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Lesional modulation of peripheral monocyte leucotactic responsiveness in leprosy
P B Campbell1, T A Tolson, L Yoder
1Department of Medicine, School of Medicine, East Carolina University, Greenville, North Carolina 27858-4354.
Abstract:
Because the accumulation and activation of mononuclear phagocytes are critical to the host response to intracellular microbial pathogens, we evaluated mechanisms of peripheral monocyte leucotactic regulation in leprosy. Plasma from 53 of 67 patients was found to inhibit the locomotion of normal human monocytes. Neither the prevalence nor the magnitude of plasma leucotactic inhibitory activity correlated with disease histology or duration, type or duration of chemotherapy, or history of erythema nodosum leprosum. Plasma leucotactic inhibitory activity resided principally in a non-immunoglobulin, cell-directed inhibitor of 230,000 daltons molecular weight. Fractionation of plasma from patients with lepromatous leprosy revealed an additional, immunoglobulin-containing inhibitor of approximately 400,000 daltons weight, possibly an IgG-IgA immune complex. Production of leucotactic inhibitors by unstimulated and concanavalin A-stimulated peripheral mononuclear cells was normal; however, cutaneous explants from these patients spontaneously produced the 230,000 dalton leucotactic inhibitor in vitro. The ability of the lesions of leprosy to impede monocyte traffic may be an important pathogenetic mechanism.
Insights
Leprosy patients exhibit plasma factors that inhibit monocyte movement, crucial for fighting infection. Lesions in leprosy patients may impede monocyte migration, contributing to disease development.
Area of Science:
- Immunology
- Cell Biology
- Pathogenesis
Background:
- Mononuclear phagocyte accumulation and activation are vital for host defense against intracellular pathogens.
- Understanding monocyte regulation is key to understanding host response in infectious diseases like leprosy.
Purpose of the Study:
- To investigate the mechanisms regulating peripheral monocyte chemotaxis in leprosy patients.
- To identify factors in leprosy patients' plasma that affect monocyte locomotion.
Main Methods:
- Assessed plasma leucotactic inhibitory activity in leprosy patients.
- Fractionated plasma to identify the molecular weight and nature of inhibitors.
- Evaluated leucotactic inhibitor production by peripheral mononuclear cells and cutaneous explants.
Main Results:
- Plasma from a majority of leprosy patients inhibited normal human monocyte locomotion.
- Inhibitory activity did not correlate with disease characteristics or treatment.
- A 230,000 dalton non-immunoglobulin inhibitor was identified, and a 400,000 dalton immunoglobulin-containing inhibitor was found in lepromatous leprosy.
- Cutaneous explants from patients spontaneously produced the 230,000 dalton inhibitor.
Conclusions:
- Leprosy lesions may impede monocyte traffic, suggesting a role in disease pathogenesis.
- Specific leucotactic inhibitors in leprosy patients' plasma and lesions contribute to altered monocyte function.
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