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Chapter 21 : Vascular Adhesion Molecules in Tuberculous Lesions
Author:
Arthur M. Dannenberg, Jr.1
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Affiliations:
1: Center for Tuberculosis Research Departments of Environmental Health Sciences, Molecular Microbiology and Immunology, and Epidemiology, Bloomberg School of Public Health Department of Pathology, School of Medicine Johns Hopkins University, Baltimore, Maryland 21205
Content Type: Monograph
Publication Year:
2006
Category: Clinical Microbiology; Bacterial Pathogenesis
Book DOI:
10.1128/9781555815684
Chapter DOI:
10.1128/9781555815684.ch21
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Abstract:
Vascular adhesion molecules enable host defense cells to leave the bloodstream and enter tuberculous lesions. After the inhalation of tubercle bacilli, Lurie’s resistant rabbits had a larger number of mononuclear cells within developing lesions than did his susceptible rabbits. Therefore, the rapid local accumulation of mononuclear cells seems to be one of the factors associated with resistance to the progress of this disease. Vascular adhesion molecules enable such an accumulation to occur. With immunohistochemical techniques, the author's group evaluated the rise and fall of three major vascular adhesion molecules as rabbit dermal BCG lesions developed and healed. Intercellular adhesion molecule 1 (ICAM- 1) is important for the adherence of polymorphonuclear leukocytes (PMN), monocytes, and lymphocytes to activated vascular endothelium before they emigrate from the bloodstream into sites of inflammation and infection. Vascular cell adhesion molecule 1 (VCAM-1) is a major factor in monocyte, lymphocyte, and eosinophil emigration. Endothelial-leukocyte adhesion molecule 1 (ELAM-1, now called E-selectin) aids the emigration of granulocytes (and some monocytes and T lymphocytes). In tuberculosis, epithelioid cells are macrophages that adhere to one another in an epithelial-like pattern. This adherence seems to be due in part to the ICAM-1 of one macrophage’s binding to its ligand LFA-1 (lymphocyte function-associated antigen 1) (CD11a/CD18) on a neighboring macrophage. ICAM, VCAM, and ELAM are markers for activated vascular endothelial cells. In tuberculous lesions, such activated endothelial cells can capture and present local mycobacterial antigens and therefore may be killed by antigen-specific cytotoxic T lymphocytes.
Citation:
Dannenberg, Jr. A.
2006.
Vascular Adhesion Molecules in Tuberculous Lesions,
p 327-338.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch21
Figures
Vascular Adhesion Molecules in Tuberculous Lesions
Citation:
Dannenberg, Jr. A.
2006.
Vascular Adhesion Molecules in Tuberculous Lesions,
p 327-338.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch21
/content/10.1128/9781555815684.ch21.ch21fig01
FIGURE 1
Microvessels in a 9-day rabbit BCG lesion, stained immunohistochemically for ICAM-1 (A) and for VCAM-1 (B). Vessels immunostained for ELAM were similar in appearance. Mouse monoclonal antibodies to rabbit ICAM-1 and VCAM-1, rabbit anti-mouse IgG, counterstained with Giemsa. Magnification, ×475. Reproduced with permission from reference 1.
10.1128/9781555815684/f0328-01_thmb.gif
10.1128/9781555815684/f0328-01.gif
FIGURE 1
Microvessels in a 9-day rabbit BCG lesion, stained immunohistochemically for ICAM-1 (A) and for VCAM-1 (B). Vessels immunostained for ELAM were similar in appearance. Mouse monoclonal antibodies to rabbit ICAM-1 and VCAM-1, rabbit anti-mouse IgG, counterstained with Giemsa. Magnification, ×475. Reproduced with permission from reference 1.
Citation:
Dannenberg, Jr. A.
2006.
