Killing of Mycobacterium tuberculosis by neutrophils: a nonoxidative process

Article Abstract:

Mycobacterium tuberculosis is the causative agent of tuberculosis in humans. M. tuberculosis lives and replicates inside macrophage cells (cells of the immune system that engulf or ingest invading organisms). When a macrophage becomes activated (in response to an invading organism) it releases reactive metabolites of oxygen, also called oxygen radicals (highly reactive atoms with unpaired electrons). Previous studies have suggested that oxygen radicals may be involved in the killing of M. tuberculosis by macrophage cells. However, other studies have shown that M. tuberculosis is resistant to oxygen radicals. During M. tuberculosis infection, neutrophils (white blood cells) are the first cells to become activated. They migrate to the site of infection and activate macrophage cells. The neutrophils have an oxidative burst that releases reactive metabolites of oxygen into the surrounding tissue. In vitro (culture), neutrophils have been shown to kill M. tuberculosis. Therefore, studies were performed to determine if oxygen radicals play a role in the killing of M. tuberculosis by neutrophils. Catalase, superoxide dismutase, taurine, deferoxamine and histidine are inhibitors of oxygen radicals. These compounds were tested for their ability to prevent neutrophils from killing M. tuberculosis. None of the oxygen radical inhibitors prevented the neutrophils from killing M. tuberculosis. Neutrophils from patients with chronic granulomatous disease (CGD) do not generate oxygen radicals. Neutrophils isolated from patients with CGD were effective in killing M. tuberculosis. These findings indicate that oxygen radicals do not play a role in the killing of M. tuberculosis by neutrophils. (Consumer Summary produced by Reliance Medical Information, Inc.)

Mycobacterium tuberculosis, Active oxygen, Active oxygen in the body

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Fungistatic activity of human neutrophils against Histoplasma capsulatum: correlation with phagocytosis

Article Abstract:

Histoplasma capsulatum is a parasitic fungus that causes histoplasmosis, a fungal respiratory disease. This disease is characterized by inflammation of the airways and lungs, and accumulation of polymorphonuclear leukocytes (PMNL), a type of white blood cell, and macrophages, a type of natural defense cell. PMNLs may act to wall off the fungal infection, thereby preventing its spread to other areas of the body. The mechanisms of resistance to H. capsulatum are not known. PMNLs and macrophages do not have the ability to kill H. capsulatum. The incidence of histoplasmosis is increased in patients with AIDS, suggesting that resistance to H. capsulatum may require an intact immune system. The effects of PMNL on H. capsulatum were assessed. The results showed that PMNL were effective in killing Candida albicans, a type of yeast, but not H. capsulatum. PMNL did not reduce the number of H. capsulatum colonies, or fungal aggregations, but did prevent further increases in the growth of this fungus, as measured at 24 and 72 hours. PMNL phagocytosed (digested) 81.3 percent of the yeast cells. Prevention of fungal growth by PMNL persisted despite deterioration of PMNL and was related to the numbers of PMNLs. (Consumer Summary produced by Reliance Medical Information, Inc.)

Evaluation, Mycoses

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Clinical prediction model for differentiation of disseminated Histoplasma capsulatum and Mycobacterium avium complex infections in febrile patients with AIDS

Article Abstract:

Blood levels of lactate dehydrogenase, alkaline phosphatase, and white blood cells can be used to distinguish disseminated histoplasmosis from Mycobacterium avium complex in AIDS patients. This was the conclusion of a study of 90 AIDS patients.

Diagnosis, Complications and side effects, AIDS (Disease), Mycobacterial infections, Mycobacterium infections

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