Impaired Cd14 and Cd36 Expression, Bacterial Clearance, and Toll-Like Receptor 4-Myd88 Signaling in Caveolin-1-Deleted Macrophages and Mice

Tsai, Tsung Huang; Chen, Shu Fen; Huang, Tai Yu; Tzeng, Chun Fu; Chiang, Ann‐Shyn; Kou, Yu Ru; Lee, Tzong‐Shyuan; Shyue, Song Kun

doi:10.1097/shk.0b013e3181ea45ca

Cited by 56 publications

(64 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One potential route of internalization of CD36 is the caveolae-dependent pathway used by TLR receptors (196). Studies showing that caveolin-1 (Cav1) gene disruption is associated with altered subcellular localization and function of CD36 (169,219) are consistent with this hypothesis. When the oral LCFA levels become sufficient to allow the binding and activation of GPR120 in lipid raft (149) triggers the GLP-1 release by TBC (121,149) (FIGURE 8, 4).…”

Section: Indirect Cooperation Hypothesissupporting

confidence: 66%

Taste of Fat: A Sixth Taste Modality?

Besnard

Passilly-Degrace

Khan

2016

Physiological Reviews

203

170

View full text Add to dashboard Cite

An attraction for palatable foods rich in lipids is shared by rodents and humans. Over the last decade, the mechanisms responsible for this specific eating behavior have been actively studied, and compelling evidence implicates a taste component in the orosensory detection of dietary lipids [i.e., long-chain fatty acids (LCFA)], in addition to textural, olfactory, and postingestive cues. The interactions between LCFA and specific receptors in taste bud cells (TBC) elicit physiological changes that affect both food intake and digestive functions. After a short overview of the gustatory pathway, this review brings together the key findings consistent with the existence of a sixth taste modality devoted to the perception of lipids. The main steps leading to this new paradigm (i.e., chemoreception of LCFA in TBC, cell signaling cascade, transfer of lipid signals throughout the gustatory nervous pathway, and their physiological consequences) will be critically analyzed. The limitations to this concept will also be discussed in the light of our current knowledge of the sense of taste. Finally, we will analyze the recent literature on obesity-related dysfunctions in the orosensory detection of lipids ("fatty" taste?), in relation to the overconsumption of fat-rich foods and the associated health risks.

show abstract

Section: Indirect Cooperation Hypothesissupporting

confidence: 66%

Taste of Fat: A Sixth Taste Modality?

Besnard

Passilly-Degrace

Khan

2016

Physiological Reviews

203

170

View full text Add to dashboard Cite

show abstract

“…Then, the upper layer was removed and the lymphocyte layer was transferred according to the manufacturer's instructions. The lymphocytes were lysed with 0.1% saponin for 15 min, serially diluted, plated onto LB agar plates, and incubated at 37°C for 18 h. CFUs of bacteria were determined by the number of colonies formed [21].…”

Section: Animal Proceduresmentioning

confidence: 99%

Cathepsin B-Mediated NLRP3 Inflammasome Formation and Activation in Angiotensin II -Induced Hypertensive Mice: Role of Macrophage Digestion Dysfunction