Vascular Adhesion Molecules in Tuberculous Lesions,
p 327-338.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch21
/content/10.1128/9781555815684.ch21.ch21fig02
FIGURE 2
(A) Size (in mm3) of rabbit dermal BCG lesions at various times after their onset. (B) Area of stained microvasculature in such lesions as a percentage of a 1-mm2 area of tissue section. The tissue sections were stained immunohistochemically for von Willebrand (vW) factor (a measure of the total functional microvasculature) and for the adhesion molecules ICAM-1, ELAM-1, and VCAM-1 (1) (see text). The microvasculature was evaluated only in the intact areas of the BCG lesions that were densely infiltrated with inflammatory cells. Normal skin values are shown at zero time. The means and their standard errors are shown. Note that peak levels of adhesion molecules preceded the peak size of the BCG lesions, because the upregulation of these molecules enabled the cell infiltration that caused the BCG lesions to grow in size. To produce this panel, each stained microvessel was circled with the probe of a computerized image analyzer, and its lumen was also circled. The two circled areas were subtracted to provide the area (in mm2) of the vessel wall. Then, the areas occupied by vessel walls in 1 mm2 of tissue section were computed. Reproduced with permission from reference 1. (C) Microvasculature stained for ICAM-1, ELAM-1, and VCAM-1 in BCG lesions as a percentage of a 1-mm2 area of tissue section. This panel confirms the data in panel B, with important 3-day measurements added. Note that ICAM and VCAM peaked at 3 days, suggesting that these adhesion molecules enabled the initial cell infiltration of mononuclear cells (macrophages and lymphocytes) into the BCG lesions. ELAM upregulation was more delayed. The means and their standard errors are shown. Reproduced with permission from reference 21. (D) Vasculature in BCG lesions stained for adhesion molecules as a percentage of the total functional vasculature (vW factor-stained vessels). Presenting the data in this way identifies the upregulation and downregulation of the adhesion molecules more precisely, because changes in the total functional vasculature have been factored out. The means and their standard errors are shown. Reproduced with permission from reference 1.
10.1128/9781555815684/f0330-01_thmb.gif
10.1128/9781555815684/f0330-01.gif
FIGURE 2
(A) Size (in mm3) of rabbit dermal BCG lesions at various times after their onset. (B) Area of stained microvasculature in such lesions as a percentage of a 1-mm2 area of tissue section. The tissue sections were stained immunohistochemically for von Willebrand (vW) factor (a measure of the total functional microvasculature) and for the adhesion molecules ICAM-1, ELAM-1, and VCAM-1 (1) (see text). The microvasculature was evaluated only in the intact areas of the BCG lesions that were densely infiltrated with inflammatory cells. Normal skin values are shown at zero time. The means and their standard errors are shown. Note that peak levels of adhesion molecules preceded the peak size of the BCG lesions, because the upregulation of these molecules enabled the cell infiltration that caused the BCG lesions to grow in size. To produce this panel, each stained microvessel was circled with the probe of a computerized image analyzer, and its lumen was also circled. The two circled areas were subtracted to provide the area (in mm2) of the vessel wall. Then, the areas occupied by vessel walls in 1 mm2 of tissue section were computed. Reproduced with permission from reference 1. (C) Microvasculature stained for ICAM-1, ELAM-1, and VCAM-1 in BCG lesions as a percentage of a 1-mm2 area of tissue section. This panel confirms the data in panel B, with important 3-day measurements added. Note that ICAM and VCAM peaked at 3 days, suggesting that these adhesion molecules enabled the initial cell infiltration of mononuclear cells (macrophages and lymphocytes) into the BCG lesions. ELAM upregulation was more delayed. The means and their standard errors are shown. Reproduced with permission from reference 21. (D) Vasculature in BCG lesions stained for adhesion molecules as a percentage of the total functional vasculature (vW factor-stained vessels). Presenting the data in this way identifies the upregulation and downregulation of the adhesion molecules more precisely, because changes in the total functional vasculature have been factored out. The means and their standard errors are shown. Reproduced with permission from reference 1.
Citation:
Dannenberg, Jr. A.
2006.
Vascular Adhesion Molecules in Tuberculous Lesions,
p 327-338.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch21
/content/10.1128/9781555815684.ch21.ch21fig03
FIGURE 3
Areas of microvasculature stained immunohistochemically for von Willebrand (vW) factor, ICAM-1, VCAM-1, and ELAM-1, as a percentage of 1-mm2 areas of tissue sections of dermal BCG lesions during the first 5 days. The functional microvasculature (per mm2) (recognized by vW staining) and the three adhesion molecules increased much more rapidly in reinfection lesions (and in tuberculin reactions) than in primary lesions. Most of the functional microvasculature stained for ICAM, but only about half as much stained for VCAM and ELAM (compare the scales on the y axes). In the primary BCG lesions, ELAM-1 was highest at 5 days, but in the reinfection BCG lesions, ELAM was highest at 3 h. The means and their standard errors are shown. Reproduced with permission from reference 22 (where P values can be found).
