Surfactant Protein D-Mediated Aggregation of Pneumocystis carinii Impairs Phagocytosis by Alveolar Macrophages

Surfactant protein D-mediated aggregation of Pneumocystis carinii impairs phagocytosis by alveolar macrophages.

Pneumocystis carinii remains an important and potentially fatal cause of opportunistic pneumonia. Animal studies reveal that substantial quantities of surfactant protein D (SP-D) accumulate in the airspaces during P. carinii pneumonia and are particularly abundant in aggregates of organisms. Due to the multimeric structure of SP-D, we hypothesized that SP-D mediates aggregation of the organism....

Surfactant protein D interacts with Pneumocystis carinii and mediates organism adherence to alveolar macrophages.

Pneumocystis carinii interacts with glycoproteins present in the lower respiratory tract through its mannose-rich surface antigen complex termed gpA. Surfactant protein D (SP-D) is a recently described component of the airspace lining material that possesses a calcium-dependent lectin domain capable of interacting with glycoconjugates present on microorganisms and leukocytes. Accordingly, we ev...

Degradation of surfactant protein D by alveolar macrophages.

Surfactant protein (SP) D is a pulmonary surfactant-associated protein that may function in lung host defense. SP-D is produced by alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells of the airway and is secreted into the air space. Here we investigated whether alveolar macrophages degraded SP-D in vitro. We also examined the effects of SP-A and lipids on SP-D metabolism...

HIV impairs alveolar macrophage mannose receptor function against Pneumocystis carinii.

Mechanism of Pneumocystis carinii attachment to cultured rat alveolar macrophages.

Pneumocystis carinii (PC) pneumonia begins as an intra-alveolar process resulting in injury to the alveolar epithelium with subsequent invasion of the lung interstitium. The clearance of PC organisms from the alveolar space is a critical function of alveolar macrophages (AM), the resident alveolar phagocytic cells. In this study the mechanism of PC attachment to AM was determined using 51Cr-lab...