Whether infection with Mycobacterium avium complex (MAC) among patients with acquired immune deficiency syndrome results from recent exposure to virulent strains or reactivation of latent infection acquired years earlier is unknown. To address this question, tissue samples from 47 simian immunodeficiency virus (SIV)-infected and 63 SIV-uninfected rhesus macaques were cultured. MAC was cultured from 14 SIV-uninfected macaques (22.2%) and 32 SIV-infected macaques (68.1%); median bacterial burdens were 33.3 and 998.7 cfu/g, respectively. Genetically distinct strains of MAC were identified for 13 SIV-uninfected macaques (20.6%) and 15 SIV-infected macaques (31.9%). A genetically identical MAC strain (K128A) was identified for 25 SIV-infected macaques (53.2%) and 1 SIV-uninfected macaque (1.6%). Multivariate analysis identified infection with SIV/Delta(B670), diagnosis of an SIV-related tumor or opportunistic infection, and birth on site as risks for MAC infection. SIV-uninfected and SIV-infected macaques yielding unique strains of MAC were considered to have latent and reactivation infection, respectively, whereas animals infected with strain K128A were considered to have recent infection, demonstrating that both mechanisms occur among rhesus macaques.

Eight-day-old embryonated hen’s eggs were used as a model to study Mycobacterium avium virulence. Strains isolated from human patients caused 20–90% mortality when eggs were infected by injection of bacterial suspensions into the amniotic sac. Virulence of examined strains subsequently decreased with passage through eggs to between 0 and 40% mortality in four passages. Virulence of the egg-attenuated strains could be restored by passage through human peripheral blood mononuclear cells. The site of infection in the egg was usually the mesodermal layer of the chorioallantoic membrane. A few small granulomas containing acid-fast bacteria were seen in the liver, but not in other organs. Death of chicken embryos may have resulted from destruction of the mesodermal layer of the chorioallantoic membrane with consequent respiratory failure. PBMCs infected with less virulent egg-passaged strains of M. avium produced higher levels of tumor necrosis factor-α than did peripheral blood mononuclear cells infected with more virulent nonpassaged strains.

Mycobacterium avium infections are the third most common opportunistic infection in patients with AIDS. Simian immunodeficiency virus (SIV)-infected rhesus macaques naturally acquire M. avium infections from the environment, and their clinical symptoms are similar to those observed in AIDS patients. We characterized concurrent infection with SIV and M. avium in monkeys on the basis of the growth of the bacteria in macrophages (Mphis) from rhesus macaques and the ability of M. avium to induce SIV replication and tumor necrosis factor alpha (TNF-alpha) production. The simian M. avium isolate grew significantly better than did an isolate from an AIDS patient or a chicken isolate (P = .001); it induced significantly more TNF-alpha production in Mphis from SIV-positive and SIV-negative monkeys than did the isolate from an AIDS patient (P = .013). No significant increase in SIV replication was seen in the M. avium isolates, and no correlation was found between increased SIV replication and increased TNF-alpha production. In addition, Mphis from monkeys infected with M. avium during late-stage SIV disease produced less TNF-alpha when stimulated with virulent M. avium.

The role of Mycobacterium avium isolates in modulating human immunodeficiency virus type 1 (HIV-1) replication was examined by use of an in vitro, resting T cell system. Two human clinical isolates (serotypes 1 and 4) but not an environmental M. avium isolate (serotype 2) enhanced HIV-1 replication. The M. avium-induced HIV-1 replication was not associated with cell activation or differential cytokine production or utilization. Addition of matrix metalloproteinase (MMP) inhibitors and their in vivo regulators, tissue inhibitors of metalloproteinases-1 and -2, abrogated M. avium-induced HIV-1 replication 80%-95%. The MMP inhibitors did not have any effect on the HIV-1 protease activity, suggesting that they may affect cellular processes. Furthermore, MMP-9 protein was differentially expressed after infection with clinical M. avium isolates and paralleled HIV-1 p24 production. Collectively, these data suggest that M. avium-induced HIV-1 replication is mediated, in part, through the induction of MMP-9.

in CD lead to generation of IFN-'/-producing Thl cells, low IL-12 levels in UC favor production of IL-5-producing T cells.Thus, activation of the IL-12/ STAT-4 pathway emerges as a central mechanism in the pathogenesis of Crohn's disease that could be an attractive target for therapeutic intervention.