10.1128/9781555815684/f0332-01_thmb.gif
10.1128/9781555815684/f0332-01.gif
FIGURE 3
Areas of microvasculature stained immunohistochemically for von Willebrand (vW) factor, ICAM-1, VCAM-1, and ELAM-1, as a percentage of 1-mm2 areas of tissue sections of dermal BCG lesions during the first 5 days. The functional microvasculature (per mm2) (recognized by vW staining) and the three adhesion molecules increased much more rapidly in reinfection lesions (and in tuberculin reactions) than in primary lesions. Most of the functional microvasculature stained for ICAM, but only about half as much stained for VCAM and ELAM (compare the scales on the y axes). In the primary BCG lesions, ELAM-1 was highest at 5 days, but in the reinfection BCG lesions, ELAM was highest at 3 h. The means and their standard errors are shown. Reproduced with permission from reference 22 (where P values can be found).
Citation:
Dannenberg, Jr. A.
2006.
Vascular Adhesion Molecules in Tuberculous Lesions,
p 327-338.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch21
/content/10.1128/9781555815684.ch21.ch21fig04
FIGURE 4
A dilated lymphatic vessel in a 1-day acute dermal inflammatory lesion produced in a rabbit by the topical application of 1% sulfur mustard (1). These lesions are markedly edematous at 1 and 2 days, but they are healed in 6 to 10 days. Note the valve in the center of the lymphatic, the nerve on the upper left of the photograph, and the capillary with three erythrocytes below. Numerous leukocytes, especially PMN, are present in the connective tissue. Lymphatics remain patent in rabbit inflammatory lesions (74). In fact, extravasated serum proteins in 1-day sulfur mustard lesions are replaced every 8 h (75). Glycol methacrylate-embedded tissue section (1 to 2 μm thick) stained with Giemsa. Magnification, ×475.
10.1128/9781555815684/f0334-01_thmb.gif
10.1128/9781555815684/f0334-01.gif
FIGURE 4
A dilated lymphatic vessel in a 1-day acute dermal inflammatory lesion produced in a rabbit by the topical application of 1% sulfur mustard (1). These lesions are markedly edematous at 1 and 2 days, but they are healed in 6 to 10 days. Note the valve in the center of the lymphatic, the nerve on the upper left of the photograph, and the capillary with three erythrocytes below. Numerous leukocytes, especially PMN, are present in the connective tissue. Lymphatics remain patent in rabbit inflammatory lesions (74). In fact, extravasated serum proteins in 1-day sulfur mustard lesions are replaced every 8 h (75). Glycol methacrylate-embedded tissue section (1 to 2 μm thick) stained with Giemsa. Magnification, ×475.
Citation:
Dannenberg, Jr. A.
2006.
Vascular Adhesion Molecules in Tuberculous Lesions,
p 327-338.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch21
/content/10.1128/9781555815684.ch21.ch21fig05
FIGURE 5
(A and B) Both photographs show a group of rather mature epithelioid cells (macrophages) surrounding a small necrotic area in a 37-day BCG lesion. The cells in panel A were immunostained for ICAM-1, whereas those in panel B were immunostained for CD11a, which is a component of LFA-1, the ligand on macrophages that binds to ICAM-1. These findings suggest that the ICAM-1–LFA-1 pair is a major contributor to the rather firm cell-cell adherence that characterizes epithelioid cells. Mouse monoclonal antibody to rabbit ICAM and CD11a, biotinylated rabbit anti-mouse IgG, counterstained with methyl green. Magnification, ×200. Reproduced with permission from reference 1.
10.1128/9781555815684/f0335-01_thmb.gif
10.1128/9781555815684/f0335-01.gif
FIGURE 5
(A and B) Both photographs show a group of rather mature epithelioid cells (macrophages) surrounding a small necrotic area in a 37-day BCG lesion. The cells in panel A were immunostained for ICAM-1, whereas those in panel B were immunostained for CD11a, which is a component of LFA-1, the ligand on macrophages that binds to ICAM-1. These findings suggest that the ICAM-1–LFA-1 pair is a major contributor to the rather firm cell-cell adherence that characterizes epithelioid cells. Mouse monoclonal antibody to rabbit ICAM and CD11a, biotinylated rabbit anti-mouse IgG, counterstained with methyl green. Magnification, ×200. Reproduced with permission from reference 1.
Citation:
Dannenberg, Jr. A.
2006.
Vascular Adhesion Molecules in Tuberculous Lesions,
p 327-338.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch21
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