Literature DB >> 9643387

Immunologic response and pathophysiology of Legionella infection.

H Friedman1, Y Yamamoto, C Newton, T Klein.   

Abstract

Legionella pneumophila, the causative agent of legionnaires' disease, is a gram-negative pleomorphic bacillus and fastidious in its growth in artificial medium. These bacteria grow readily intracellularly, including growth in macrophages and other phagocytic cells. Humoral antibodies develop readily to these bacteria not only in infected patients, but also in persons who have had subclinical exposure. High-levels of serum antibodies may also occur in individuals who recover from infection. However, cell-mediated immunity based on lymphocytes reacting with the organisms and cytokines produced by such lymphocytes are important in resistance. Vaccines prepared from killed Legionella or their components readily induce cell-mediated immunity. Immune resistance to disease depends on lymphocyte-based immunity, activating cytokine formation, some of which activate macrophages to resist infection. Resistance to Legionella infection by experimental animals such as mice correlates with activation of macrophages, which can inhibit replication of the bacteria. Much recent experimental work has involved studies using inbred animals, including inbred mice genetically resistant to Legionella versus mice genetically susceptible. Detailed studies show that regulation of macrophage resistance versus susceptibility to infection is mediated by specific genetic mechanisms. Induction of cytokines by Legionella can activate immune cells, especially helper T cells. Th 1 type helper cells that produce type 1 class cytokines, such as interferon gamma and interleukin-2 (IL-2), are known to be important in cellular immunity to Legionella as well as to other opportunistic intracellular bacteria. In contrast, Th 2 type helper cells, which secrete type 2 class cytokines such as IL-4, IL-5, and IL-6, activate B lymphocytes to produce humoral antibodies important in resistance to extracellular bacteria which secrete toxins and extracellular factors as compared to intracellular bacteria such as Legionella. Although Legionella, similar to other ubiquitous opportunistic pathogens, can cause serious infection in immunocompromised individuals, these bacteria have many distinguishing characteristics, such as very rapid replication in macrophages from susceptible individuals. However, activated macrophages restrict the growth of these bacteria. Infection by Legionella, if recognized clinically, can be readily treated with appropriate antibiotics. Currently, many studies are in progress concerning the mechanism of pathogenicity and assessment of the molecular biologic mechanisms of protective immune responses to this bacterium, which causes serious infection in immunocompromised individuals.

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Year:  1998        PMID: 9643387

Source DB:  PubMed          Journal:  Semin Respir Infect        ISSN: 0882-0546


  5 in total

1.  Legionella.

Authors: 
Journal:  Curr Infect Dis Rep       Date:  1999-04       Impact factor: 3.725

2.  Involvement of fractalkine/CX3CL1 expression by dendritic cells in the enhancement of host immunity against Legionella pneumophila.

Authors:  Toshiaki Kikuchi; Sita Andarini; Hong Xin; Kazunori Gomi; Yutaka Tokue; Yasuo Saijo; Tasuku Honjo; Akira Watanabe; Toshihiro Nukiwa
Journal:  Infect Immun       Date:  2005-09       Impact factor: 3.441

3.  Differential effects of virulent versus avirulent Legionella pneumophila on chemokine gene expression in murine alveolar macrophages determined by cDNA expression array technique.

Authors:  N Nakachi; K Matsunaga; T W Klein; H Friedman; Y Yamamoto
Journal:  Infect Immun       Date:  2000-10       Impact factor: 3.441

4.  Detection of Legionella species in respiratory specimens using PCR with sequencing confirmation.

Authors:  J L Cloud; K C Carroll; P Pixton; M Erali; D R Hillyard
Journal:  J Clin Microbiol       Date:  2000-05       Impact factor: 5.948

5.  Integrating Antimicrobial Therapy with Host Immunity to Fight Drug-Resistant Infections: Classical vs. Adaptive Treatment.

Authors:  Erida Gjini; Patricia H Brito
Journal:  PLoS Comput Biol       Date:  2016-04-14       Impact factor: 4.475

  5 in total

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