In vitro TNF, IL-6 and IL-2 production by rat milk cells following Trichinella spiralis infection

Trichinella spiralis-specific immunity can be transferred from immune mothers to suckling neonates via lactation, suggesting that milk from immune dams contains specific factors to T. spiralis. TNF and IL-6 are important cytokines in inflammatory processes, and IL-2 is essential in lymphocyte activa...

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Veröffentlicht in:Journal of reproductive immunology 1993-11, Vol.25 (2), p.119-131
Hauptverfasser: Na, Hyung R., Seelig, Leonard L.
Format: Artikel
Sprache:eng
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Zusammenfassung:Trichinella spiralis-specific immunity can be transferred from immune mothers to suckling neonates via lactation, suggesting that milk from immune dams contains specific factors to T. spiralis. TNF and IL-6 are important cytokines in inflammatory processes, and IL-2 is essential in lymphocyte activation. Using cell line bioassays, we examined the capacity of rat milk mononuclear cells from immune and non-immune control dams to produce these cytokines following in vitro stimulation with mitogens or T. spiralis antigen. Milk cells were capable of producing IL-2, IL-6 and TNF upon Con A stimulation, and TNF and IL-6 upon LPS stimulation. The amount of these cytokines produced by mitogen-stimulated milk cells from T. spiralis-infected rats was similar to that produced by non-infected controls, although lower than that of corresponding blood mononuclear cells. Upon stimulation with T. spiralis antigen, milk cells from infected rats produced a significantly higher amount of TNF (158 ± 39U/10 6 cells) compared to non-infected controls (16 ± 6 U/10 6 cells, P < 0.01), and also higher than that of the corresponding blood cells (60 ± 10 U/10 6 cells, P < 0.01). Only small amounts of IL-6 and no IL-2 was secreted by milk cells from control or infected groups after stimulation with antigen. This study shows that rat milk cells are capable of synthesizing cytokines, and TNF produced by immune mothers may play a role in augmenting the neonate resistance to T. spiralis infection.
ISSN:0165-0378
1872-7603
DOI:10.1016/0165-0378(93)90053-K