Effects of Activated Macrophages on Nocardia asteroides

Abstract

The mechanism(s) of host resistance against Nocardia asteroides has not been well defined. Since disease due to N. asteroides frequently occurs in patients with impaired cell-mediated immunity, we studied the interaction of N. asteroides with activated and control mouse peritoneal macrophages. Activated macrophages were from mice infected with Toxoplasma gondii or injected with Corynebacterium parvum. N. asteroides in the early stationary phase (>99% in the coccobacillary form) was used for challenge of macrophage monolayers. Growth of two strains of N. asteroides was markedly inhibited in activated macrophages, whereas N. asteroides grew well in control macrophages. Quantitation of macrophage-associated N. asteroides indicated that activated macrophages killed 40 to 50% of N. asteroides within 6 h ( P < 0.002). In control macrophage preparations, it appeared as if Nocardia filaments extended from within macrophages to the outside, and many of these filaments appeared to have extended to and then grown through neighboring macrophages. In activated macrophage preparations, Nocardia remained in the coccobacillary form in most macrophages. Control macrophage monolayers were almost completely overgrown with and destroyed by Nocardia 20 h after challenge, whereas activated macrophage monolayers remained intact. Nocardia that grew in control macrophages were not acid-alcohol fast or only weakly so, whereas the few Nocardia that grew in activated macrophages were strongly acid-alcohol fast. Our results indicate that activated macrophages may be important in host defense against N. asteroides.

Nocardiosis cerebral parvosintomática, en pacientes inmunocomprometidos

“…Así mismo dentro de los fagocitos, es capaz de resistir los mecanismos deletéreos dependientes de oxígeno, debido a catalasas y superóxido-dismutasas que expresa 1 . Ciertas cepas bacteriales son capaces de liberarse de los macrófagos y reactivarse 30 . Dos mecanismos de sobrevivencia como la capacidad de transformarse a formas-L y la de metabolizar la fosfatasa ácida lisosomal como fuente de carbono, parecieran estar involucrados en la permanencia de las bacterias en el huésped por tiempo indefinido 1 .…”

Role of L-forms of Nocardia caviae in the development of chronic mycetomas in normal and immunodeficient murine models

“…The data suggested that as N. caviae grew within the host during the early stages of infection there was a cell-mediated response that involved T-lymphocytes, macrophages, and polymorphonuclear leukocytes that could effectively inhibit the growth of the organism. The organisms that were thus contained were gradually stripped of their cell wall, probably by the interaction of highly activated macrophages (8,15,16). The resulting protoplasts or spheroplasts appeared to be refractile to the milieu of degradative enzymes that were released, and the cells survived within certain tissues.…”

Isolation and purification of two immunodominant antigens from Nocardia brasiliensis

“…Nocardia asteroides also produces mycetoma and is the main etiologic agent of pulmonary nocardiosis, which causes about 500 to 1,000 cases per year in the United States (4,22). Although the pathogenic mechanisms of nocardial infections have not been completely elucidated, some authors have reported experiments indicating that the cellular immune response plays an important role in resistance (10,12). The role of the humoral immune response in nocardial infections is not well known, although some authors have observed that antibody production is associated with worsening lesions (18).…”