Journal of Pediatric Gastroenterology and NutritionVolume 26, Issue 5 p. 545-545 Abstracts: ESPGHAN-NASPGN 5th Joint Meeting ORAL IMMUNIZATION WITH A HELICOBACTER PYLORI (Hp) VACCINE DECREASES ENDOSCOPIC AND HISTOLOGIC DISEASE AND BACTERIAL LOAD IN H. MUSTELAE (Hm) CHALLENGED FERRETS. B D Gold, B D Gold Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorB Williams, B Williams Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorD Adams, D Adams Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorD Ngo, D Ngo Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorB Khanna, B Khanna Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorL Herman, L Herman Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorG W Newman, G W Newman Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this author B D Gold, B D Gold Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorB Williams, B Williams Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorD Adams, D Adams Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorD Ngo, D Ngo Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorB Khanna, B Khanna Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorL Herman, L Herman Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this authorG W Newman, G W Newman Morehouse School of Medicine, Emory University School of Medicine, Centers for Disease Control and Prevention, Atlanta, GA Armed Forces Institute of Pathology, Washington, D.C.Search for more papers by this author First published: 01 May 1998 https://doi.org/10.1002/j.1536-4801.1998.tb00927.xRead the full textAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume26, Issue5May 1998Pages 545-545 RelatedInformation

Microbial pathogenicity has been defined as "the biochemical mechanisms whereby microorganisms cause disease" (Smith 1968); however, the actual process is much more dramatic. The interaction between host and pathogen during disease is a dynamic confrontation where the microbe's strategies for survival meet face to face with the formidable defenses of the immune system. The tactics employed by both participants provide fascinating topics for researchers of many disciplines. Advances, fueled largely by the application of molecular biology, have been made in the biochemistry, immunology, and cell biology of the host-parasite interaction. Among the many new insights is the recognition that bacterial pathogens have evolved sophisticated signal transduction systems controlling the coordinate expression of virulence determinants.

Annals of the New York Academy of SciencesVolume 797, Issue 1 p. 255-256 Models for Pathogenesis of Mycobacterium avium E. G. LONG, Corresponding Author E. G. LONG National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333b Address for correspondence: Earl G. Long, PhD, G-11, DASTLR/NCID, Centers for Disease Control, Atlanta, GA 30333.Search for more papers by this authorK. A. BIRKNESS, K. A. BIRKNESS National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorG. W. NEWMAN, G. W. NEWMAN National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorF. D. QUINN, F. D. QUINN National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorE. P. EWING Jr, E. P. EWING Jr National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorJ. H. BARTLETT, J. H. BARTLETT National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorC. H. KING, C. H. KING National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorM. A. YAKRUS, M. A. YAKRUS National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorC. R. HORSBURGH Jr, C. R. HORSBURGH Jr Emory University School of Medicine, Atlanta, Georgia 30333Search for more papers by this author E. G. LONG, Corresponding Author E. G. LONG National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333b Address for correspondence: Earl G. Long, PhD, G-11, DASTLR/NCID, Centers for Disease Control, Atlanta, GA 30333.Search for more papers by this authorK. A. BIRKNESS, K. A. BIRKNESS National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorG. W. NEWMAN, G. W. NEWMAN National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorF. D. QUINN, F. D. QUINN National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorE. P. EWING Jr, E. P. EWING Jr National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorJ. H. BARTLETT, J. H. BARTLETT National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorC. H. KING, C. H. KING National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorM. A. YAKRUS, M. A. YAKRUS National Center for Infectious Diseases Centers for Disease Control and Prevention, Atlanta, Georgia 30333Search for more papers by this authorC. R. HORSBURGH Jr, C. R. HORSBURGH Jr Emory University School of Medicine, Atlanta, Georgia 30333Search for more papers by this author First published: October 1996 https://doi.org/10.1111/j.1749-6632.1996.tb52969.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1 Morita, Y., M. Arai, O. Nomura, S. Maruyama & Y. Katsube. 1994. Avian tuberculosis which occurred in an imported pigeon and pathogenesis of the isolates. J. Vet. Med. Sci. 56: 585– 587. 2 Reddy, V. M., K. Parikh, J. Luna-Herrera, J. O. Falkingham, III, S. Brown & P. R. J. Gangadharam. 1994. Comparison of virulence of Mycobacterium avium complex (MAC) strains isolated from AIDS and non-AIDS patients. Microb. Pathog. 16: 121– 130. 3 Moehring, J. M. & M. R. Solotorovsky. 1965. Pathogenicity of transparent, opaque and rough variants of Mycobacterium avium in chickens and mice. Am. Rev. Respir. Dis. 92: 499– 506. 4 Schaefer, W. B., C. L. Davis & M. L. Cohn. 1970. Pathogenesis of transparent, opaque, and rough variants of Mycobacterium avium in chickens and mice. Am. Rev. Respir. Dis. 102: 499– 506. Volume797, Issue1Microbial Pathogenesis and Immune Response IIOctober 1996Pages 255-256 ReferencesRelatedInformation

