1887

Chapter 22 : and Interleukin-12 Production: In Vitro Infection Model

Authors: Kazuto Matsunaga1, Thomas W. Klein1, Catherine Newton1, Herman Friedman1, Yoshimasa Yamamoto1
VIEW AFFILIATIONS HIDE AFFILIATIONS
Affiliations: 1: Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, FL 33612-4799
Content Type: Monograph
Publication Year: 2002

Category: Bacterial Pathogenesis

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.

Preview this chapter:
Preview Magnify
Zoom in
Zoomout

and Interleukin-12 Production: In Vitro Infection Model, Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555817985/9781555812300_Chap22-1.gif /docserver/preview/fulltext/10.1128/9781555817985/9781555812300_Chap22-2.gif

Abstract:

Interleukin-12 (IL-12), one of the key cytokines in regulating the development of Th1 response, is a heterodimeric cytokine composed of two disulfide-linked p35 and p40 subunits. Both subunits have to be expressed within the same cell to produce biologically active p70 heterodimer. The production of IL-12 by monocytes/macrophages is induced by exposing responsive cells to a variety of microbial products such as lipopolysaccharide (LPS). The suppression of IL-12 by infection may be occurring at the level of gene transcription. The analysis of the steady-state levels of IL-12 p35 and IL-12 p40 mRNA determined by reverse transcriptase-PCR (RT-PCR) showed that infection induced the suppression of mRNA accumulation for the IL-12 p40 gene in response to LPS stimulation, but not the IL-12 p35 gene, which was constitutive in all macrophages treated. infection induced production of MCP-1 protein and up-regulated the LPS-induced production of MCP-1 protein regardless of the virulence of and its viability in the macrophages. The experimental mouse infection with resulted in certain levels of IL-12. Since IL-12 production is regulated by multiple mechanisms, including cytokines produced by other cells, it can be speculated that the suppressed IL-12 by infection may be overcome by other systems in vivo, such as the host defense system.

Citation: Matsunaga K, Klein T, Newton C, Friedman H, Yamamoto Y. 2002. and Interleukin-12 Production: In Vitro Infection Model, p 120-123. 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.ch22
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

References

/content/book/10.1128/9781555817985.chap22
1. Braun, M. C.,, E. Lahey,, and B. L. Kelsall. 2000. Selective suppression of IL-12 production by chemoattractants. J. Immunol. 164: 3009– 3017.
2. Brieland, J. K.,, D. G. Remick,, M. L. Le-gendre,, N. C. Engleberg,, and J. C. Fantone. 1998. In vivo regulation of replicative Legionella pneumophila lung infection by endogenous interleukin-12. Infect. Immun. 66: 65– 69.
3. Chehimi, J.,, S. E. Starr,, I. Frank,, A. D'Andrea,, X. Ma,, R. R. McGregor,, J. Sennelier,, and G. Trinchieri. 1994. Impaired interleukin 12 production in human immunodeficiency virus-infected patients. J. Exp. Med. 179: 1361– 1366.
4. Cooper, A. M.,, A. D. Roberts,, E. R. Rhoades,, J. E. Callahan,, D. M. Getzv,, and I. M. Orme. 1995. The role of interleukin-12 in acquired immunity to Mycobacterium tuberculosis infection. Immunology 84: 423– 432.
5. D'Andrea, A.,, M. Rengaraju,, N. M. Val-iante,, J. Chehimi,, M. Kubin,, M. Aste,, S. H. Chan,, M. Kobayashi,, D. Young,, E. Nick-barg,, R. Chizzonite,, S. F. Wolf,, and G. Trinchieri. 1992. Production of natural killer cell stimulatory factor (NKSF/IL-12) by peripheral blood mononuclear cells. J. Exp. Med. 176: 1387– 1398.
6. Gubler, U.,, A. Chua,, D. S. Schoenhaut,, C. M. Dwyer,, W. McComas,, R. Motyka,, N. Nabavi,, A. G. Wolitzky,, P. M. Quinn,, P. C. Familletti,, and M. C. Gately. 1991. Coexpression of two distinct genes is required to generate secreted bioactive cytotoxic lymphocyte maturation factor. Proc. Natl. Acad. Sci. USA 88: 4143– 4147.
7. Gui-Jie, F.,, H. S. Goodridge,, M. M. Harnet,, X. Wei,, A. V. Nikolaev,, A. P. Higson,, and F. Liew. 1999. Extracellular signal-related kinase (ERK) and p38 mitogen-activated protein (MAP) kinases differentially regulate the lipopo-lysaccharide-mediated induction of inducible nitric oxide synthase and IL-12 in macrophages: Leishmania phosphoglycans subvert macrophage IL-12 production by targetting ERK MAP kinase. J. Immunol. 163: 6403– 6412.
8. Heinzel, F. P.,, D. S. Schoenhaut,, R. M. Rerco,, L. E. Rosser,, and M. C. Gately. 1993. Recombinant interleukin-12 cures mice infected with Leishmania major. J. Exp. Med. 177: 1505– 1512.
9. Klein, T. W.,, C. Newton, Y. Yamamoto, and H. Friedman. 1999. Immune responses to Legionella, p. 149– 166. In L. J. Paradise,, H. Friedman,, and M. Bendinelli (éd.), Opportunistic Intracellular Bacteria and Immunity. Plenum Press, New York, N.Y.
10. Nash, T. W.,, D. M. Libby,, and D. M. Hor-witz. 1988. IFN-γ activated human alveolar macrophages inhibit the intracellular multiplication of Legionella pneumophila. J. Immunol. 140: 3978– 3981.
11. Sypek, J. P.,, C. L. Chung,, S. E. H. Mayor,, J. M. Subramanyam,, S. J. Goldman,, D. S. Sieburth,, S. F. Wolf,, and R. G. Schaub. 1993. Resolution of cutaneous leishmaniasis: interleukin-12 initiates a protective T helper type 1 immune response. J. Exp. Med. 177: 1797– 1802.
12. Trinchieri, G. 1993. Interleukin-12 and its role in the generation of Th1 cells. Immunol. Today 14: 335– 337.
13. Wagner, R. D.,, H. Steinberg,, J. F. Brown,, and C. J. Czuprynski. 1994. Recombinant interleukin-12 enhances resistance of mice to Lis-teria monocytogenes infection. Microb. Pathog. 17: 175– 186.
14. Yamamoto, Y.,, T. W. Klein,, and H. Friedman. 1993. Legionella pneumophila virulence conserved after multiple single-colony passage on agar. Curr. Microbiol. 27: 241– 245.

