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Cited by 148

The DOI matches its Crossref record; 200 of the 200 references it cites were found in a registry or an index.

Chronic granulomatous disease: a review of the infectious and inflammatory complications

Song, EunKyung, Jaishankar, Gayatri Bala, Saleh, Hana, Jithpratuck, Warit, Sahni, Ryan, Krishnaswamy, Guha·2011·Clinical and Molecular Allergy
DOI 10.1186/1476-7961-9-10PMC PMC3128843
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Abstract

Chronic Granulomatous Disease is the most commonly encountered immunodeficiency involving the phagocyte, and is characterized by repeated infections with bacterial and fungal pathogens, as well as the formation of granulomas in tissue. The disease is the result of a disorder of the NADPH oxidase system, culminating in an inability of the phagocyte to generate superoxide, leading to the defective killing of pathogenic organisms. This can lead to infections with Staphylococcus aureus,Psedomonas species,Nocardia species, and fungi (such as Aspergillus species and Candida albicans). Involvement of vital or large organs can contribute to morbidity and/or mortality in the affected patients. Major advances have occurred in the diagnosis and treatment of this disease, with the potential for gene therapy or stem cell transplantation looming on the horizon.

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Figures

Figure 1 Distribution of Common Immunodeficiencies. Primary immune deficiencies can involve either the adaptive (T- and B-lymphocyte deficiencies) or the innate (phagocyte, complement or other defects) immune response (Figure 1). Of these, defects in phagocyte function constitute only about 18%, with the larger portion of the defects seen in the B cell/antibody and/or T cell components of immunity.
Figure 1 Distribution of Common Immunodeficiencies. Primary immune deficiencies can involve either the adaptive (T- and B-lymphocyte deficiencies) or the innate (phagocyte, complement or other defects) immune response (Figure 1). Of these, defects in phagocyte function constitute only about 18%, with the larger portion of the defects seen in the B cell/antibody and/or T cell components of immunity.CC BY · PubMed Central
Figure 2 Defects Leading to Immunodeficiency Disease. The various defects are summarized in Figure 2, which describe the potential sequence of events, starting from T- and B cell interactions and antibody synthesis to the involvement of phagocyte and complement components of the innate immune response. Explanation for the various aspects of the immune response is provided at the bottom of the figure (components 1-8); Components 5 and 6 deal with phagocytic/neutrophil defects.
Figure 2 Defects Leading to Immunodeficiency Disease. The various defects are summarized in Figure 2, which describe the potential sequence of events, starting from T- and B cell interactions and antibody synthesis to the involvement of phagocyte and complement components of the innate immune response. Explanation for the various aspects of the immune response is provided at the bottom of the figure (components 1-8); Components 5 and 6 deal with phagocytic/neutrophil defects.CC BY · PubMed Central
Figure 3 Role of Macrophages in Host Defenses. Macrophages are generated from bone marrow precursor cells in the presence of stem cell hematopoietic factors (such as granulocyte-macrophage colony stimulating factor/GM-CSF and macrophage colony stimulating factor/M-CSF). The activation of macrophages (in the presence of specific receptors and T lymphocytes as shown in the figure- CD40/CD40L, CD28/B7, interleukin-interleukin receptor etc) results in functional consequences such as microbicidal activity directed especially towards intracellular pathogens and aided by the expression of peroxides and superoxide radicals. These processes are defective in CGD (see text). Other secretory effects of macrophages result in the production of a plethora of mediators that assist in immunity (these are shown in the figure and include complement, enzymes, interleukins, interferons and growth factors).
Figure 3 Role of Macrophages in Host Defenses. Macrophages are generated from bone marrow precursor cells in the presence of stem cell hematopoietic factors (such as granulocyte-macrophage colony stimulating factor/GM-CSF and macrophage colony stimulating factor/M-CSF). The activation of macrophages (in the presence of specific receptors and T lymphocytes as shown in the figure- CD40/CD40L, CD28/B7, interleukin-interleukin receptor etc) results in functional consequences such as microbicidal activity directed especially towards intracellular pathogens and aided by the expression of peroxides and superoxide radicals. These processes are defective in CGD (see text). Other secretory effects of macrophages result in the production of a plethora of mediators that assist in immunity (these are shown in the figure and include complement, enzymes, interleukins, interferons and growth factors).CC BY · PubMed Central
Figure 4 The NADPH Oxidase System. The assembly of the various subunits of NADPH oxidase is shown in the figure, while the molecular genetics, rough prevalence, inheritance pattern and chromosomal localization of CGD subtypes are shown in the bottom of the figure. There are several components of NADPH oxidase: of these the cytochrome-b558 heterodimer is located in the membrane and consists of the gp91phox and p22phox units, while three cytosolic components exist- including the p67phox , p47phox and a p40phox. Following cellular activation, the soluble cytosolic components, p67phox , p47phox , and a p40phox , move to the membrane and bind to components of the cytochrome-b558 heterodimer. This is also accompanied by the binding of the GTPase protein, Rac, culminating by unclear mechanisms in flavocytochrome activation. This catalyzes the transfer of electrons from NADPH to oxygen, resulting in the formation of superoxide in the extracellular compartment (phagolysosome). Subsequent reactions via superoxide dismutase (SOD), catalase or myeloperoxidase (MPO), occurring in the phagolysome, can result in formation of H2O2, H2O or HOCl- respectively.
Figure 4 The NADPH Oxidase System. The assembly of the various subunits of NADPH oxidase is shown in the figure, while the molecular genetics, rough prevalence, inheritance pattern and chromosomal localization of CGD subtypes are shown in the bottom of the figure. There are several components of NADPH oxidase: of these the cytochrome-b558 heterodimer is located in the membrane and consists of the gp91phox and p22phox units, while three cytosolic components exist- including the p67phox , p47phox and a p40phox. Following cellular activation, the soluble cytosolic components, p67phox , p47phox , and a p40phox , move to the membrane and bind to components of the cytochrome-b558 heterodimer. This is also accompanied by the binding of the GTPase protein, Rac, culminating by unclear mechanisms in flavocytochrome activation. This catalyzes the transfer of electrons from NADPH to oxygen, resulting in the formation of superoxide in the extracellular compartment (phagolysosome). Subsequent reactions via superoxide dismutase (SOD), catalase or myeloperoxidase (MPO), occurring in the phagolysome, can result in formation of H2O2, H2O or HOCl- respectively.CC BY · PubMed Central

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Research works printed but not linked: 1

  1. Janeway CA: Hypergammaglobulinemia associated with severe, recurrent and chronic non-specific infection. Am J Dis Child. 1954, 88: 388-392.

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Metadata

Authors
Song, E., Jaishankar, G. B., Saleh, H., Jithpratuck, W., Sahni, R., & Krishnaswamy, G.
Venue
Clinical and Molecular Allergy
Publisher
Springer Science and Business Media LLC
Published
2011-05-31
Volume
9
Issue
1
ISSN
1476-7961
DOI
10.1186/1476-7961-9-10
PMC
PMC3128843
Cited by
148
References
200
Language
en

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CoChat. (2026). Citation check: Chronic granulomatous disease: a review of the infectious and inflammatory complications. https://app.cochat.ai/papers/10.1186/1476-7961-9-10
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Song, E., Jaishankar, G. B., Saleh, H., Jithpratuck, W., Sahni, R., & Krishnaswamy, G. (2011). Chronic granulomatous disease: a review of the infectious and inflammatory complications. Clinical and Molecular Allergy. https://doi.org/10.1186/1476-7961-9-10

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