Journal of Pediatric Gastroenterology and NutritionVolume 23, Issue 3 p. 346-346 Annual Meeting of the North American Society for Pediatric Gastroenterology and Nutrition 17 COMPARISON OF HELICOBACTER PYLORI AND HELICOBACTER HEPATICUS INTERACTIONS WITH EUKARYOTIC CELLS IN VITRO. W C lfeadike, W C lfeadike Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorM A Nicholson, M A Nicholson Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorK A Birkness, K A Birkness Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorF D Quinn, F D Quinn Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorE H White, E H White Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorG W Newman, G W Newman Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorJ H Bartlett, J H Bartlett Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorD Adams, D Adams Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorB D Gold, B D Gold Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this author W C lfeadike, W C lfeadike Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorM A Nicholson, M A Nicholson Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorK A Birkness, K A Birkness Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorF D Quinn, F D Quinn Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorE H White, E H White Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorG W Newman, G W Newman Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorJ H Bartlett, J H Bartlett Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorD Adams, D Adams Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this authorB D Gold, B D Gold Centers for Disease Control and Prevention and Emory University School of Medicine, Atlanta, GASearch for more papers by this author First published: 01 October 1996 https://doi.org/10.1002/j.1536-4801.1996.tb01599.x POSTER SESSION I: Poster Theme Symposium I: Epithelial Cell Biology: H. Pylori Pathogenesis: Read the full textAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume23, Issue3October 1996Pages 346-346 RelatedInformation

Journal of Pediatric Gastroenterology and NutritionVolume 23, Issue 3 p. 348-348 Annual Meeting of the North American Society for Pediatric Gastroenterology and Nutrition 23 MACROPHAGE INFILTRATION OF THE GASTRIC MUCOSA IN CHILDREN WITH AND WITHOUT HELICOBACTER PYLORI INFECTION. A E Whitney, A E Whitney Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorT S Emory, T S Emory Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorA M Marty, A M Marty Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorP A O'Shea, P A O'Shea Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorG W Newman, G W Newman Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorV Otterbeck, V Otterbeck Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorB D Gold, B D Gold Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this author A E Whitney, A E Whitney Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorT S Emory, T S Emory Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorA M Marty, A M Marty Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorP A O'Shea, P A O'Shea Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorG W Newman, G W Newman Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorV Otterbeck, V Otterbeck Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this authorB D Gold, B D Gold Centers for Disease Control and Emory University School of Medicine (EU), Atlanta, GA Armed Forces Institute of Pathology (AFIP), Washington, DCSearch for more papers by this author First published: 01 October 1996 https://doi.org/10.1002/j.1536-4801.1996.tb01558.x POSTER SESSION I: Poster Theme Symposium I: Epithelial Cell Biology: H. Pylori Pathogenesis: Read the full textAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume23, Issue3October 1996Pages 348-348 RelatedInformation

Journal of Pediatric Gastroenterology and NutritionVolume 23, Issue 3 p. 344-344 Annual Meeting of the North American Society for Pediatric Gastroenterology and Nutrition 10 AN IN VITRO MODEL TO STUDY HOST CELLULAR RESPONSES TO HELICOBACTER PYLORI. B D Gold, B D Gold Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorK A Birkness, K A Birkness Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorF D Quinn, F D Quinn Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorD Adams, D Adams Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorW C Ifeadike, W C Ifeadike Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorE P^Jr. Ewing, E P^Jr. Ewing Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorE H White, E H White Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorD T Smoot, D T Smoot Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorJ H Bartlett, J H Bartlett Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorG W Newman, G W Newman Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this author B D Gold, B D Gold Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorK A Birkness, K A Birkness Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorF D Quinn, F D Quinn Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorD Adams, D Adams Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorW C Ifeadike, W C Ifeadike Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorE P^Jr. Ewing, E P^Jr. Ewing Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorE H White, E H White Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorD T Smoot, D T Smoot Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorJ H Bartlett, J H Bartlett Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this authorG W Newman, G W Newman Centers for Disease Control and Prevention, Atlanta, GA Emory University School of Medicine, Atlanta, GA Howard University, Washington, D.C.Search for more papers by this author First published: 01 October 1996 https://doi.org/10.1002/j.1536-4801.1996.tb01594.x PLENARY SESSIONS: Read the full textAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume23, Issue3October 1996Pages 344-344 RelatedInformation

