Effects of Hyperthermia on Intracellular Chloride

Amorino, George P.; Fox, Michael H.

doi:10.1007/s002329900099

Cited by 15 publications

(4 citation statements)

References 29 publications

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“…Sodium absorption from the apical membrane of cells is regulated by various ion channels, including a basolateral potassium channel, a Na + /K + /2Cl co-transporter and Na + /K + -ATPase [24, 30]. Intracellular free sodium levels induce sodium transport outside of cells across the basolateral membrane [24] and regulate membrane integrity [25], whereas high temperature decreases intracellular free sodium levels [31]. Therefore, these effects of high temperature may be associated with the decreased in the number of domes formed on cell monolayers.…”

Section: Discussionmentioning

confidence: 99%

Effects of high temperature on pandemic and seasonal human influenza viral replication and infection-induced damage in primary human tracheal epithelial cell cultures

Yamaya

Nishimura

Kalonji

et al. 2019

Heliyon

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High temperature reduces influenza viral replication; however, the treatment of fevers is thought to be necessary to improve patients' conditions. We examined the effects of high temperature on viral replication and infection-induced damage to human tracheal epithelial cells. Cell viability and dome formation were reduced, the number of detached cells was increased and lactate dehydrogenase (LDH) levels tended to be increased from 72 h to 120 h in uninfected cells cultured at 40 °C. Long-term (72 h and/or 120 h) exposure to high temperatures (39 °C and/or 40 °C) decreased RNA levels and/or viral titers of eight influenza virus strains. Cell viability and dome formation were reduced, and the number of detached cells and LDH levels were increased to a similar extent after infection with the A/H1N1 pdm 2009 virus at 37 °C and 40 °C. High temperature increased the endosomal pH, where the viral RNA enters the cytoplasm, in uninfected cells. High temperature reduced the production of IL-6, which mediate viral replication processes, and IL-1β and IL-8 in uninfected and infected cells. Based on these findings, high temperature may cause similar levels of airway cell damage after infection to cells exposed normal temperatures, although high temperature reduces viral replication by affecting the function of acidic endosomes and inhibiting IL-6-mediated processes.

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Section: Discussionmentioning

confidence: 99%

Effects of high temperature on pandemic and seasonal human influenza viral replication and infection-induced damage in primary human tracheal epithelial cell cultures

Yamaya

Nishimura

Kalonji

et al. 2019

Heliyon

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“…Thus we can normalize the intracellular MQAE concentration by using the EV, even if the cell volume is changed during [Cl Ϫ ] i measurement period. Until now, MQAE is reported to be used to monitor [Cl Ϫ ] i changes in CHO cells by using a fluorescence/forward angle light scatter (FALS) to normalize the dye content (2). The data from FALS are obtained in a laser flow cytometry for identification of cell populations based on their approximate size and granularity.…”

Section: Discussionmentioning

confidence: 99%

Physiological significance of hypotonicity-induced regulatory volume decrease: reduction in intracellular Cl⁻concentration acting as an intracellular signaling

Mitsuya

Shiozaki²,

Niisato³

et al. 2007

American Journal of Physiology-Renal Physiology

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Regulatory volume decrease (RVD) occurs after hypotonicity-caused cell swelling. RVD is caused by activation of ion channels and transporters, which cause effluxes of K(+), Cl(-), and H(2)O, leading to cell shrinkage. Recently, we showed that hypotonicity stimulated transepithelial Na(+) reabsorption via elevation of epithelial Na(+) channel (alpha-ENaC) expression in renal epithelia A6 cells in an RVD-dependent manner and that reduction of intracellular Cl(-) concentration ([Cl(-)](i)) stimulated the Na(+) reabsorption. These suggest that RVD would reveal its stimulatory action on the Na(+) reabsorption by reducing [Cl(-)](i). However, the reduction of [Cl(-)](i) during RVD has not been definitely analyzed due to technical difficulties involved in halide-sensitive fluorescent dyes. In the present study, we developed a new method for the measurement of [Cl(-)](i) change during RVD by using a high-resolution flow cytometer with a halide-specific fluorescent dye, N-(6-methoxyquinolyl) acetoethyl ester. The [Cl(-)](i) in A6 cells in an isotonic medium was 43.6 +/- 3.1 mM. After hypotonic shock (268 to 134 mosmol/kgH(2)O), a rapid increase of cell volume followed by RVD occurred. The RVD caused drastic diminution of [Cl(-)](i) from 43.6 to 10.8 mM. Under an RVD-blocked condition with NPPB (Cl(-) channel blocker) or quinine (K(+) channel blocker), we did not detect the reduction of [Cl(-)](i). Based on these observations, we conclude that one of the physiological significances of RVD is the reduction of [Cl(-)](i) and that RVD shows its action via reduction of [Cl(-)](i) acting as an intracellular signal regulating cellular physiological functions.

