Highlighted Text:
Show |
Hide
Full text loading...
Chapter 22 : Acquired Immunity: Chronic Bacterial Infections
Authors:
Andrea M. Cooper1,
Richard Robinson2
VIEW AFFILIATIONS
HIDE AFFILIATIONS
Affiliations:
1: Trudeau Institute, Inc, 154 Algonquin Ave., Saranac Lake, NY;
2: Trudeau Institute, Inc, 154 Algonquin Ave., Saranac Lake, NY
Content Type: Monograph
Publication Year:
2011
Category: Immunology; Clinical Microbiology
Book DOI:
10.1128/9781555816872
Chapter DOI:
10.1128/9781555816872.ch22
MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.
Preview this chapter:
Acquired Immunity: Chronic Bacterial Infections, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555816872/9781555815141_Chap22-1.gif /docserver/preview/fulltext/10.1128/9781555816872/9781555815141_Chap22-2.gif
Abstract:
This chapter discusses what happens when the immune response is capable of controlling a bacterial pathogen but not eliminating it. In this case, acquired immunity is defined not as the response capable of eliminating the pathogen but the response that allows survival of the host. The presence of ongoing infection and inflammation is likely to severely interfere with the generation of acquired specific memory. In this chapter the authors have consider the acquired cellular response to bacterial challenge with a focus on members of the genus Mycobacterium. The chapter focuses on the elements of the acquired immune response that mediate both immunity as well as the immunopathologic consequences that are often concomitant with expression of immunity to chronic bacterial pathogens. More recent studies, made possible by the development of tools capable of dissecting the nature of the T-cell response during an infection, have highlighted the truly complex nature of acquired immunity. The nature of the inflammatory response to Mycobacterium tuberculosis in the absence of acquired immune response suggests that the pathogen makes use of the acquired response to generate the damage required for transmission. The relative importance of cytokine cross-regulation, regulatory T-cell control, and the active cytotoxic activity of the bacteria in regulating the acquired response to Mycobacterium ulcerans has yet to be fully defined.
Citation:
Cooper A, Robinson R.
2011.
Acquired Immunity: Chronic Bacterial Infections,
p 279-287.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch22
Figures
Acquired Immunity: Chronic Bacterial Infections
[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555816872.ch22-1,webId=/content/author/10.1128/9781555816872.ch22-1,properties={foaf_givenname=Andrea M., foaf_name=Andrea M. Cooper, foaf_surname=Cooper, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555816872.ch22-aff1]]}], com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555816872.ch22-2,webId=/content/author/10.1128/9781555816872.ch22-2,properties={foaf_givenname=Richard, foaf_name=Richard Robinson, foaf_surname=Robinson, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555816872.ch22-aff2]]}]]
Citation:
Cooper A, Robinson R.
2011.
Acquired Immunity: Chronic Bacterial Infections,
p 279-287.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch22
/content/10.1128/9781555816872.ch22.ch22fig01
FIGURE 1
Chronic bacterial infection influences the host immune response. When the acquired cellular response of the host rapidly eliminates an invading bacterial population, it rapidly contracts and a memory population capable of rapidly responding to reinfection is generated (a). In a chronic infection (b), there are several potential outcomes for the host response that depend upon bacterial burden, the level of immunosuppression from the bacteria, the extent of immunoregulation, and the inflammatory environment. The response could maintain a high level (long dashed line, A), fluctuate in response to bacterial number (dot/dash line, B), contract to a level capable of controlling bacterial growth (short dash, C), or become depleted as the bacterial infection persists (short to long dash, D). In tuberculosis, it appears that curve C is the pattern of host response; however, curve D may also apply as the infected host ages.
10.1128/9781555816872/f0280-01_thmb.gif
10.1128/9781555816872/f0280-01.gif
FIGURE 1
Chronic bacterial infection influences the host immune response. When the acquired cellular response of the host rapidly eliminates an invading bacterial population, it rapidly contracts and a memory population capable of rapidly responding to reinfection is generated (a). In a chronic infection (b), there are several potential outcomes for the host response that depend upon bacterial burden, the level of immunosuppression from the bacteria, the extent of immunoregulation, and the inflammatory environment. The response could maintain a high level (long dashed line, A), fluctuate in response to bacterial number (dot/dash line, B), contract to a level capable of controlling bacterial growth (short dash, C), or become depleted as the bacterial infection persists (short to long dash, D). In tuberculosis, it appears that curve C is the pattern of host response; however, curve D may also apply as the infected host ages.
