Dirofilaria immitis: Heartworm Products Contract Rat Trachea in Vitro

Collins, Janay; Williams, J. F.; Kaiser, Lana

doi:10.1006/expr.1994.1007

Cited by 8 publications

(3 citation statements)

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“…This step may be one of the events of direct action of a protein on the epithelial cells together with the multitude of effects which are observed as a consequence of immunomodulation during acute inflammatory response. A recently reported study with heartworm (Dirofilaria immitis) products on rat tracheal smooth muscle in relation to the epithelial cells in vitro suggested that the filarial factors play a role in the pathogenesis of the disease (John et al, 1994). Earlier reports reveal that the tracheal and bronchial smooth muscle contraction is increased by the removal of epithelial cells (Barnes et ai., 1985, Flavhan et al, 1985, Munakata et al, 1989, Kaiser et ai., 1992 and that the epithelial cells exert an inhibitory effect on the smooth muscle contraction via the release of epithelium derived inhibitory factors (Inoue et al, 1986, Laitinen et al, 1985.…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively circulating filarial "shed proteins" could cause airway hyperactivity. It has been already reported that the pathogenesis of pulmonary abnormalities seen in TPE patients may be due to the circulating filarial factors (John et al, 1994). In this study we delineate the role of lung epithelial cells when exposed to these filarial shed proteins in vitro and whether there is any epithelial cell modulation in the pathophysiology of TPE.…”

Section: Introductionmentioning

confidence: 87%

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Interaction of filarial proteins on growth regulation of normal lung epithelial cells in vitro

Maya

Usha

Jayaraman

et al. 1995

Cell Biology International

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An in vitro model to examine the effects of filarial proteins on lung epithelial cells has been developed. Several of these proteins appear in circulation of infected individuals. A close association between tropical pulmonary eosinophilia (TPE) and filariasis has been reported by several workers. [3H]-thymidine studies do indicate that when optimum concentration of these filarial proteins were added to lung cultures in proliferating and basal/maintenance media a further increase in growth stimulation was observed early in culture. However, on longer exposures and at higher concentrations an inhibitory effect with distinct morphological changes were noted. The dual role of these proteins on lung epithelial cells in vitro may highlight the possibility of a direct interaction of these proteins with lung cells during disease also contributing to tissue damage.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 87%

Interaction of filarial proteins on growth regulation of normal lung epithelial cells in vitro

Maya

Usha

Jayaraman

et al. 1995

Cell Biology International

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“…A few factors produced by adult HWs depress agonist-induced, endothelium-dependent relaxations of isolated rat aorta and increase acetylcholine-induced contractions of the rat trachea in vitro [1, 5, 8, 11]. However, relaxation of the rat aorta by substances contained in HWs has not been reported.…”

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confidence: 99%

Heartworm extract induces relaxation of isolated rat thoracic aorta

Kitoh

Nakamura

Kitagawa

et al. 2017

The Journal of Veterinary Medical Science

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Isolated rat thoracic aortic strips undergoing noradrenaline-induced contraction were treated with an adult heartworm (HW) crude extract and then examined for isometric changes in tension. HW extract caused relaxation of endothelium-intact strips, but not endothelium-denuded strips. This effect was inhibited by treatment with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) and could be reversed by additional treatment with L-arginine. However, HW extract at a high concentration caused slight relaxation of endothelium-denuded strips, and relaxation persisted after L-NAME treatment in endothelium intact-strips. These data suggested that the relaxation induced by HW extract was mainly endothelium-dependent, nitric oxide-mediated, but in part, also endothelium-independent. In addition, a bioassay using isolated rat thoracic aortas may be a useful tool for investigating vasoactive substances in the HW extract.

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NECROSIS OF LUNG EPITHELIAL CELLS BY FILARIAL PARASITIC PROTEIN VIA AN EARLY INDUCTION OF c‐H‐rasAND TNFα EXPRESSION

Maya¹

1997

Cell Biology International

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The direct interaction of filarial proteins with lung epithelial cells was examined to determine the possible mechanism of inducing cell death, an event that is observed in patients with tropical pulmonary eosinophilia. Exposure of lung epithelial cells to filarial parasitic proteins, Brugia malayi (BmA), Setaria digitata (Sd), and recombinant filarial protein (pGT 7) in vitro for more than 2 days, causes the appearance of DNA fragments both in the cytoplasm and culture supernatants, while no fragmentation was observed in the untreated controls. The release of DNA fragments both in the cytoplasm and the culture supernatants simultaneously, indicates that cell death is induced by a necrotic event rather than apoptosis. Fluorescent-labelled studies also indicate the fragmentation of DNA increasing in a time-dependent manner. Normal cellular function is controlled through several oncogenes. The modulation of specific proto-oncogenes like myc, ras and TNF alpha during exposure to filarial parasitic proteins reveal elevated levels of expression of ras and TNF alpha as early as 2 hours, implicating their involvement prior to DNA fragmentation leading to pathogenesis.

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Dirofilaria immitis: Heartworm Products Contract Rat Trachea in Vitro

Cited by 8 publications

References 0 publications

Interaction of filarial proteins on growth regulation of normal lung epithelial cells in vitro

Interaction of filarial proteins on growth regulation of normal lung epithelial cells in vitro

Heartworm extract induces relaxation of isolated rat thoracic aorta

NECROSIS OF LUNG EPITHELIAL CELLS BY FILARIAL PARASITIC PROTEIN VIA AN EARLY INDUCTION OF c‐H‐rasAND TNFα EXPRESSION

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