Pneumocystis carinii induces an oxidative burst in alveolar macrophages

Abstract

There is evidence that alveolar macrophages (AM) play a role in the clearing of Pneumocystis carinii from the lungs. To investigate the mechanisms involved in this process, we studied in vitro the induction of an oxidative burst by P. carinii in a cell line of macrophages (NR8383) and AM from normal rats. P. carinui was added to macrophage monolayers (106 cells), and the H202 produced after 4 h of incubation was measured. Both NR8383 macrophages and normal rat AM produced H202 in response to P. carinii cysts and trophozoites isolated from dexamethasone-treated rats, although the amount of H202 induced in AM from normal rats was larger. NR8383 macrophages bound and phagocytized both P. carinii cysts and trophozoites and produced increasing amounts of H202 as a dose-related response to cysts and trophozoites. Opsonization ofP. carinii with normal rat serum increased H202 production by both types of macrophages; this enhancement was decreased, but not abolished, when the serum was first depleted of complement by heat treatment. These findings demonstrate that NR8383 macrophages and normal rat AM produce an oxidative burst in response to P. carinii and that this response is enhanced by complement.

Pneumocystis carinii-induced activation of the respiratory burst in human monocytes and macrophages

“…and through an increased potential of supcroxidc production, since the PMA response was also increased in IFN--,treated cells. The ability of macrophages to activate the respiratory burst when challenged with pneumocysts is in agreement with the findings of Hidalgo et ai [6] and Taylor ct al. [5], who used a macrophage cell line and alveolar macrophages from rats and rat serum for opsonization.…”

“…is known to be important for the ability of phagocytic cells to kill ingested microorganisms. Previous studies, using chemoluminescence or peroxidase assay for HiO; determination, showed that pneumocysts were able to activate the respiratory burst in rat macrophages and a macrophage cell line [5,6]. We have studied the ability of human monocytes and monocyte-derived maerophages to produee Oi , when stimulated with P. carinii.…”

Alveolar Macrophage–mediated Killing of Pneumocystis carinii f. sp. muris Involves Molecular Recognition by the Dectin-1 β-Glucan Receptor

“…Nevertheless, previous studies have reported a role for both reactive oxygen species in the killing of P. carinii. Some reports have shown that both hydrogen peroxide and superoxide are directly toxic to P. carinii (12)(13)(14). Furthermore, studies have shown that P. carinii can elicit an oxidative burst of both hydrogen peroxide and superoxide from macrophages (12,13).…”

Interleukin 1: an important mediator of host resistance against Pneumocystis carinii.

“…II.-1 elicits local accumulation and activation of inflammatory cells (8,11,21). These cells are considered important in host defenses against P. carinii (3,4,6,(22)(23)(24)(25)(26) and, indeed, reconstitution of P. carinii-infected SCID mice with immunocompetent spleen cells induces significant recruitment of inflammatory cells into bronchoalveolar lumina (3,5). The effect of 35F5 treatment on pulmonary inflammation in reconstituted SCID mice was therefore investigated.…”