Citation:
Cooper A, Robinson R.
2011.
Acquired Immunity: Chronic Bacterial Infections,
p 279-287.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch22
/content/10.1128/9781555816872.ch22.ch22fig02
FIGURE 2
Chronic infection allows for increased transmission. A bacterial pathogen with multiple transmission strategies such as Y. pestis can afford to grow rapidly and kill one host (the human) as the alternative hosts provide a reservoir and the possibility of further spread. In contrast, in the absence of an alternative vector for transmission, it is advantageous for bacteria to persist within a host and thereby maximize the exposure of the infected host to target hosts (e.g., M. tuberculosis).
10.1128/9781555816872/f0280-02_thmb.gif
10.1128/9781555816872/f0280-02.gif
FIGURE 2
Chronic infection allows for increased transmission. A bacterial pathogen with multiple transmission strategies such as Y. pestis can afford to grow rapidly and kill one host (the human) as the alternative hosts provide a reservoir and the possibility of further spread. In contrast, in the absence of an alternative vector for transmission, it is advantageous for bacteria to persist within a host and thereby maximize the exposure of the infected host to target hosts (e.g., M. tuberculosis).
Citation:
Cooper A, Robinson R.
2011.
Acquired Immunity: Chronic Bacterial Infections,
p 279-287.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch22
/content/10.1128/9781555816872.ch22.ch22fig03
FIGURE 3
The nature of acquired immune response to chronic bacterial infection. The nature and extent of the acquired cellular response to chronic bacterial infection depend upon a variety of factors. The nature of the bacterial stimulus will determine the initial and extended activation of the acquired response by determining the levels of APC activation and inflammatory cytokines. The ability of the bacteria to affect the architecture and function of the lymph node as well as the site of infection greatly influences the continued activation of the acquired specific responses as well as defines the ability of the protective cellular response to be expressed.
10.1128/9781555816872/f0281-01_thmb.gif
10.1128/9781555816872/f0281-01.gif
FIGURE 3
The nature of acquired immune response to chronic bacterial infection. The nature and extent of the acquired cellular response to chronic bacterial infection depend upon a variety of factors. The nature of the bacterial stimulus will determine the initial and extended activation of the acquired response by determining the levels of APC activation and inflammatory cytokines. The ability of the bacteria to affect the architecture and function of the lymph node as well as the site of infection greatly influences the continued activation of the acquired specific responses as well as defines the ability of the protective cellular response to be expressed.
Citation:
Cooper A, Robinson R.
2011.
Acquired Immunity: Chronic Bacterial Infections,
p 279-287.
In
Kaufmann S, Rouse B, Sacks D (ed),
The Immune Response to Infection.
ASM Press, Washington, DC.
doi: 10.1128/9781555816872.ch22
References
/content/book/10.1128/9781555816872.ch22
1.
Alcaïs, A.,, A. Alter,, G. Antoni,, M. Orlova,, V. Nguyen,, M. Singh,, P. Vanderborght,, K. Katoch,, M. Mira,, H. Vu,, T. Ngyuen,, N. Nguyen,, M. Moraes,, N. Mehra,, E. Schurr, and, L. Abel. 2007. Stepwise replication identifies a low-producing lymphotoxin-alpha allele as a major risk factor for early-onset leprosy. Nat. Gene. 39: 517– 522.
2.
Batista, M.,, A. Porro,, S. Maeda,, E. Gomes,, M. Yoshioka,, M. Enokihara, and, J. Tomimori. 2008. Leprosy reversal reaction as immune reconstitution inflammatory syndrome in patients with AIDS. Clin. Infect. Dis. 46: e56– 60.
3.
Blaser, M., and, J. Atherton. 2004. Helicobacter pylori persistence: biology and disease. J. Infect. Dis. 113: 321– 333.
4.
Cooper, A. 2009. Cell mediated immune responses in tuberculosis. Ann. Rev. Immunol. 27: 393– 422.
5.