Tables

Legionella pneumophila and Interleukin-12 Production: In Vitro Infection Model
[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555817985.chap22-1,webId=/content/author/10.1128/9781555817985.chap22-1,properties={foaf_givenname=Kazuto, foaf_name=Kazuto Matsunaga, foaf_surname=Matsunaga, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555817985.chap22-aff1]]}], com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555817985.chap22-2,webId=/content/author/10.1128/9781555817985.chap22-2,properties={foaf_givenname=Thomas W., foaf_name=Thomas W. Klein, foaf_surname=Klein, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555817985.chap22-aff1]]}], com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555817985.chap22-3,webId=/content/author/10.1128/9781555817985.chap22-3,properties={foaf_givenname=Catherine, foaf_name=Catherine Newton, foaf_surname=Newton, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555817985.chap22-aff1]]}], com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555817985.chap22-4,webId=/content/author/10.1128/9781555817985.chap22-4,properties={foaf_givenname=Herman, foaf_name=Herman Friedman, foaf_surname=Friedman, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555817985.chap22-aff1]]}], com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555817985.chap22-5,webId=/content/author/10.1128/9781555817985.chap22-5,properties={foaf_givenname=Yoshimasa, foaf_name=Yoshimasa Yamamoto, foaf_surname=Yamamoto, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555817985.chap22-aff1]]}]]
Citation: Matsunaga K, Klein T, Newton C, Friedman H, Yamamoto Y. 2002. and Interleukin-12 Production: In Vitro Infection Model, p 120-123. 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.ch22
/content/10.1128/9781555817985.chap22.tab22-1
TABLE 1

Effect of infection of macrophages on the protein levels of IL-12 p40/p70 production induced by LPS

10.1128/9781555817985/tab22-1_thmb.gif
10.1128/9781555817985/tab22-1.gif
Generic image for table
TABLE 1

Effect of infection of macrophages on the protein levels of IL-12 p40/p70 production induced by LPS

Citation: Matsunaga K, Klein T, Newton C, Friedman H, Yamamoto Y. 2002. and Interleukin-12 Production: In Vitro Infection Model, p 120-123. 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.ch22
/content/10.1128/9781555817985.chap22.tab22-2
TABLE 2

Effect of virulent (LP-V) infection of macrophages on the protein levels of IL-l, IL-6, and IL-10 production induced by LPS

10.1128/9781555817985/tab22-2_thmb.gif
10.1128/9781555817985/tab22-2.gif
Generic image for table
TABLE 2

Effect of virulent (LP-V) infection of macrophages on the protein levels of IL-l, IL-6, and IL-10 production induced by LPS

Citation: Matsunaga K, Klein T, Newton C, Friedman H, Yamamoto Y. 2002. and Interleukin-12 Production: In Vitro Infection Model, p 120-123. 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.ch22

Back to top
This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error