Natural killer cells mediate protection induced by a Salmonella aroA mutant

Schafer, Rosana; Eisenstein, Toby K.

doi:10.1128/iai.60.3.791-797.1992

Cited by 54 publications

(25 citation statements)

References 22 publications

(36 reference statements)

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“…sponses are not involved. Since other bacterial particles such as HK C. parvum, but not 1.1-m latex beads, also induced comparable levels of IFN-␥, these responses might be common with microbial particulate components (30,44). Taken together, the capacities of particles to prime alveolar M in vivo closely parallel the responses of our in vitro cell system.…”

Section: Discussionsupporting

confidence: 59%

Alveolar macrophage priming by intravenous administration of chitin particles, polymers of N-acetyl-D-glucosamine, in mice

et al. 1997

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Intravenous (i.v.) administration of phagocytosable chitin particles (1 to 10 m) in C57BL/6 mice and SCID mice primed alveolar macrophages (M) within 3 days to yield up to a 50-fold increase in their oxidative burst when elicited in vitro with phorbol myristate acetate (PMA). C57BL/6 mice pretreated with monoclonal antibodies (MAbs) against mouse gamma interferon (IFN-␥) or NK1.1 showed a markedly decreased level of alveolar M priming following injection of chitin particles. To confirm IFN-␥ production in vitro, spleen cells isolated from normal C57BL/6 mice and SCID mice were cultured with chitin particles. Significant IFN-␥ production was observed following stimulation with chitin but not with chitosan or latex beads. When spleen cells were treated with anti-NK1.1 MAb, IFN-␥ production was significantly inhibited. Another set of experiments showed that when C57BL/6 mice were pretreated i.v. with a small dose IFN-␥, a higher level of priming was induced with not only phagocytosable chitin particles but also phagocytosable chitosan and even latex beads. Likewise, the spleen cell cultures preconditioned with IFN-␥ provided an up-regulation of IFN-␥ production by these phagocytosable particles. Taken together, the in vivo and in vitro results suggest that (i) the alveolar M priming mechanism is due, at least in part, to direct activation of M by IFN-␥, which is produced by NK1.1 ؉ CD4 ؊ cells; (ii) IFN-␥ would have an autocrine-like effect on M and make them more responsive to particle priming; and (iii) phagocytosis of particulates, probably by a postmembrane event such as interiorization, appears to be important for the up-regulation of alveolar M priming and IFN-␥ production.

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Section: Discussionsupporting

confidence: 59%

Alveolar macrophage priming by intravenous administration of chitin particles, polymers of N-acetyl-D-glucosamine, in mice

et al. 1997

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“…During the initial stages of infection, cell wall components of Salmonella such as lipopolysaccharide (LPS) and certain lipoproteins induce a massive inflammatory response in the surrounding tissue, resulting in the expression of inflammatory cytokines [e.g., TNF-␣, interleukin (IL)-1, IL-6, IL-12, and IL-18] and a variety of chemokines that recruit cells of the immune system to these sites [26][27][28][29]. IFN-␥ is also produced during early infection, with natural killer (NK) cells being an important source during this stage [30,31]. Additional potential sources for IFN-␥ are macrophages, B cells, and specialized T cell populations, such as NK T cells, that are able to recognize conserved structural patterns of bacteria [32][33][34].…”

Section: The Immune Response To Salmonellamentioning

confidence: 99%

Immune response to infection with Salmonella typhimurium in mice

Mittrücker

Kaufmann

2000

Journal of Leukocyte Biology

254

213

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Infection of mice with Salmonella typhimurium results in systemic infection and a disease similar to that seen in humans after infection with S. typhi. The innate immune system can restrict replication of S. typhimurium to a certain degree, but for effective control and eradication of bacteria, acquired immunity is essential. Salmonella infection induces the generation of specific CD4 ؉ and CD8 ؉ T cells, and both T cell populations are important for protection during primary and secondary responses, although the mechanisms underlying T cell-mediated protection are not yet completely understood. Infection with S. typhimurium also results in a strong antibody response to Salmonella antigens and, in contrast to most other intracellular bacteria, this antibody response participates in protection. In summary, the response to S. typhimurium involves both T and B cell-mediated immunity, and mechanisms mediated by both lymphocyte populations are important for control of primary infection and protection against secondary infection.

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“…Several studies have demonstrated the importance of the innate immune response in limiting bacterial multiplication and thereby controlling infection, ascribing impor-tant roles for macrophages and natural killer cells in the acute phase of the infection. [50][51][52] Macrophages are the host cells for Salmonella and also initiate the innate immune response to pathogens by producing pro-inflammatory cytokines, such as IL-12 and TNF-a. Interleukin-12 is a known growth factor for natural killer cells, which have the capacity to rapidly secrete IFN-c, a cytokine with a potent macrophage-activating capacity.…”

Section: Discussionmentioning

confidence: 99%

Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium

et al. 2010

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SummaryThe cholinergic nervous system has been demonstrated to attenuate the inflammatory response during sepsis via the inhibitory action of acetylcholine (ACh) on macrophages. These findings were largely based on experimental sepsis models using endotoxin as the inducing agent. Herein, however, we report that the specific inhibition of acetylcholinesterase (AChE) renders animals more resistant to infection by a virulent strain of Salmonella enterica serovar Typhimurium, a Gram-negative enteric pathogen. Inhibition of AChE was induced by a subchronic exposure to paraoxon, a potent anti-cholinesterase metabolite of the organophosphorous compound parathion. Our findings indicate that inhibition of AChE enhanced survival of infected mice in a dose-dependent fashion and this correlated with efficient control of bacterial proliferation in target organs. Immunologically, inhibition of AChE enabled the animals to mount a more effective inflammatory anti-microbial response, and to secrete higher levels of interleukin-12, a key T helper type 1-promoting cytokine. The ACh-induced enhancement in resistance to infection was abrogated by co-administration of an oxime which can reactivate AChE. Hence, in a model of Gram-negative bacterial infection, cholinergic stimulation is shown to enhance the anti-microbial immune response leading to effective control of bacterial proliferation and enhanced animal survival.

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Natural killer cells mediate protection induced by a Salmonella aroA mutant

Cited by 54 publications

References 22 publications

Alveolar macrophage priming by intravenous administration of chitin particles, polymers of N-acetyl-D-glucosamine, in mice

Alveolar macrophage priming by intravenous administration of chitin particles, polymers of N-acetyl-D-glucosamine, in mice

Immune response to infection with Salmonella typhimurium in mice

Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium

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