Cooper, A.M.,, L.B. Adams,, D.K. Dalton,, R. Appelberg, and, S. Ehlers. 2002. IFN-γ and NO in mycobacterial disease: new jobs for old hands. Trends Microbiol. 10: 221– 226.
6.
Cruz, A.,, S. Khader,, E. Torrado,, A. Fraga,, J. Pearl,, J. Pedrosa,, A. Cooper, and, A. Castro. 2006. CE:IFN-γ regulates the induction and expansion of IL-17-producing CD4 T cells during mycobacterial infection. J. Immunol. 177: 1416– 1420.
7.
Dannenberg, A.J., and, F. Collins. 2001. Progressive pulmonary tuberculosis is not due to increasing numbers of viable bacilli in rabbits, mice and guinea pigs, but is due to a continuous host response to mycobacterial products. Tuberculosis 81: 229– 242.
8.
de Noronha, A.,, A. Báfica,, L. Nogueira,, A. Barral, and, M. Barral-Netto. 2008. Lung granulomas from Mycobacterium tuberculosis/HIV-1 co-infected patients display decreased in situ TNF production. Pathology - Research and Practice 204: 155– 161.
9.
Demangel, C.,, T. Stinear, and, S. Cole. 2009. Buruli ulcer: reductive evolution enhances pathogenicity of Mycobacterium ulcerans. Nat. Rev. Microbiol. 7: 50– 60.
10.
Dobos, K.,, E. Spotts,, B. Marston,, C. J. Horsburgh, and, C. King. 2000. Serologic response to culture filtrate antigens of Mycobacterium ulcerans during Buruli ulcer disease. Emerg. Infect. Dis. 6: 158– 164.
11.
Dye, C. 2006. Global epidemiology of tuberculosis. Lancet 367: 938– 940.
12.
Feng, C.,, D. Jankovic,, M. Kullberg,, A. Cheever,, C. Scanga,, S. Hieny,, P. Caspar,, G. Yap, and, A. Sher. 2005. Maintenance of pulmonary Th1 effector function in chronic tuberculosis requires persistent IL-12 production. J. Immunol. 174: 4185– 92.
13.
Feng, C.,, L. Zheng,, D. Jankovic,, A. Báfica,, J. Cannons,, W. Watford,, D. Chaussabel,, S. Hieny,, P. Caspar,, P. Schwartzberg,, M. Lenardo, and, A. Sher. 2008. The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-gamma-induced cell death. Nat. Immunol. 9: 1279– 1287.
14.
Gonzalez-Juarrero, M.,, O. Turner,, J. Turner,, P. Marietta,, J. Brooks, and, I. Orme. 2001. Temporal and spatial arrangement of lymphocytes within lung granulomas induced by aerosol infection with Mycobacterium tuberculosis. Infect. Immun. 69: 1722– 1728.
15.
Gooding, T.,, P. Johnson,, D. Campbell,, J. Hayman,, E. Hartland,, A. Kemp, and, R. Robins-Browne. 2001. Immune response to infection with Mycobacterium ulcerans. Infect. Immun. 69: 1704– 1707.
16.
Gooding, T.,, P. Johnson,, M. Smith,, A. Kemp, and, R. Robins-Browne. 2002. Cytokine profiles of patients infected with Mycobacterium ulcerans and unaffected household contacts. Infect. Immun. 70: 5562– 5567.
17.
Gringhuis, S.,, J. den Dunnen,, M. Litjens,, M. van der Vlist, and, T. Geijtenbeek. 2009. Carbohydrate-specific signaling through the DC-SIGN signalosome tailors immunity to Mycobacterium tuberculosis, HIV-1 and Helicobacter pylori. Nat. Immunol. 10: 1081– 1088.
18.
Hagge, D.,, B. Saunders,, G. Ebenezer,, N. Ray,, V. Marks,, W. Britton,, J. Krahenbuhl, and, L. Adams. 2009. Lymphotoxin-alpha and TNF have essential but independent roles in the evolution of the granulomatous response in experimental leprosy. Am. J. Path. 174: 1379– 1389.
19.
Hurtado, A.,, K. Hill,, W. Rosenblatt,, J. Bender, and, T. Scharmen. 2003. Longitudinal study of tuberculosis outcomes among immunologically naive Aché natives of Paraguay. Am. J. Phys. Anthropol. 121: 134– 150.
