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Defective production of reactive oxygen intermediates (ROI) in a patient with recurrent amebic liver abscess
Patricia Morán1, Guadalupe Rico, Manuel Ramiro
1Departamento de Medicina Experimental, Facultad de Medicina, UNAM, México, DF México.
Abstract:
Previously, we reported the case of a man in the fourth decade of life afflicted with three independent episodes of amebic liver abscesses over a period of 4 years. Previous evidence has indicated that the cellular immune response is involved in protection against recurrent invasive amebic infection, and macrophage-mediated effector mechanisms appear important for host resistance to Entamoeba histolytica infection. The aim of the present work was to investigate locomotor activity and oxidative burst function of peripheral mononuclear cells of this individual after healing of the third amebic liver abscess. A locomotion assay using Boyden chemotaxis chambers and the respiratory burst evaluated by chemiluminescence were performed in both mononuclear phagocytes (MPs) and polymorphonuclear (PMN) leukocytes. Levels of salivary IgA and serum IgG anti-amebic antibodies were followed during 48 months after the second amebic liver abscess. Results obtained showed a deficiency in MP but not in PMN leukocyte respiratory burst. Respiratory burst is a major microbicidal mechanism in MP leukocytes; this also has been considered as a host resistance strategy against E. histolytica. It may be at least one risk factor in our patient that was responsible for recurrence of amebic liver abscess.
Insights
A patient with recurrent amebic liver abscesses showed a deficiency in mononuclear phagocyte respiratory burst function. This cellular immune defect may explain the repeated Entamoeba histolytica infections.
Area of Science:
- Immunology
- Infectious Diseases
Background:
- Recurrent invasive amebic infections highlight the importance of cellular immunity.
- Macrophage-mediated mechanisms are crucial for host resistance against Entamoeba histolytica.
Observation:
- This study investigated the immune cell function in a patient with three amebic liver abscesses over four years.
- Locomotor activity and oxidative burst function of peripheral mononuclear cells were assessed post-recovery from the third abscess.
Findings:
- A significant deficiency was observed in the respiratory burst function of mononuclear phagocytes (MPs), but not polymorphonuclear (PMN) leukocytes.
- The respiratory burst in MPs is a key microbicidal mechanism and a host resistance strategy against E. histolytica.
Implications:
- The identified MP respiratory burst deficiency may be a contributing risk factor for the patient's recurrent amebic liver abscesses.
- Understanding specific immune deficiencies can guide strategies for managing recurrent parasitic infections.
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