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“…Data were analyzed using CellQuest software. The intracellular Cl Ϫ concentration was measured using MQAE (2). Red blood cells (2 ϫ 10 6 /ml in RPMI 1640) were loaded at 5 mM at 37°C for 2 h and washed three times with RPMI 1640.…”

Section: Methodsmentioning

confidence: 99%

Hemolysis of Erythrocytes by Granulysin-Derived Peptides but Not by Granulysin

Dong

Deng

et al. 2005

Antimicrob Agents Chemother

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Granulysin, a 9-kDa protein localized in human cytolytic T lymphoctyes and natural killer cell granules, is cytolytic against tumors and microbes but not against red blood cells. Synthetic peptides corresponding to the central region of granulysin recapitulate the lytic activity of the intact molecule, and some peptides cause hemolysis of red blood cells. Peptides in which cysteine residues were replaced by serine maintain their activity against microbes but lose activity against human cells, suggesting their potential as antibiotics. Studies were undertaken to determine the mechanism of resistance of red blood cells to granulysin and sensitivity to a subset of granulysin-derived peptides. Granulysin lyses immature reticulocytes, which have mitochondria, but not red blood cells. Granulysin lyses U937 cells but not U937 cells lacking mitochondrial DNA and a functional respiratory chain (U937°cells), further demonstrating the requirement of intact mitochondria for granulysinmediated death. Peptide G8, which corresponds to helix 2/loop 2/helix 3, lyses red blood cells, while peptide G9, which is identical except that the cysteine residues were replaced by serine, does not lyse red blood cells. Granulysin peptide-induced hemolysis is markedly inhibited by an anion transporter inhibitor and by Na ؉ , K ؉ , and Ca 2؉ channel blockers but not by Na ؉ /K ؉ pump, cotransport, or Cl ؊ channel blockers. Although recombinant granulysin and G9 peptide do not induce hemolysis, they both competitively inhibit G8-induced hemolysis. The finding that some derivatives of granulysin are hemolytic may have important implications for the design of granulysin-based antimicrobial therapeutics.

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Effects of Hyperthermia on Intracellular Chloride

Cited by 15 publications

References 29 publications

Effects of high temperature on pandemic and seasonal human influenza viral replication and infection-induced damage in primary human tracheal epithelial cell cultures

Effects of high temperature on pandemic and seasonal human influenza viral replication and infection-induced damage in primary human tracheal epithelial cell cultures

Physiological significance of hypotonicity-induced regulatory volume decrease: reduction in intracellular Cl⁻concentration acting as an intracellular signaling

Hemolysis of Erythrocytes by Granulysin-Derived Peptides but Not by Granulysin

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Effects of Hyperthermia on Intracellular Chloride

Cited by 15 publications

References 29 publications

Effects of high temperature on pandemic and seasonal human influenza viral replication and infection-induced damage in primary human tracheal epithelial cell cultures

Effects of high temperature on pandemic and seasonal human influenza viral replication and infection-induced damage in primary human tracheal epithelial cell cultures

Physiological significance of hypotonicity-induced regulatory volume decrease: reduction in intracellular Cl−concentration acting as an intracellular signaling

Hemolysis of Erythrocytes by Granulysin-Derived Peptides but Not by Granulysin

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Physiological significance of hypotonicity-induced regulatory volume decrease: reduction in intracellular Cl⁻concentration acting as an intracellular signaling