Increased Survival of Swiss Mice Given Sublethal Infections of Trichinella spiralis

Weatherly, Norman F.

doi:10.2307/3277722

Cited by 52 publications

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“…In addition, tumour patients which responded to radiation therapy with a blood eosinophilia [444,445] showed double the median survival of those who did not [445]. Also, the incidence of naturally-occurring mammary tumours in mice was reduced when they developed an eosinophilia following infection with Trichinella spiralis [446]. Furthermore, development of sarcoma was completely suppressed in rats infected with Nippostrongulus brasiliensis, five days before tumour inoculation [447].…”

Section: Bronchogenic Tumoursmentioning

confidence: 99%

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part II)

Kroegel¹,

Warner²,

Jc³

et al. 1994

Eur Respir J

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The second part of this review on eosinophils focuses on biological cell functions and surveys the various deleterious mechanisms involved in the eosinophil-dominated inflammatory reaction. It discusses the possible pathogenic role of eosinophils in several eosinophil-related diseases, such as parasitic infections, interstitial lung disorders and bronchial diseases, graft rejection, vasculitic granulomatous disorders, pleural effusion, and bronchogenic tumours.The final section of the article highlights the possible recent pharmacological and future therapeutic approaches in modifying eosinophil recruitment and function. Eur Respir J., 1994, 7, 743-760 This paper is published as a follow-on to "Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)"* (Eur Respir J, 1994; 7: 519-543). Biological cell functionsThe eosinophil mediates its effector functions through various distinct cellular mechanisms, namely nonoxidative, oxidative, and humoral mechanisms ( fig. 7). Nonoxidative mechanismsAs mentioned previously, the three basic proteins as well as eosinophil peroxidase (EPO) have toxic properties independent of molecular oxygen species. For instance, major basic protein (MBP) [323], eosinophil cationic protein (ECP) [324] and EPO in the presence of hydrogen superoxide and a halide [99] kill helminthic parasites in vitro. In addition, these proteins are toxic for tumour cells and/or mammalian cells [325], including human pulmonary parenchyma and interstitial matrix [326,327], cultured human lung epithelial cells [328], and guinea-pig respiratory epithelium [252, 253,329]. Furthermore, it has been demonstrated that MBP damages human bronchial epithelium, which consists of desquamation and destruction of ciliated cells [329]. Finally, release of their granule proteins by plateletactivating factor (PAF)-activated intact eosinophils has been shown to imitate the characteristic pathological findings of airway epithelium in asthma [330].In addition to their cytotoxic action, eosinophil cationic proteins at certain subtoxic concentrations also stimulate other inflammatory cells. For instance, MBP and ECP have been shown to degranulate platelets [305], induce histamine release from mast cells and basophils [240, 245,331], as well as superoxide anion generation and lysosomal enzyme release by human neutrophils [264].Finally, eosinophil proteins may affect airway muscle function and hyperresponsiveness. Recent reports investigating the effects of direct intratracheal instillation of purified eosinophil granule proteins on pulmonary function and airway responsiveness in primates [281,332] have shown that MBP induces a dose-related increase in airway responsiveness to inhaled methacholine. In the same model, both MBP and EPO caused a transient bronchoconstriction immediately after instillation, that resolved within 1 h. Interestingly, other eosinophil granular proteins failed to effect airway responsiveness or pulmonary function.Mode of action. The mode of action of these basic proteins is n...

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Section: Bronchogenic Tumoursmentioning

confidence: 99%

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part II)

Kroegel¹,

Warner²,

Jc³

et al. 1994

Eur Respir J

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“…In the T. spiralis system, infection with this nematode was shown to prolong the mean survival time of Swiss mice that were subsequently chal lenged with Sarcoma-180 (S-180) ascites tu mors [13]. In addition, Weatherly [16] found that mulliparous, female SW mice be came markedly resistant to the development of spontaneous mammary neoplasia after natural infection with T. spiralis. In this re spect, the nematode appeared to act in a manner similar to other nonspecific stimu lants of the lymphoid system, such as BCG and Corynebacterium parvum.…”

Section: Introductionmentioning

confidence: 99%

Antineoplastic Effects of Long-Term <i>Trichinella spiralis</i> Infection on B-16 Melanoma

Molinari

Ebersole

1977

Int Arch Allergy Immunol

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Oral infection of mice with Trichinella spiralis has been shown to induce a potentiation of the delayed hypersensitive (DTH) response to BCG. The present investigation was initiated to determine whether nematode-induced potentiation of DTH influenced the induction and progression of a transplantable mouse tumor. B6D2F1/J mice were orally infected with 200 T. spiralis larvae 176 days preceding subcutaneous administration of 5 × 10⁵ viable B-16 melanoma cells. The antineoplastic effects of long-term nematode infection were assessed by daily observation of the animals monitoring development and progression of neoplastic nodules. Control mice developed tumors by day 28 following tumor challenge, while none of the corresponding T. spiralis-infected animals demonstrated any signs of neoplasia. All control mice died within 60 days, while none of the nematode-infected animals developed detectable neoplasms. This phenomenon suggested that the presence of well-established larval cysts was capable of stimulating host antineoplastic activity.

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“…Infections caused by certain intracellular parasites and bacteria are associated with increased resistance to tumor growth [4, 10, Brulev-Rosset/F lorentin/Kj u l il /M athe 595 11,15,27,28] and the macrophages from these infected animals can kill, nonspecifically, tumor cells in vitro [12]. The in vitro cytopathic activities of macrophages can be increased by nonspecific stimulants of the monon uclear phagocyte cell system: BCG [8,21], complete Freund's adjuvant [13], peptone [17], Corynebacterium parvum [9,23], and poly I:C [16].…”

Section: Introductionmentioning

confidence: 99%

Nonspecific Macrophage Activation by Systemic Adjuvants

Bruley-Rosset¹,

Florentin²,

Khalil³

et al. 1976

Int Arch Allergy Immunol

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Six systemic adjuvants: living bacillus Calmette-Guérin (BCG), hydrosoluble extracts from BCG and from Mycobacterium smegmatis, bacterial lipopolysaccharide, lentinan and levamisole, have been tested for their ability to induce macrophage activation in mice. The first four adjuvants mentioned increase phosphatase activity of peritoneal macrophages and make them nonspecifically cytotoxic for tumor cells in vitro. The intensity of these phenomena vary with route and time of administration. In contrast, lentinan and levamisole depress both these macrophage activities. Living BCG, extracts from BCG and from M. smegmatis, and the lipopolysaccharide increase the cytotoxic potential of normal macrophages in vitro, suggesting that these agents may exert a direct action on macrophages. Levamisole did not activate normal macrophages in vitro. The existence of a correlation between the capacity of adjuvants to stimulate macrophage tumoricidal activity and their efficiency in active cancer immunotherapy is discussed.

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Increased Survival of Swiss Mice Given Sublethal Infections of Trichinella spiralis

Cited by 52 publications

References 0 publications

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part II)

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part II)

Antineoplastic Effects of Long-Term <i>Trichinella spiralis</i> Infection on B-16 Melanoma

Nonspecific Macrophage Activation by Systemic Adjuvants

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