Comment on “Some immunomodulatory effects of probiotic bacteria might be due to porcine neutrophil elastase inhibitor, a serpin present in MRS broth” [Immunol. Lett. (December) (in press) 1]

Foligné, Benoît; Pot, Bruno

doi:10.1016/j.imlet.2009.01.006

Cited by 1 publication

(1 citation statement)

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“…Kv1.3 has an immunoregulatory function and is an important factor in regulating the activity and differentiation of T cells [11] . Blocking Kv1.3 can inhibit Ca 2+ signaling, T cell proliferation, and IL-2 secretion [12,13] . While the role of the Kv1.3 channel has been established in regulating T cell function, few studies have examined its role in macrophages.…”

Section: Discussionmentioning

confidence: 99%

Blockage of Kv1.3 regulates macrophage migration in acute liver injury by targeting δ-catenin through RhoA signaling

Liu

Bian

et al. 2020

Int. J. Biol. Sci.

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Background: Activation of macrophages and infiltration are key events in acute liver injury (ALI). Kv1.3 plays an important role in regulating immunologic functions of macrophages and is extensively recognized as a potential ion channel for immunological diseases. Objective: We hypothesized that blockage of Kv1.3 may influence ALI by inhibiting macrophages infiltration in damaged liver tissues. Methods: Margatoxin was administered into the peritoneal cavity of ALI mice. The impact of this treatment on ALI and macrophage migration in vivo and in vitro was determined using immunohistochemistry, transwell migration, and wound healing assays. Results: MgTX treatment alleviated ALI in mice, as evidenced by reduced macrophage infiltration in liver tissues and lower serum levels of liver ALT and AST. RNA-seq profiling analysis showed that the most obvious change by MgTX treatment was downregulation of δ-catenin, a protein known to be associated with macrophage migration. The effect of MgTX on macrophage migration and involvement of δ-catenin was confirmed by transwell and wound healing assays. Overexpression of δ-catenin in RAW264.7 cells promoted migration, an event that was suppressed upon silencing of δ-catenin. Mechanistically, the expression of RhoA was regulated by the overexpression or knockdown of δ-catenin. Conclusion: These findings suggest a role for blockage of Kv1.3 channel in macrophage migration and reveal a new target in the treatment of ALI.

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Section: Discussionmentioning

confidence: 99%