and 100 kDa components. It was shown that immunization with isolated proteins failed to protect mice against lethal Listeria monocytogenes infection. Possible reasons for failure are discussed.

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PubMed1986

Vaccination against Listeria infection in mice with a mutant strain of reduced virulence.

Killed Listeria monocytogenes (L.m.) or living Listeria innocua, being unable to afford noticeable immunity against L.m. challenge in mice, the efficacy of a living strain of L.m. of reduced virulence was studied. This strain was obtained from a field strain of low virulence by successive mutations for streptomycin dependence, reversion to independence and resistance to erythromycin. Its protective immunity was checked in mice against IV, SC and intra-gastric challenges. Vaccinated mice were protected against a IV challenge, lethal for controls, and they were rid of infection in a much shorter time than controls after SC or intra-gastric challenges. They were also protected against abortion when the challenge was done by SC, but not by IV route. The level of immunity was shown to be dose-dependent. Appearing very early after vaccination, immunity remained stable for at least four months, then decreased slowly afterwards, but could be restored and even enhanced by a recall. The protection was equally effective against L.m. serovars 1 or 4 challenges.

Animals↗
PubMed1988

T-cell subsets in delayed-type hypersensitivity, protection, and granuloma formation in primary and secondary Listeria infection in mice: superior role of Lyt-2+ cells in acquired immunity.

Immunity to Listeria monocytogenes was studied in mice treated with rat monoclonal antibodies (MAbs) specific for the Thy-1.2, L3T4, and Lyt-2 T-cell markers. Three characteristic T-cell-mediated phenomena were investigated. Delayed-type hypersensitivity (DTH) to listerial antigen was totally abolished in mice treated with anti-Thy-1.2 or anti-L3T4 MAbs, whereas anti-Lyt-2 MAb treatment had no effect, regardless of whether the MAb was given during the induction or the expression of DTH. On the other hand, the elimination of bacteria from the spleens of infected animals was inhibited only by the application of either anti-Thy-1.2 MAb or anti-Lyt-2 MAb. This could be shown most impressively during the secondary infection of immune mice with a normally lethal dose of listeriae. In this situation, treatment with anti-Lyt-2 MAb sufficed to completely abolish immunologic memory, whereas anti-L3T4 MAb had only a marginal effect on antibacterial protection. However, the accelerated development of mononuclear cell foci in the livers of immune mice was inhibited by the application of both anti-L3T4 MAb and anti-Lyt-2 MAb. It is concluded that in murine listeriosis, DTH and acquired immunity to reinfection are dissociable phenomena. Although DTH is a function of L3T4+ T lymphocytes, Lyt-2+ T cells are necessary and sufficient for the expression of acquired resistance to L. monocytogenes. The roles of the different T-cell subsets in granuloma formation warrant further investigation.

Animals↗
PubMed1974

Effects of antithymocyte sera and antimacrophage sera on cell-mediated immune reactions in Listeria-infected mice.

The cell-mediated immune responses of allograft rejection, delayed hypersensitivity, and resistance to Listeria monocytogenes were suppressed by injections of antithymocyte serum (ATS), but the immune responses were not significantly altered by antimacrophage serum (AMS) or normal rabbit serum (NRS). Antisera were prepared in rabbits against purified mouse thymocytes and purified peritoneal macrophages. When mice were injected with ATS near the time of skin grafting, allografts survived significantly longer. Similar administration of AMS or NRS failed to alter the course of graft rejection. Decreased footpad swelling indicated the suppression of delayed hypersensitivity in mice injected with ATS 6 days after a sublethal inoculation of Listeria cells. None of the serum treatments affected the ultimate survival of mice infected with a small number of bacteria. Either ATS or NRS was injected into immunized mice 1 day before and 2 days after a challenge inoculation of Listeria cells. Pronounced suppression of delayed hypersensitivity was found in the ATS-treated groups, along with extensive mortalities that reached 100% in the group receiving the largest dose of ATS. All control animals survived and demonstrated strong delayed hypersensitivity reactions. Antimacrophage serum had no significant effect on the three mechanisms of cell-mediated immunity that were tested. The lymphoid cells which mediate delayed hypersensitivity, antimicrobial cellular immunity, and allograft rejection possess antigenic determinants in common with thymocytes.

