A Clinicopathologic Study With Presentation of Five Cases and Review of the Literature

Callahan, William P.; Russell, William O.; Smith, Marvin E.

doi:10.1097/00005792-194612000-00001

Cited by 101 publications

(14 citation statements)

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“…LT mediate multiple important inflammatory mechanisms, including the attraction and localization of circulating neutrophils and monocytes. Of note, both neutrophils and blood monocytes readily kill T. gondii (9,15,26) but are not a prominent feature of the host inflammatory response to this infection (27). The inability of resident macrophages to generate LT during the phagocytosis of viable T. gondii would be consistent with these in vivo observations.…”

Section: Discussionsupporting

confidence: 52%

Alteration of leukotriene release by macrophages ingesting Toxoplasma gondii.

Locksley¹,

Fankhauser²,

Henderson³

1985

Proc. Natl. Acad. Sci. U.S.A.

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Mouse resident peritoneal macrophages incubated with ionophore A23187 or opsonized zymosan released leukotrienes (LT) B4 and C4 (LTB4 and LTC4) and LTC4 and LTD4, respectively. In contrast, incubation with Toxoplasma gondii, an obligate intracellular protozoan, led to the formation of 11-, 12-, and 15-hydroxyicosatetraenoic acids (HETEs), together with an unidentified compound, designated compound X. Each of these compounds incorporated [3H]arachidonic acid from the macrophage during phagocytosis of T. gondi. Compound X migrated immediately prior to 15-HETE by reversephase HPLC and was distinct from authentic monoHETE, monohydroperoxyicosatetraenoic acid (mono-HPETE), and dihydroxyicosatetraenoic acid (diHETE) standards. The generation of compound X by macrophages correlated with the extent of phagocytosis of T. gondii and with intracellular survival of the organisms. Prior antibody-coating of T. gondii or activation of macrophages, either of which inhibited survival and replication of ingested organisms, was associated with production of LTD4 but not compound X. Killed organisms also stimulated LTD4 release only. Although T. gondii concentrated arachidonic acid, they did not metabolize the compound to identifiable lipoxygenase products. Preincubation of macrophages with the relative lipoxygenase inhibitors nordihydroguaiaretic acid or 5,8,11,14-icosatetraynoic acid inhibited the formation of compound X. The absence of leukotriene production by macrophages ingesting T. gondji may explain the relative lack of a neutrophil inflammatory response in diseases due to obligate intracellular organisms. Alternatively, compound X may have functional activities that might mediate some of the host responses to cellular parasitism.The leukotrienes (LT) have been identified as potentially important inflammatory mediators of host defense (1, 2). LTB4 is a potent neutrophil chemoattractant and stimulus for aggregation, degranulation, and adherence to endothelium. The sulfidopeptide leukotrienes LTC4, LTD4, and LTE4, which collectively constitute the slow-reacting substance of anaphylaxis (SRS), promote vasoconstriction and enhance permeability across the postcapillary venule. Resident tissue macrophages are major sources of the LT (3-5). The plasma membrane of these cells is rich in esterified arachidonate that is released during membrane perturbation and is then available to Ca2+-dependent 5-lipoxygenase that regulates the formation of the LT (6, 7). Traditional stimuli for LT production by macrophages in vitro include both soluble (calcium ionophore A23187, endotoxin, phorbol myristate acetate) and particulate (zymosan, immunocomplexes) stimuli; LT production in response to the latter has been related directly to the degree of phagocytosis (3-5).Resident tissue macrophages are the initial target of many obligate intracellular pathogens that infect man, but the capacity of viable organisms to trigger the release of inflammatory mediators from macrophages has not been systematically investigated. The pathogenic protozoa...

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Section: Discussionsupporting

confidence: 52%

Alteration of leukotriene release by macrophages ingesting Toxoplasma gondii.

Locksley¹,

Fankhauser²,

Henderson³

1985

Proc. Natl. Acad. Sci. U.S.A.

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“…Many studies from the Western world have emphasized a decline in the prevalence of toxoplasmosis. Studies conducted by Eichenwald and others [13][14][15][16][17] have shown that congenital toxoplasmosis can lead to sensorineural deafness. In some studies, serologic and skin test surveys among deaf patients have suggested a cause and effect relationship, whereas in others, no such relationship has been found.…”

Section: Discussionmentioning

confidence: 99%

Toxoplasmosis and Congenital Sensorineural Hearing Loss in Saudi Arabia

Al-Amari

Kameswaran

1996

Ann Saudi Med

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“…This question cannot be answered definitively at the present time; however, several lines of evidence suggest that the mechanism described here may have an in vivo counterpart. Moderate numbers of eosinophils are found in foci of inflammation in human toxoplasmosis (47,48). Further, intraperitoneal infection of mice with Toxoplasma (2 X 103) causes an increase in peritoneal fluid eosinophils from 0.1% of total cells (1.6 x 103 eosinophils) to 9% (7.5 X 105 eosinophils) at 5 d postinfection.…”

Section: Discussionmentioning

confidence: 99%