Caenorhabditis elegans mom-4 is required for the activation of the p38 MAPK signaling pathway in the response to Pseudomonas aeruginosa infection

Xu, Ajing; Shi, Guojun; Liu, Feng; Ge, Baoxue

doi:10.1007/s13238-012-2080-z

Cited by 12 publications

(9 citation statements)

References 55 publications

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“…Next, we test whether pmk-1 was required for scav-5 mutants lifespan extension after P. aeruginosa PA14 infection. Our results in line with previous studies that loss-and reductionof-function mutations of p38 MAPK PMK-1 pathway components lead to a reduced lifespan of worms fed on P. aeruginosa PA14 (Figure 7A) (Xu et al, 2013;Head et al, 2017). Besides, we found pmk-1 RNAi treatment suppressed the extended lifespan phenotype of scav-5 mutants when cultured on P. aeruginosa PA14 (Figure 7B), demonstrating the requirement of pmk-1 pathway for scav-5 mutants lifespan extension infected by P. aeruginosa PA14.…”

Section: Scav-5 Mutants Are Resistant To P Aeruginosa Pa14 Through Activation Of Pmk-1 P38 Mapk Pathwaysupporting

confidence: 93%

Loss of Function of Scavenger Receptor SCAV-5 Protects C. elegans Against Pathogenic Bacteria

Luo

Jing

Yuan

et al. 2021

Front. Cell. Infect. Microbiol.

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Scavenger receptors play a critical role in innate immunity by acting as the pattern-recognition receptors. There are six class B scavenger receptors homologs in C. elegans. However, it remains unclear whether they are required for host defense against bacterial pathogens. Here, we show that, of the six SCAV proteins, only loss of function scav-5 protect C. elegans against pathogenic bacteria S. typhimurium SL1344 and P. aeruginosa PA14 by different mechanism. scav-5 mutants are resistant to S. typhimurium SL1344 due to dietary restriction. While scav-5 acts upstream of or in parallel to tir-1 in conserved PMK-1 p38 MAPK pathway to upregulate the innate immune response to defend worms against P. aeruginosa PA14. This is the first demonstration of a role for SCAV-5 in host defense against pathogenic bacteria. Our results provide an important basis for further elucidating the underlying molecular mechanism by which scav-5 regulates innate immune responses.

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Section: Scav-5 Mutants Are Resistant To P Aeruginosa Pa14 Through Activation Of Pmk-1 P38 Mapk Pathwaysupporting

confidence: 93%

Loss of Function of Scavenger Receptor SCAV-5 Protects C. elegans Against Pathogenic Bacteria

Luo

Jing

Yuan

et al. 2021

Front. Cell. Infect. Microbiol.

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“…In mammalian cells, NaHS is the donor of H 2 S, and it generates H 2 S through the catalytic reactions of cystathion ine lyase, cystathionineβsynthase, and aminotransferase, and exists in the forms of H 2 S gas and NaHS in vivo [23 25]. A study by Yan et al found that low doses of NaHS (3050 µmol/L) could reduce intracellular free radical gen eration and enhance cell survival, while high dose NaHS (1 mmol/L) was able to inhibit cell proliferation and in duce apoptosis [26]. In addition, Abrahamsen H. et al also showed that H 2 S could induce cell death by activating the apoptotic mechanism [27].…”

Section: Discussionmentioning

confidence: 99%

The role of sodium hydrosulfide in the proliferation and apoptosis of exogenous SB203580 pre-treated human ovarian cancer cells

2020

European Journal of Gynaecological Oncology

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Explore the regulatory function of sodium hydrosulfide (NaHS) on the proliferation and apoptosis of exogenous SB203580 pretreated human ovarian cancer SKOV3 cells. Methods: SKOV3 cells cultured in vitro were assigned to the control group, NaHS group, SB203580 group, and NaHS combined with SB203580 group. The effects and influences on cell proliferation were detected by MTT assay. Effects on the cell cycle and apoptosis were detected by flow cytometry. Western blot was used to detect the expression of Pp38MAPK. Results: Proliferation of SKOV3 cells were remarkably decreased in the NaHS, SB203580, and NaHS combined with SB203580 groups. Cell quantity in G1 phase and S phase increased and decreased remarkably, respectively. Obviously, cell apoptosis rate was increased in the combination group compared to singledrug treatment groups. Pp38MAPK expression in NaHS group was upregulated by comparing with that in control group, and that was markedly enhanced in the combination group compared to single drug treatment group. Conclusions: NaHS inhibited proliferation and promoted apoptosis of SKOV3 cells by blocking the p38MAPK signaling pathway. Furthermore, coordination between NaHS and SB203580 regulated the proliferation and apoptosis of SKOV3 cells.

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“…The p38 MAPK (also called PMK-1) pathway is activated through phosphorylation by upstream MAPKK (SEK-1), which is activated by MAPKKK (NSY-1). It has a role in regulating life expectancy by modulating the specific immune response of the worm and has been shown to be required in its resistance to bacterial infection ( 109 ). Under the control of PMK-1, potential antimicrobials are secreted such as C-type lectins, ShK toxins, or CUB-like genes in response to P. aeruginosa infection.…”

Section: Probiotic Microorganisms Influence On C Elegans mentioning

confidence: 99%

Caenorhabditis elegans, a Host to Investigate the Probiotic Properties of Beneficial Microorganisms

Poupet

Chassard

Nivoliez³

et al. 2020

Front. Nutr.

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Caenorhabditis elegans, a non-parasitic nematode emerges as a relevant and powerful candidate as an in vivo model for microorganisms-microorganisms and microorganisms-host interactions studies. Experiments have demonstrated the probiotic potential of bacteria since they can provide to the worm a longer lifespan, an increased resistance to pathogens and to oxidative or heat stresses. Probiotics are used to prevent or treat microbiota dysbiosis and associated pathologies but the molecular mechanisms underlying their capacities are still unknown. Beyond safety and healthy aspects of probiotics, C. elegans represents a powerful way to design large-scale studies to explore transkingdom interactions and to solve questioning about the molecular aspect of these interactions. Future challenges and opportunities would be to validate C. elegans as an in vivo tool for high-throughput screening of microorganisms for their potential probiotic use on human health and to enlarge the panels of microorganisms studied as well as the human diseases investigated.

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Caenorhabditis elegans mom-4 is required for the activation of the p38 MAPK signaling pathway in the response to Pseudomonas aeruginosa infection

Cited by 12 publications

References 55 publications

Loss of Function of Scavenger Receptor SCAV-5 Protects C. elegans Against Pathogenic Bacteria

Loss of Function of Scavenger Receptor SCAV-5 Protects C. elegans Against Pathogenic Bacteria

The role of sodium hydrosulfide in the proliferation and apoptosis of exogenous SB203580 pre-treated human ovarian cancer cells

Caenorhabditis elegans, a Host to Investigate the Probiotic Properties of Beneficial Microorganisms

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