Contribution of intracellular calcium stores to an increase in cytosolic calcium concentration induced byMannheimia haemolyticaleukotoxin

Abstract

The contribution of intracellular calcium stores to Mannheimia haemolytica leukotoxin (LKT)-induced increase in cytosolic calcium concentration was studied by pharmacologically inhibiting transport of calcium across the plasma and endoplasmic reticulum membranes of bovine neutrophils exposed to LKT. Active intracellular storage of calcium by sarcoplasmic/endoplasmic reticulum calcium ATPase, influx of extracellular calcium across the plasma membrane, and release of stored calcium via inositol triphosphate receptors and ryanodine-sensitive calcium channels were inhibited using thapsigargin, lanthanum chloride, xestospongin C, and magnesium chloride, respectively. Pre-incubation with thapsigargin attenuated the increase in cytosolic calcium concentration produced by LKT, thus confirming the involvement of intracellular calcium stores. Inhibitory effects of lanthanum chloride, xestospongin C, and magnesium chloride indicated that the increase in cytosolic calcium concentration induced by LKT resulted from both influx of calcium across the plasma membrane and release of calcium from intracellular stores.

SK3 channel and mitochondrial ROS mediate NADPH oxidase-independent NETosis induced by calcium influx

“…S2). However, the calcium ionophores also induce the release of stored calcium (43,44). Thus, it is likely that release of stored calcium leads to a partial activation of the NOX-independent pathway.…”

Actinobacillus actinomycetemcomitans leukotoxin requires lipid microdomains for target cell cytotoxicity

“…The ability of 2‐APB (Bootman et al ., 2002), a reliable blocker of store‐operated Ca 2+ pathways, to inhibit these increases (Fig. 3C) reinforces this premise and is consistent with observations made with other RTX toxins (Uhlen et al ., 2000; Cudd et al ., 2003). The fact that Ltx stimulates [Ca 2+ ] c elevations of equal magnitudes in both toxin‐sensitive cells, such as wild‐type Jn.9 and LFA‐1‐reconstituted Jβ2.7/hCD11a cells, and the toxin‐resistant Jβ2.7 cells (Fig.…”

Functional Consequences of Calcium Influx Promoted by Bacterial Pore-Forming Toxins

“…For intracellular bacteria, pore formation and ion flux can also occur within the phagosome [ 6 ]. Other mechanisms have been described, such as the activation of endogenous ion channels, either located in the plasma membrane or in organelles accumulating Ca 2+ , like the endoplasmic reticulum (ER) and lysosomes ( Figure 1 ) [ 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 ].…”