TLR2 mediates phagocytosis and autophagy through JNK signaling pathway in Staphylococcus aureus-stimulated RAW264.7 cells

Fang, Lei; Wu, Hui-Mei; Ding, Peishan; Liu, Rong‐Yu

doi:10.1016/j.cellsig.2013.12.016

Cited by 116 publications

(85 citation statements)

References 38 publications

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“…Although the role of TLRs in the engulfment of pathogens remains controversial, it has been reported that TLR2 enhances phagocytosis of Listeria monocytogenes by macrophages [33] and plays an important role in phagocytosis of Streptococcus pneumonia by mouse neutrophils [34]. Furthermore, it was recently demonstrated that TLR2 could mediate the phagocytosis of Staphylococcus aureus in a mouse macrophage cell line through the MAPK signaling pathway [35]. Although the infection rate and number of internalized parasites were reduced by anti-TLR2–neutralizing antibody, based on our results, we cannot unequivocally state that TLR2 is a phagocytic receptor for Leishmania .…”

Section: Discussionmentioning

confidence: 99%

Understanding the Mechanisms Controlling Leishmania amazonensis Infection In Vitro: The Role of LTB4 Derived From Human Neutrophils

Tavares

Araújo-Santos

Afonso

et al. 2014

The Journal of Infectious Diseases

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Neutrophils are rapidly recruited to the site of Leishmania infection and play an active role in capturing and killing parasites. They are the main source of leukotriene B4 (LTB4), a potent proinflammatory lipid mediator. However, the role of LTB4 in neutrophil infection by Leishmania amazonensis is not clear. In this study, we show that L. amazonensis or its lipophosphoglycan can induce neutrophil activation, degranulation, and LTB4 production. Using pharmacological inhibitors of leukotriene synthesis, our findings reveal an LTB4-driven autocrine/paracrine regulatory effect. In particular, neutrophil-derived LTB4 controls L. amazonensis killing, degranulation, and reactive oxygen species production. In addition, L. amazonensis infection induces an early increase in Toll-like receptor 2 expression, which facilitates parasite internalization. Nuclear factor kappa B (NFkB) pathway activation represents a required upstream event for L. amazonensis–induced LTB4 synthesis. These leishmanicidal mechanisms mediated by neutrophil-derived LTB4 act through activation of its receptor, B leukotriene receptor 1 (BLT1).

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Section: Discussionmentioning

confidence: 99%

Understanding the Mechanisms Controlling Leishmania amazonensis Infection In Vitro: The Role of LTB4 Derived From Human Neutrophils

Tavares

Araújo-Santos

Afonso

et al. 2014

The Journal of Infectious Diseases

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“…Recently, several studies reported that TLR2 stimulation by various pathogens induces autophagy (14, 15). In response to Listeria monocytogenes , macrophages deficient in the TLR2 and NOD/receptor-interacting protein 2 (RIP2) pathways show defective autophagy induction and fail to colocalize bacteria within autophagosomes [Figure 1B; Ref.…”

Section: Tlrs and Autophagymentioning

confidence: 99%

“…Another study showed that Staphylococcus aureus -mediated stimulation of TLR2 in RAW 264.7 mouse macrophages induces phagocytosis and autophagy. In particular, knockdown of TLR2 was shown to attenuate S. aureus -induced phosphorylation of macrophage c-Jun N-terminal kinase (JNK) but not phosphorylation of p38 or ERK (15). Collectively, these data indicate that TLR2 stimulated by invading microbes could mediate autophagy induction and promote the clearance of pathogens, despite the different pathways involved.…”

Section: Tlrs and Autophagymentioning

confidence: 99%

Pattern Recognition Receptors and Autophagy

Lee

2014

Front. Immunol.

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The immune system senses exogenous threats or endogenous stress through specialized machinery known as pattern recognition receptors (PRRs). These receptors recognize conserved molecular structures and initiate downstream signaling pathways to control immune responses. Although various immunologic pathways mediated by PRRs have been described, recent studies have demonstrated a link between PRRs and autophagy. Autophagy is a specialized biological process involved in maintaining homeostasis through the degradation of long-lived cellular proteins and organelles. In addition to this fundamental function, autophagy plays important roles in various immunologic processes. In this review, we focus on the reciprocal influences of PRRs and autophagy in modulating innate immune responses.

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“…It has been reported that S. aureus infection induces upregulation of TLR-2 expression (Zhao et al 2008). In addition, TLR2 mediates phagocytosis and autophagy through JNK signaling pathway in S. aureus-stimulated macrophages (Fang et al 2014). Regulation of TLR2 and TLR2-related apoptotic factors by baicalin leads to inhibition of S. aureusinduced apoptosis in mouse mammary glands (Guo et al 2014).…”

Section: Discussionmentioning

confidence: 98%

The herbal-derived honokiol and magnolol enhances immune response to infection with methicillin-sensitive Staphylococcus aureus (MSSA) and methicillin-resistant S. aureus (MRSA)

Choi

Kim

et al. 2015

Appl Microbiol Biotechnol

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The emergence of antibiotic resistant strains such as methicillin-resistant Staphylococcus aureus (MRSA) reminds us an urgent need to develop a new immune-modulating agent for preventing S. aureus infection. In this study, we found that herbal medicines, honokiol and magnolol, caused a significant cellular immune modulatory effect during S. aureus infection. In mouse macrophages, these compounds drove upregulation of an antioxidant effect in response to S. aureus, resulting in a dampened total cellular reactive oxygen species (ROS) production and decreased production of inflammatory cytokines/chemokines, whereas honokiol induced increased types I and III interferon messenger RNA (mRNA) expression levels in response to MSSA infection. Moreover, the internalization of S. aureus by human alveolar epithelial cells was inhibited by these compounds. Furthermore, honokiol and magnolol treatment promoted a delay in killing during MSSA infection in Caenorhabditis elegans, suggesting antimicrobial function in vivo. In conclusion, honokiol and magnolol may be considered as attractive immune-modulating treatment for S. aureus infection.

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TLR2 mediates phagocytosis and autophagy through JNK signaling pathway in Staphylococcus aureus-stimulated RAW264.7 cells

Cited by 116 publications

References 38 publications

Understanding the Mechanisms Controlling Leishmania amazonensis Infection In Vitro: The Role of LTB4 Derived From Human Neutrophils

Understanding the Mechanisms Controlling Leishmania amazonensis Infection In Vitro: The Role of LTB4 Derived From Human Neutrophils

Pattern Recognition Receptors and Autophagy

The herbal-derived honokiol and magnolol enhances immune response to infection with methicillin-sensitive Staphylococcus aureus (MSSA) and methicillin-resistant S. aureus (MRSA)

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