Annals of the New York Academy of SciencesVolume 797, Issue 1 p. 19-25 Genetic and Tissue Culture Systems for the Study of Bacterial Pathogenesis FREDERICK D. QUINN, FREDERICK D. QUINN Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorKRISTIN A. BIRKNESS, KRISTIN A. BIRKNESS Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorLYNNE C. KIKUTA-OSHIMA, LYNNE C. KIKUTA-OSHIMA Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorGALE W. NEWMAN, GALE W. NEWMAN Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorEFRAIN M. RIBOT, EFRAIN M. RIBOT Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorC. HAROLD KING, C. HAROLD KING Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this author FREDERICK D. QUINN, FREDERICK D. QUINN Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorKRISTIN A. BIRKNESS, KRISTIN A. BIRKNESS Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorLYNNE C. KIKUTA-OSHIMA, LYNNE C. KIKUTA-OSHIMA Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorGALE W. NEWMAN, GALE W. NEWMAN Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorEFRAIN M. RIBOT, EFRAIN M. RIBOT Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this authorC. HAROLD KING, C. HAROLD KING Division of AIDS, STD, and TB Laboratory Research Centers for Disease Control and Prevention Atlanta, Georgia 30333Search for more papers by this author First published: October 1996 https://doi.org/10.1111/j.1749-6632.1996.tb52945.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References 1 Roth, J. A., C. A. Bolin, K. A. Brogden, F. C. Minion & M. J. Wannemuehler. 1995. Virulence Mechanisms of Bacterial Pathogens. ASM Press. Washington , DC . 2 Moulder, J. W. 1985. Microbiol. Rev. 49: 298– 337. 3 Zychlinsky, A., J. J. Perdomo & P. J. Sansonetti. 1994. Ann. N.Y. Acad. Sci. 730: 197– 208. 4 Portnoy, D. A., T. Chakraborty, W. Goebel & P. Cossart. 1992. Infect. Immun. 60: 1263– 1267. 5 Stadnyk, A. W. 1994. FASEB J. 8: 1041– 1047. 6 Lukacs, N. W., S. L. Kunkel, R. Allen, H. L. Evanoff, C. L. Shaklee, J. S. Sherman, M. D. Burdick & R. M. Strieter. 1995. Am. J. Physiol. 268: L856-L861. 7 Alexander, J. J., R. Miguel & D. Graham. 1991. J. Vasc. Surg. 13: 444– 451. 8 Birkness, K. A., B. L. Swisher, E. H. White, E. G. Long, E. P. Ewing, Jr. & F. D. Quinn. 1995. Infect. Immun. 63: 402– 409. 9 Falkow, S. 1988. Rev. Infect. Dis. 10: 5274– 5276. 10 Alouf, J. E. & J. Freer. 1991. Source Book of Bacterial Toxins. Academic Press. New York . 11 Freer, J., R. Aitken & J. E. Alouf. 1994. Bacterial Protein Toxins. Gustav Fischer Verlag. New York . 12 Welch, R. A., T. Felmlee, F. Pellett & D. E. Chenoweth. 1986. The Escherichia coli haemolysin: Its gene organization and interaction with neutrophil receptors. 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D. Quinn. 1994. Ann. N.Y. Acad. Sci. 730: 263– 265. 24 Plum, G. & J. E. Clark-Curtiss. 1994. Infect. Immun. 62: 476– 483. 25 Zhang, L. & D. Medina. 1993. Mol. Carcinog. 8: 123– 136. 26 Wong, K. K. & M. McClelland. 1994. Proc. Natl. Acad. Sci. USA 88: 639– 643. 27 Liang, P. & A. B. Pardee. 1992. Science 257: 967– 971. Volume797, Issue1Microbial Pathogenesis and Immune Response IIOctober 1996Pages 19-25 ReferencesRelatedInformation

The long term survival of peripheral blood derived human macrophages (M phi) from normal, healthy donors after infection with Mycobacterium avium intracellulare (MAI) correlates with the increased induction of TNF-alpha and IL-6 mRNA and protein by the infected M phi. This conclusion is based on the following observations: M phi from approximately 30% of the blood donors in our study die 3 to 4 days after inoculation (MAI-growth nonsupportive (NS], whereas M phi from the other donors survive inoculation with MAI for 7-10 days (MAI-growth supportive (S)). S-type M phi when infected with MAI had markedly increased amounts of TNF-alpha and IL-6 mRNA and protein when compared to NS-type M phi. The effect of LPS on the induction of TNF-alpha mRNA and protein was also significantly enhanced in S-type M phi in comparison to NS cells. In contrast, IL-1 beta mRNA and protein production had similar increases in both donor types when infected with MAI or stimulated with LPS. The phenotype of the donors in the amount of TNF-alpha and IL-6 produced in response to MAI infection remained stable for a period of more than 1 yr. Pretreatment of NS M phi with recombinant human granulocyte-macrophage-CSF, but not IFN-gamma, however, converted NS M phi into a S-type cell phenotype. These granulocyte-macrophage-CSF pretreated NS M phi survived infection with MAI for a longer period of time and also had increased production of both TNF-alpha and IL-6 mRNA and protein. Cultures of S-type M phi infected with MAI had higher numbers of intracellular bacteria when compared to cultures of NS-infected M phi. Thus, increased survival of MAI-infected human M phi in vitro is correlated to increased production of TNF-alpha and IL-6 in response to infection with MAI.