ATF3 inhibits the inflammation induced by<i>Mycoplasma pneumonia</i>in vitro and in vivo

Wang, Jing; Cheng, Wei; Wang, Zhen; Xin, Lihong; Zhang, Wen

doi:10.1002/ppul.23705

Cited by 15 publications

(10 citation statements)

References 35 publications

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“…In mouse models, ATF3 could be superinduced by reactive oxygen species and protect against endotoxic shock by inhibiting innate cytokines (Hoetzenecker et al, 2011). In addition, ATF3 facilitates the pathogen clearance in S. pneumoniae infection by promoting IL-17A production in γδ T cells (Lee et al, 2018), and it inhibits the secretion of inflammatory cytokines induced by Mycoplasma pneumonia in vitro and in vivo (Wang et al, 2017). As evidenced by our analysis, the ATF3 + B cells highly expressed genes associated with regulation of transmembrane transport, cell adhesion, and Th17 cell differentiation.…”

Section: Discussionmentioning

confidence: 99%

Signatures of B Cell Receptor Repertoire Following Pneumocystis Infection

et al. 2021

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B cells play vital roles in host defense against Pneumocystis infection. However, the features of the B cell receptor (BCR) repertoire in disease progression remain unclear. Here, we integrated single-cell RNA sequencing and single-cell BCR sequencing of immune cells from mouse lungs in an uninfected state and 1–4 weeks post-infection in order to illustrate the dynamic nature of B cell responses during Pneumocystis infection. We identified continuously increased plasma cells and an elevated ratio of (IgA + IgG) to (IgD + IgM) after infection. Moreover, Pneumocystis infection was associated with an increasing naïve B subset characterized by elevated expression of the transcription factor ATF3. The proportion of clonal expanded cells progressively increased, while BCR diversity decreased. Plasma cells exhibited higher levels of somatic hypermutation than naïve B cells. Biased usage of V(D)J genes was observed, and the usage frequency of IGHV9-3 rose. Overall, these results present a detailed atlas of B cell transcriptional changes and BCR repertoire features in the context of Pneumocystis infection, which provides valuable information for finding diagnostic biomarkers and developing potential immunotherapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Signatures of B Cell Receptor Repertoire Following Pneumocystis Infection

et al. 2021

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“…The persistence of inflammatory response is unfavorable to the body ( Wang et al., 2017 ). A strong inflammatory response leads to local tissue damage, epithelial cell damage, and increased vascular leakage, all of which can lead to lung dysfunction and even death ( Grommes and Soehnlein, 2011 ).…”

Section: Cytokines-medicated Communications Between Ams and Aecs Duri...mentioning

confidence: 99%

Interaction between alveolar macrophages and epithelial cells during Mycoplasma pneumoniae infection

Xue

Wang

Han

2023

Front. Cell. Infect. Microbiol.

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Mycoplasma pneumoniae, as one of the most common pathogens, usually causes upper respiratory tract infections and pneumonia in humans and animals. It accounts for 10% to 40% of community-acquired pneumonia in children. The alveolar epithelial cells (AECs) are the first barrier against pathogen infections, triggering innate immune responses by recruiting and activating immune cells when pathogens invade into the lung. Alveolar macrophages (AMs) are the most plentiful innate immune cells in the lung, and are the first to initiate immune responses with pathogens invasion. The cross-talk between the alveolar epithelium and macrophages is necessary to maintain physiological homeostasis and to eradicate invaded pathogen by regulating immune responses during Mycoplasma pneumoniae infections. This review summarizes the communications between alveolar macrophages and epithelial cells during Mycoplasma pneumoniae infections, including cytokines-medicated communications, signal transduction by extracellular vesicles, surfactant associated proteins-medicated signal transmission and establishment of intercellular gap junction channels.

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“…By forming dimers with ATF3-itself and various other bZip proteins, such as ATF2, c-Jun, JunB, and JunD, ATF3 can function as a transcriptional activator or repressor[ 19 20 ]. Evidence have suggested that ATF3 plays a role in a variety of biological processes, such as metabolism[ 20 21 ] cell motility [ 22 ] cell cycle [ 23 ] DNA repair [ 24 ] cell death [ 25 ] and various functions on maintaining the homeostasis[ 26 27 28 29 30 31 32 33 34 35 36 37 ]. ATF3 can be up-regulated by stimulations from wide spectrum of toll-like receptors (TLRs), including TLR4, 2/6, 3, 5, 7, and 9, and serves as a negative feedback regulator [ 38 ].…”

Section: Taconate-induced Anti-inflammatory Atf3 Pathwaymentioning

confidence: 99%

Emerging role of the itaconate-mediated rescue of cellular metabolic stress

Chang

Sun

2022

Tzu Chi Medical Journal

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Metabolic regulations play vital roles on maintaining the homeostasis of our body. Evidence have suggested that ATF3 and nuclear factor erythroid 2–related factor 2 (NRF2) are critical for maintaining cell function, metabolism, and inflammation/anti-inflammation regulations when cells are under stress, while the upstream regulators in the stressed cells remain elusive. Recent findings have shown that tricarboxylic acid cycle metabolites such as itaconate and succinate are not just mitochondrial metabolites, but rather important signaling mediators, involving in the regulations of metabolism, immune modulation. Itaconate exerts anti-inflammatory role through regulating ATF3 and NRF2 pathways under stressed conditions. In addition, itaconate inhibits succinate dehydrogenase, succinate oxidation and thus blocking succinate-mediated inflammatory processes. These findings suggest itaconate-ATF3 and itaconate-NRF2 axes are well-coordinated machineries that facilitate the rescue against cellular stress. Here, we review these fascinating discoveries, a research field may help the development of more effective therapeutic approach to manage stress-induced inflammation, tissue damage, and metabolic disorder.

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ATF3 inhibits the inflammation induced byMycoplasma pneumoniain vitro and in vivo

Abstract: ATF3 inhibit the expression and release of TNF-α, IL-1β, IL-6, and IL-18 induced by MP in vitro and in vivo, which is associated with its negative regulation of Egr-1/Fyn signaling pathway.

Cited by 15 publications

References 35 publications

Signatures of B Cell Receptor Repertoire Following Pneumocystis Infection

Signatures of B Cell Receptor Repertoire Following Pneumocystis Infection

Interaction between alveolar macrophages and epithelial cells during Mycoplasma pneumoniae infection

Emerging role of the itaconate-mediated rescue of cellular metabolic stress

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