Lian

Lai

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Angiotensin II (Ang II) is an octapeptide hormone that plays a significant role in mediating hypertension. Although hypertension is considered a chronic inflammatory disease, the molecular basis of the sterile inflammatory response involved in hypertension remains unclear. Methods: We investigated the role of macrophage NLRP3 inflammasomes in engulfing and digesting microbes, a key macrophage function, and in early onset of hypertension-associated macrophage injury using biochemical analyses, gene silencing, molecular biotechnology, immunofluorescence, and microbiology. Results: Ang II stimulation decreased nitric oxide (NO) release and macrophage digestion in cultured THP-1 cells and markedly increased NLRP3 inflammasome formation and activation. NO release and macrophage digestion were restored by NLRP3 inflammasome inhibition with isoliquiritigenin and gene silencing. This Ang II-induced upregulation of NLRP3 inflammasomes in macrophages was attributed to lysosomal damage and release of cathepsin B. Mechanistically, losartan, a nonpeptide Ang II receptor antagonist, decreased Ang II-induced NLRP3 inflammasome activation, lysosomal membrane permeability, lysosomal cathepsin B release, and macrophage digestion dysfunction. Similarly, Ang II-induced macrophage microbe digestion and NO production, which were blocked by ATI gene silencing. In addition, in vivo experiments showed that the bacteria scavenging function was clearly decreased in macrophages from Ang II-induced hypertensive mice. Conclusion: Angiotensin II enhances lysosomal membrane permeabilization and the consequent release of lysosomal cathepsin B, resulting in activation of the macrophage NLRP3 inflammasome. This may contribute to NO mediation of dysfunction in digesting microbes.

show abstract

“…This receptor complex is expressed on numerous cell types, including cells of the immune system and parenchymal cells (9). Studies using mouse strains deficient in TLR4 signaling (10)(11)(12), TLR4 expression (10,(13)(14)(15)(16), or using inhibitors of TLR function in wild type (WT) mice (1,17) confirmed that TLR4 contributes to bacterial clearance and the host inflammatory response in the setting of Gram-negative bacterial infection. Furthermore, the TLR4 Asp 299 Gly polymorphism, which results in depressed LPS-TLR4 signaling (18), is associated with increased susceptibility to Gramnegative infections in humans (19).…”

mentioning

confidence: 99%

Lipopolysaccharide Clearance, Bacterial Clearance, and Systemic Inflammatory Responses Are Regulated by Cell Type–Specific Functions of TLR4 during Sepsis

Deng

Scott

Loughran

et al. 2013

The Journal of Immunology

171

137

View full text Add to dashboard Cite

The morbidity associated with bacterial sepsis is the result of host immune responses to pathogens, which are dependent on pathogen recognition by pattern recognition receptors, such as TLR4. TLR4 is expressed on a range of cell types, yet the mechanisms by which cell-specific functions of TLR4 lead to an integrated sepsis response are poorly understood. To address this, we generated mice in which TLR4 was specifically deleted from myeloid cells (LysMTLR4KO) or hepatocytes (HCTLR4KO) and then determined survival, bacterial counts, host inflammatory responses, and organ injury in a model of cecal ligation and puncture (CLP), with or without antibiotics. LysM-TLR4 was required for phagocytosis and efficient bacterial clearance in the absence of antibiotics. Survival, the magnitude of the systemic and local inflammatory responses, and liver damage were associated with bacterial levels. HCTLR4 was required for efficient LPS clearance from the circulation, and deletion of HCTLR4 was associated with enhanced macrophage phagocytosis, lower bacterial levels, and improved survival in CLP without antibiotics. Antibiotic administration during CLP revealed an important role for hepatocyte LPS clearance in limiting sepsis-induced inflammation and organ injury. Our work defines cell type–selective roles for TLR4 in coordinating complex immune responses to bacterial sepsis and suggests that future strategies for modulating microbial molecule recognition should account for varying roles of pattern recognition receptors in multiple cell populations.

show abstract

Impaired Cd14 and Cd36 Expression, Bacterial Clearance, and Toll-Like Receptor 4-Myd88 Signaling in Caveolin-1-Deleted Macrophages and Mice

Cited by 56 publications

References 34 publications

Taste of Fat: A Sixth Taste Modality?

Taste of Fat: A Sixth Taste Modality?

Cathepsin B-Mediated NLRP3 Inflammasome Formation and Activation in Angiotensin II -Induced Hypertensive Mice: Role of Macrophage Digestion Dysfunction

Lipopolysaccharide Clearance, Bacterial Clearance, and Systemic Inflammatory Responses Are Regulated by Cell Type–Specific Functions of TLR4 during Sepsis

Contact Info

Product

Resources

About