20.
Khader, S., and, A. Cooper. 2008a. IL-23 and IL-17 in tuberculosis. Cytokine 41: 79– 83.
21.
Khader, S., and, A. Cooper. 2008b. The role of cytokines in the initiation, expansion and control of cellular immunity to tuberculosis. Immunol. Rev. 226: 191– 204.
22.
Khader, S. A.,, J. Rangel-Moreno,, J. J. Fountain,, C. A. Martino,, W. W. Reiley,, J. E. Pearl,, G. M. Winslow,, D. L. Woodland,, T. D. Randall, and, A. M. Cooper. 2009. In a murine tuberculosis model, the absence of homeostatic chemokines delays granuloma formation and protective immunity. J. Immunol. 183: 8004– 8014.
23.
Koch, M. A.,, G. Tucker-Heard,, N. R. Perdue,, J. R. Killebrew,, K. B. Urdahl, and, D. J. Campbell. 2009. The transcription factor T-bet controls regulatory T cell homeostasis and function during type 1 inflammation. Nat. Immunol. 10: 595– 602. doi:10.1038/ni.1731.
24.
Li, X.,, K. McKinstry,, S. Swain, and, D. Dalton. 2007. IFN-gamma acts directly on activated CD4+ T cells during mycobacterial infection to promote apoptosis by inducing components of the intracellular apoptosis machinery and by inducing extracellular proapoptotic signals. J. Immunol. 179: 939– 949.
25.
Maglione, P., and, J. Chan. 2009. How B cells shape the immune response against Mycobacterium tuberculosis. Eur. J. Immunol. 39: 676– 686.
26.
Marsollier, L.,, E. Deniaux,, P. Brodin,, A. Marot,, C. Wondje,, J. Saint-André,, A. Chauty,, C. Johnson,, F. Tekaia,, E. Yeramian,, P. Legras,, B. Carbonnelle,, G. Reysset,, S. Eyangoh,, G. Milon,, S. Cole, and, J. Aubry. 2007. Protection against Mycobacterium ulcerans lesion development by exposure to aquatic insect saliva. PLoS Medicine 4: e64.
27.
Mira, M.,, A. Alcaïs,, V. Nguyen,, M. Moraes,, C. Di Flumeri,, H. Vu,, C. Mai,, T. Nguyen,, N. Nguyen,, X. Pham,, E. Sarno,, A. Alter,, A. Montpetit,, M. Moraes,, J. Moraes,, C. Doré,, C. Gallant,, P. Lepage,, A. Verner,, E. Van De Vosse,, T. Hudson,, L. Abel, and, E. Schurr. 2004. Susceptibility to leprosy is associated with PARK2 and PACRG. Nature 427: 636– 640.
28.
Mossman, T., and, R. Coffman. 1989. Th1 and Th2 cells: different patterns of lymphokine secretion lead to different functional properties. Ann. Rev. Immunol. 7: 145– 173.
29.
Mueller, S.,, K. Hosiawa-Meagher,, B. Konieczny,, B. Sullivan,, M. Bachmann,, R. Locksley,, R. Ahmed, and, M. Matloubian. 2007a. Regulation of homeostatic chemokine expression and cell trafficking during immune responses. Science 3 17: 670– 674.
30.
Mueller, S.,, M. Matloubian,, D. Clemens,, A. Sharpe,, G. Freeman,, S. Gangappa,, C. Larsen, and, R. Ahmed. 2007b. Viral targeting of fibroblastic reticular cells contributes to immunosuppression and persistence during chronic infection. Proc. Nat. Acad. Sci. USA 104: 15430– 15435.
31.
North, R., and, Y. Jung. 2004. Immunity to tuberculosis. Ann. Rev. Immunol. 22: 599– 623.
32.
Okenu, D.,, L. Ofielu,, K. Easley,, J. Guarner,, E. Spotts Whitney,, P. Raghunathan,, Y. Stienstra,, K. Asamoa,, T. van der Werf,, W. van der Graaf,, J. Tappero,, D. Ashford, and, C. King. 2004. Immunoglobulin M antibody responses to Mycobacterium ulcerans allow discrimination between cases of active Buruli ulcer disease and matched family controls in areas where the disease is endemic. Clin. Diagn. Lab. Immunol. 11: 387– 391.