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PubMed2004

Roles of caspase-1 in Listeria infection in mice.

Caspase-1 [IL-1beta-converting enzyme (ICE)] processes substrate precursor molecules to yield the biologically active form of IL-1beta and IL-18, both of which are considered to play important roles in the host defense by activation of both innate and adaptive immunity. We evaluated the immune response of caspase-1(-/-) mice to Listeria monocytogenes (LM) infection. LM eradication in the early phase of infection was impaired in the mutant mice with a prominent decrease in IL-18 and IFN-gamma production, but not in IL-12. Caspase-1(-/-) spleen cells including dendritic cells and NK cells produced less IFN-gamma in response to heat-killed LM than wild-type cells in vitro. IFN-gamma production and bactericidal activity in LM-infected caspase-1(-/-) mice was reconstituted to normal levels by adding back IL-18 at the initial phase of infection, suggesting that the lack of this cytokine is primarily responsible for the susceptibility of caspase-1(-/-) mice against LM infection. Moreover, IFN-gamma injection of caspase-1(-/-) mice corrected the deficiency in pathogen clearance. In contrast, LM-specific acquired immunity in caspase-1(-/-) mice was normal and they successfully cleared the pathogen following secondary infection, in spite of a moderate skewing of cytokine profile to T(h)2 when compared to wild-type mice. These data shed light on the importance of caspase-1-mediated IL-18 processing in innate immunity against facultative intracellular pathogens.

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PubMed2005

Membrane tumor necrosis factor confers partial protection to Listeria infection.

Tumor necrosis factor (TNF) plays a critical role in the host response to the intracellular pathogen Listeria monocytogenes (LM). TNF exists in soluble and membrane-bound forms and exhibits both unique and overlapping activities. We examined the role of membrane TNF in the absence of secreted TNF for host resistance in knockin mice in which the endogenous TNF was replaced by a regulated, noncleavable allele (mem-TNF). Macrophages expressing mem-TNF produced nitric oxide and displayed normal bactericidal activity. Although mice completely deficient in TNF (TNF(-/-)) succumbed to LM infection within 4 days, mem-TNF mice controlled LM infection at a low dose (10(4) CFU) but succumbed at a higher dose of infection (10(5) CFU). In contrast to complete TNF deficiency, mem-TNF mice developed confined microabscesses that expressed inducible nitric oxide synthase. The transfer of lymphocytes from immunized mem-TNF, but not TNF(-/-), mice protected TNF(-/-) mice from fatal infection. Taken together the data suggest that in the absence of soluble TNF, the presence of membrane-expressed TNF on phagocytes and lymphocytes partially restores host defense to LM infection.

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PubMed1995

Secondary response to Listeria infection requires IFN-gamma but is partially independent of IL-12.

During a secondary immune response to Listeria monocytogenes (LM), the production of IFN-gamma was still required for resistance, but it was considerably less dependent on IL-12 production. When IL-12 was neutralized in vivo using specific hamster antimurine IL-12 mAbs, there was a dramatically increased susceptibility to infection during primary listeriosis but much less during a secondary infection. However, neutralization of IFN-gamma in vivo resulted in a similar increased susceptibility during both primary and secondary listeriosis. In culture, splenocytes isolated from unimmunized mice produced IFN-gamma in response to heat-killed L. monocytogenes (hk-LM) that was absolutely dependent upon IL-12 production. However, directly stimulating the TCR with anti-CD3-epsilon mAbs resulted in IFN-gamma production that was unaffected by neutralizing IL-12 in vitro. In contrast, splenocytes isolated from LM-immune mice produced IFN-gamma in response to hk-LM, part of which was independent on IL-12 production. However, anti-CD3-epsilon Ab-stimulated IFN-gamma production remained independent of IL-12 production. The source of hk-LM-induced, IL-12-independent IFN-gamma production was the T cell because anti-Thy1.2 Ab plus complement treatment in vitro completely abolished it. Together, these data support a model of memory T cells being produced during the primary infection with LM that can be stimulated to produce IFN-gamma during the secondary response to LM, partially independent of macrophage IL-12 production.

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