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Neutrophil gelatinase-associated lipocalin (NGAL) has recently been identified in myeloperoxidase-negative neutrophil granules. Members of the lipocalin family are thought to bind and transport small lipophilic molecules such as retinoids and roles in cell regulation have been proposed. Recently, NGAL has also been demonstrated in the colonic mucosa in certain pathologic conditions. The aim of this study was to examine the distribution of NGAL in normal and neoplastic tissues by immunohistochemistry. Interestingly, NGAL was found in a variety of normal and pathological human tissues. A cell type-specific pattern of expression was seen in bronchus, stomach, small intestine, pancreas, kidney, prostate gland, and thymus. The comparative analysis of the putative rat homologue neu-related lipocalin showed a very similar pattern of expression with the exception of pancreas and kidney. Neoplastic human tissues showed a very heterogeneous expression of NGAL protein. High NGAL levels were found in adenocarcinomas of lung, colon and pancreas. In contrast, renal cell carcinomas of various subtypes and prostate cancers contained low NGAL levels. Lymphomas and thymic tumours were negative for NGAL immuno-labeling. Knowledge about the location of NGAL in normal cells and in disease states provides the first clues towards understanding its biological function.

When Schistosoma mansoni miracidia penetrate resistant individuals of the intermediate host snail Biomphalaria glabrata, the sporocyst is encapsulated by hemocytes (macrophagelike cells of the snail circulation) and killed. In our in vitro model the same fate requires only sporocysts and snail hemolymph. However, when cultured in plasma alone (cell-free hemolymph), sporocysts remain viable for more than 3 days, regardless of whether the plasma is from susceptible or resistant snails. When hemolymph is used from susceptible snails, the sporocysts retain a normal healthy appearance. Furthermore, the parasite appears to express an offensive response to the hemocytes of susceptible snails. Ultrastructural study reveals that resistant-strain hemocytes destroy the parasite tegument; within 24 hr the sporocyst is damaged severely throughout. This cell-mediated, internal, defensive response of an invertebrate host closely resembles antibody-dependent, cell-mediated damage to schistosomula in mammalian hosts.

Dynamic aspects of the cellular responses of juvenile (2-3 mm shell diameter) 10-R2 strain Biomphalaria glabrata to newly penetrated Schistosoma mansoni (NIH-Sm-PR-1 strain) were studied at the ultrastructural level. As early as 3 hr postexposure (PE), host hemocytes had contacted the parasite's surface and by 7.5 hr, had phagocytosed sporocyst microvilli and small pieces of underlying tegument. Most sporocysts observed at 24 hr PE lacked tegumental cytoplasm, and germinal cells and other internal structures showed extensive pathological changes. By 48 hr, capsules were filled with hemocytes containing numerous, large phagosomes, and only scattered remnants of sporocyst material remained. Capsules were difficult to find at 4 days PE, suggesting that hemocytes participating in the encapsulation response had dispersed. Hemocytes responsible for the rapid and consistent destruction of S. mansoni sporocysts in the head-foot region typically formed extensive pseudopodia and contained large numbers of lysosomelike bodies, characteristics associated with granulocytes of B. glabrata. No evidence was found to suggest that hemocytes were lysed, or formed multinuclear syncytia, during the encapsulation response.

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