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Chapter 23 : Differential Cytokine Response Following Challenge of A/J Mice with Virulent and Avirulent

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Differential Cytokine Response Following Challenge of A/J Mice with Virulent and Avirulent , Page 1 of 2

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Abstract:

causes a severe atypical pneumonia in humans, the so-called Legionnaires' disease. Although the disease mostly occurs in immunocompromised subjects, several virulence factors of have been described that confer to the microorganism an intrinsic aggressive potential. The ability of this pathogen to replicate in host macrophages is considered a major virulence trait. For this reason, the susceptibility to the experimental infection with observed in guinea pigs and in selected mouse strains has been generally explained by the permissiveness of macrophages of these animals for invasion and intracellular replication in vitro, as reported, for elicited peritoneal macrophages from susceptible A/J mice. Researchers found that the i.p. inoculation of virulent cells from the VIR+ strain was rapidly lethal for A/J mice, since 100 and 60% of the animals acutely died within 2 days following the challenge with 2 X 10 or 2 X 10 bacterial cells. Unchecked TNF-α production upon i.v. inoculation has recently been reported as the causative factor in the death of replication-unpermissive BALB/c mice. Accordingly, the protection afforded by IL-10 treatment or TNF-α neutralization in the mice model also indicates that the release of TNF-α, a well-known toxic shock-related cytokine, plays a major role in mediating the lethal effects of the virulent legionellae. Therefore induction of proinflammatory cytokines, in particular TNF-α, besides being an important factor facilitating the resolution of infections, might also be regarded as a possible contributory factor to the pathogenic action of virulent strains.

Citation: Torosantucci A, Chiani P, Ricci M, Pastoris M. 2002. Differential Cytokine Response Following Challenge of A/J Mice with Virulent and Avirulent , p 124-128. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch23

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Tumor Necrosis Factor alpha
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Figures

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FIGURE 1

Mortality of A/J mice and recovery of PEC-associated viable cells after an i.p. challenge with VIR+ or VIR— strain. (A) Differential lethality of VIR+ and VIR— strain for A/J mice. Groups of 12 mice were inoculated i.p. at day 0 with the indicated dose of cells, VIR+ or VIR— strain. Data represent cumulative percent mortality of animals at the indicated day postchaUenge. (B) Recovery of cells from PECs of A/J mice injected i.p. with VIR+ or VIR— strain. Mice were given 2 X 10 to 3 X 10 bacterial cells. CFU in PECs were enumerated, as described in the text, at the indicated time post-inoculation. Values are expressed as means ± standard error of the individual CFU counts measured in four mice from two independent experiments. The asterisk marks a statistically significant difference ( < 0.05, Student's test, two tailed) with respect to values measured for the VIR+ strain.

Citation: Torosantucci A, Chiani P, Ricci M, Pastoris M. 2002. Differential Cytokine Response Following Challenge of A/J Mice with Virulent and Avirulent , p 124-128. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch23
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Image of FIGURE 2
FIGURE 2

Release of proinflammatory cytokines in the peritoneal cavity and in serum of VIR+ or VIR— challenged mice. Mice were injected i.p. with saline (control) or with 2 X 10 to 5 X 10 cells of the indicated strain. Twenty-four hours after the bacterial challenge, cytokine levels in individual peritoneal lavage fluids (eight mice for each experimental group) and in serum (four mice for each experimental group) were measured by ELISA. Values respresent mean cytokine concentrations ± standard error measured in mice from each experimental group. The asterisks indicate a statistically significant difference ( < 0.01; Mann-Whitney U test, two tailed) with respect to saline-injected, control mice.

Citation: Torosantucci A, Chiani P, Ricci M, Pastoris M. 2002. Differential Cytokine Response Following Challenge of A/J Mice with Virulent and Avirulent , p 124-128. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch23
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References

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1. Beutler, B.,, and A. Cerami. 1986. Cachectin and tumor necrosis factor as two sides of the same biological coin. Nature 320:584588.
2. Brieland, J.,, P. Freeman,, R. Kunkel,, C. Chrisp,, M. Hurley,, J. Fantone,, and C. En-gleberg. 1994. Replicative Legionella pneumophila lung infection in intratracheally inoculated A/J mice. Am. J. Pathol. 145:15371546.
3. Brieland, J. K.,, D. G. Remick,, P. T. Freeman,, M. C. Hurley,, J. C. Fantone,, and N. C. Engleberg. 1995. In vivo regulation of replicative Legionella pneumophila lung infection by endogenous tumor necrosis factor alpha and nitric oxide. Infect. Immun. 63:32533258.
4. Castellani Pastoris, M.,, E. Proietti,, C. Mauri,, P. Chiani,, and A. Cassone. 1997. Suckling CD1 mice as an animal model for studies of Legionella pneumophila virulence. J. Med. Microbiol. 46:647655.
5. Cianciotto, N.,, B. I. Eisenstein,, C. Engleberg,, and H. Shuman. 1989. Genetics and molecular pathogenesis of Legionella pneumophila, an intracellular parasite of macrophages. Mol. Biol. Med. 6:409424.
6. Fiorentino, D.,, A. Zlotnik,, T. Mosmann,, M. Howard,, and A. O'Garra. 1991. IL-10 inhibits cytokine production by activated macrophages. J Immunol. 147:38153822.
7. Gerard, C.,, C. Bruyns,, A. Marchant,, D. Abramowicz,, P. Vandenabeele,, A. Delvaux,, W. Fiers,, M. Goldman,, and T. Velu. 1993. Interleukin-10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia. J. Exp. Med. 177:12051208.
8. Newton, C.,, S. McHugh,, R. Widen,, N. Nakachi,, T. Klein,, and H. Friedman. 2000. Induction of interleukin-4 (IL-4) by Legionella pneumophila infection in BALB/c mice and regulation of tumor necrosis factor alpha, IL-6 and IL-1β. Infect. Immun. 68:52345240.
9. Swanson, M. S.,, and Hammer, B. K. 2000. Legionella pneumophila pathogenesis: a fateful journey from amoeba to macrophages. Annu. Rev. Microbiol. 54:567613.
10. Tracey, K. J.,, Y. Fong,, D. G. Hesse,, K. R. Manogue,, A. T. Lee,, G. C. Kuo,, S. F. Lowry,, and A. Cerami. 1987. Anti-cachectin/ TNF monoclonal antibodies prevent septic shock during lethal bacteraemia. Nature 330:662664.
11. Yamamoto, Y.,, T. W. Klein,, C. A. Newton,, R. Widen,, and H. Friedman. 1988. Growth of Legionella pneumophila in thioglycollate-elicited macrophages from A/J mice. Infect. Immun. 56: 370375.
12. Yoshida, S.,, and Y. Mizuguchi. 1986. Multiplication of Legionella pneumophila Philadelphia 1 in cultured peritoneal macrophages and its correlation to susceptibility of animals. Can. J. Microbiol. 32:438442.

Tables

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TABLE 1

Effect of the treatment with IL-10 or with anti-mouse TNF- or IL-6 antibodies on the course of a lethal VIR+ challenge

Citation: Torosantucci A, Chiani P, Ricci M, Pastoris M. 2002. Differential Cytokine Response Following Challenge of A/J Mice with Virulent and Avirulent , p 124-128. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch23

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