Chloroquine attenuates lipopolysaccharide-induced inflammatory responses through upregulation of USP25

Ding, Changyu; Li, Fangfang; Long, Yupeng; Zheng, Jie

doi:10.1139/cjpp-2016-0303

Cited by 15 publications

(14 citation statements)

References 42 publications

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“…We assumed that LPS may increase USP25 protein level to stabilize HBO1 via enhancing HBO1 deubiquitination. As predicted, LPS increased USP25 protein level in a time-dependent manner in THP-1 cells, consistent with other reports [23, 35] (Fig. 5A).…”

Section: Resultssupporting

confidence: 93%

LPS promotes HBO1 stability via USP25 to modulate inflammatory gene transcription in THP-1 cells

Chen

Lai

et al. 2018

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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The histone acetyltransferase HBO1 (Histone acetyltransferase binding to origin recognition complex 1, Myst2/Kat7) participates in a range of life processes including DNA replication and tumorigenesis. Recent studies revealed that HBO1 is involved in gene transcriptional activation. However, the molecular behavior of HBO1 in inflammation is yet to be studied. Here we report that endotoxin lipopolysaccharide (LPS) elevates HBO1 protein level via up-regulating UPS25 (ubiquitin specific peptidase 25) and alters inflammatory gene transcription in THP-1 monocytes and in human primary macrophages. LPS protects HBO1 from ubiquitin proteasomal degradation without significantly altering its transcription. By immunoprecipitation, we identified that HBO1 associates with a deubiquitinating enzyme USP25 in THP-1 cells. LPS increases protein level of USP25 resulting in accumulation of HBO1 by suppression of HBO1 ubiquitination. Stabilized-HBO1 modulates inflammatory gene transcription in THP-1 cells. These findings indicate that USP25 promotes stability of HBO1 in bacterial infection thereby enhances HBO1-mediated inflammatory gene transcription.

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Section: Resultssupporting

confidence: 93%

LPS promotes HBO1 stability via USP25 to modulate inflammatory gene transcription in THP-1 cells

Chen

Lai

et al. 2018

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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“…We conclude that increased intestinal permeability indicates impaired barrier function and that increased uncontrolled passage of substances through the barrier causes increased inflammatory responses [33]. Indeed, RAPA-treated piglets with disrupted intestinal integrity showed higher levels of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, compared to the control treatment.…”

Section: Discussionmentioning

confidence: 76%

“…These effects may contribute to the alleviation of the weaning stress response in piglets. The results from previous studies showed CQ promoted injury recovery by preventing the degradation of the autophagic and ubiquitinated protein and inhibiting autophagy-associated inflammation [33,35].…”

Section: Discussionmentioning

confidence: 97%

Chloroquine Downregulation of Intestinal Autophagy to Alleviate Biological Stress in Early-Weaned Piglets

Liao

Tang

Chang

et al. 2020

Animals

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Early weaning stress impairs the development of gastrointestinal barrier function, causing immune system dysfunctions, reduction in feed intake, and growth retardation. Autophagy was hypothesized to be a key underlying cellular process in these dysfunctions. We conjectured that rapamycin (RAPA) and chloroquine (CQ), as two autophagy-modifying agents, regulate the autophagy process and may produce deleterious or beneficial effects on intestinal health and growth. To explore the effect of autophagy on early weaning stress in piglets, 18 early-weaned piglets were assigned to three treatments (each treatment of six piglets) and treated with an equal volume of RAPA, CQ, or saline. The degree of autophagy and serum concentrations of immunoglobulins and cytokines, as well as intestinal morphology and tight junction protein expression, were evaluated. Compared with the control treatment, RAPA-treated piglets exhibited activated autophagy and had decreased final body weight (BW) and average daily gain (ADG) (p < 0.05), impaired intestinal morphology and tight junction function, and higher inflammatory responses. The CQ-treated piglets showed higher final BW, ADG, jejuna and ileal villus height, and lower autophagy and inflammation, compared with control piglets (p < 0.05). Throughout the experiment, CQ treatment was beneficial to alleviate early weaning stress and intestinal and immune system dysfunction.

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“…USP25 deficient mice have been shown to be more susceptible to virus infection and LPS-induced septic shock [63,65].IL-17-mediated inflammation is also attenuated by USP25 through TRAF5 and TRAF6 deubiquitination [66]. The anti-malarial drug chloroquine is suggested to alleviate LPS-induced inflammation by up regulatingUSP25 in macrophages [125].…”

Section: Uspsmentioning

confidence: 99%

The Role of Deubiquitinating Enzymes in Acute Lung Injury and Acute Respiratory Distress Syndrome

Zou

2020

IJMS

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Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) are characterized by an inflammatory response, alveolar edema, and hypoxemia. ARDS occurs most often in the settings of pneumonia, sepsis, aspiration of gastric contents, or severe trauma. The prevalence of ARDS is approximately 10% in patients of intensive care. There is no effective remedy with mortality high at 30–40%. Most functional proteins are dynamic and stringently governed by ubiquitin proteasomal degradation. Protein ubiquitination is reversible, the covalently attached monoubiquitin or polyubiquitin moieties within the targeted protein can be removed by a group of enzymes called deubiquitinating enzymes (DUBs). Deubiquitination plays an important role in the pathobiology of ALI/ARDS as it regulates proteins critical in engagement of the alveolo-capillary barrier and in the inflammatory response. In this review, we provide an overview of how DUBs emerge in pathogen-induced pulmonary inflammation and related aspects in ALI/ARDS. Better understanding of deubiquitination-relatedsignaling may lead to novel therapeutic approaches by targeting specific elements of the deubiquitination pathways.

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Chloroquine attenuates lipopolysaccharide-induced inflammatory responses through upregulation of USP25

Cited by 15 publications

References 42 publications

LPS promotes HBO1 stability via USP25 to modulate inflammatory gene transcription in THP-1 cells

LPS promotes HBO1 stability via USP25 to modulate inflammatory gene transcription in THP-1 cells

Chloroquine Downregulation of Intestinal Autophagy to Alleviate Biological Stress in Early-Weaned Piglets

The Role of Deubiquitinating Enzymes in Acute Lung Injury and Acute Respiratory Distress Syndrome

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