33.
Phillips, R.,, C. Horsfield,, S. Kuijper,, S. Sarfo,, J. Obeng-Baah,, S. Etuaful,, B. Nyamekye,, P. Awuah,, K. Nyarko,, F. Osei-Sarpong,, S. Lucas,, A. Kolk, and, M. Wansbrough-Jones. 2006. Cytokine response to antigen stimulation of whole blood from patients with Mycobacterium ulcerans disease compared to that from patients with tuberculosis. Clin. Vaccine Immunol. 13: 253– 257.
34.
Portaels, F.,, M. Silva, and, W. Meyers. 2009. Buruli ulcer. Clin. Dermatol. 27: 291– 305.
35.
Prévot, G.,, E. Bourreau,, H. Pascalis,, R. Pradinaud,, A. Tanghe,, K. Huygen, and, P. Launois. 2004. Differential production of systemic and intralesional gamma interferon and interleukin-10 in nodular and ulcerative forms of Buruli disease. Infect. Immun. 72: 958– 965.
36.
Schurr, E.,, A. Alcaís,, L. de Léséleuc, and, L. Abel. 2006. Genetic predisposition to leprosy: A major gene reveals novel pathways of immunity to Mycobacterium leprae. Semin Immunol 18: 404– 410.
37.
Schütte, D.,, A. Umboock, and, G. Pluschke. 2009. Phagocytosis of Mycobacterium ulcerans in the course of rifampicin and streptomycin chemotherapy in Buruli ulcer lesions. Br J Dermatol 160: 273– 283.
38.
Scott-Browne, J.,, S. Shafiani,, G. Tucker-Heard,, K. Ishida-Tsubota,, J. Fontenot,, A. Rudensky,, M. Bevan, and, K. Urdahl. 2007. Expansion and function of Foxp3-expressing T regulatory cells during tuberculosis. J. Exp. Med. 204: 2159– 2169.
39.
Silva, M. T.,, F. Portaels, and, J. Pedrosa. 2009. Pathogenetic mechanisms of the intracellular parasite Mycobacterium ulcerans leading to Buruli ulcer. Lancet Infect. Dis. 9: 699– 710.
40.
Ustianowski, A.,, S. Lawn, and, D. Lockwood. 2006. Interactions between HIV infection and leprosy: a paradox. Lancet Infect. Dis 6: 350– 360.
41.
Walker, S., and, D. Lockwood. 2008. Leprosy type 1 (reversal) reactions and their management. Lepr. Rev. 79: 372– 386.
42.
Wei, G.,, L. Wei,, J. Zhu,, C. Zang,, J. Hu-Li,, Z. Yao,, K. Cui,, Y. Kanno,, T. Roh,, W. Watford,, D. Schones,, W. Peng,, H. Sun,, W. Paul,, J. O’Shea, and, K. Zhao. 2009. Global mapping of H3K4me3 and H3K27me3 reveals specificity and plasticity in lineage fate determination of differentiating CD4+ T cells. Immunity 30: 155– 167.
43.
Westenbrink, B.,, Y. Stienstra,, M. Huitema,, W. Thompson,, E. Klutse,, E. Ampadu,, H. Boezen,, P. Limburg, and, T. van der Werf. 2005. Cytokine responses to stimulation of whole blood from patients with Buruli ulcer disease in Ghana. Clin. Diag. Lab. Immunol. 12: 125– 129.
44.
Winslow, G.,, A. Roberts,, M. Blackman, and, D. Woodland. 2003. Persistence and turnover of antigen-specific CD4 T cells during chronic tuberculosis infection in the mouse. J. Immunol. 170: 2046– 2052.
45.
Yeboah-Manu, D.,, E. Peduzzi,, E. Mensah-Quainoo,, A. Asante-Poku,, D. Ofori-Adjei,, G. Pluschke, and, C. Daubenberger. 2006. Systemic suppression of interferon-gamma responses in Buruli ulcer patients resolves after surgical excision of the lesions caused by the extracellular pathogen Mycobacterium ulcerans. J. Leukocyte Biol. 79: 1150– 1156.
46.
Zhou, L.,, M. Chong, and, D. Littman. 2009. Plasticity of CD4 + T cell lineage differentiation. Immunity 30: 646– 655.