Staphylococcus aureus stimulates neutrophil itaconate production that suppresses the oxidative burst

Tomlinson, Kira L.; Riquelme, Sebastián A.; Baskota, Swikrity Upadhyay; Drikic, Marija; Monk, Ian R.; Stinear, Timothy P.; Lewis, Ian A.; Prince, Alice

doi:10.1016/j.celrep.2023.112064

Cited by 45 publications

(31 citation statements)

References 55 publications

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“…Instead, the tissue damage mediated by cytolytic T cells may provide the environment for S. aureus to invade and replicate in this patient population. This would be consistent with the ability of S. aureus to colonize broken skin and soft tissue ( 27 , 28 ). However, the enrichment of genes associated with both cytolysis and IL-1 in S. aureus –dominant lesions is a feature of L. braziliensis –infected patients compared with other skin diseases complicated by S. aureus colonization and infection.…”

Section: Discussionsupporting

confidence: 80%

“…In other contexts, itaconate was reported to inhibit the inflammasome activation and downstream IL-1β release ( 29 ), but we did not observe lower expression of IL1B in samples with high levels of ACOD1. However, it has also been reported that S. aureus increases itaconate, which limits bacterial killing, indicating a possible role in the increased Staphylococcus burdens ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

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Multiomic profiling of cutaneous leishmaniasis infections reveals microbiota-driven mechanisms underlying disease severity

Farias Amorim,

Lovins,

Singh

et al. 2023

Sci. Transl. Med.

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Leishmania braziliensis is a parasitic infection that can result in inflammation and skin injury with highly variable and unpredictable clinical outcomes. Here, we investigated the potential impact of microbiota on infection-induced inflammatory responses and disease resolution by conducting an integrated analysis of the skin microbiome and host transcriptome on a cohort of 62 patients infected with L. braziliensis . We found that overall bacterial burden and microbiome configurations dominated with Staphylococcus spp. were associated with delayed healing and enhanced inflammatory responses, especially by IL-1 family members. Quantification of host and bacterial transcripts on human lesions revealed that high lesional S. aureus transcript abundance was associated with delayed healing and increased expression of IL-1β. This cytokine was critical for modulating disease outcomes in L. braziliensis –infected mice colonized with S. aureus , given that its neutralization reduced pathology and inflammation. These results highlight how the human microbiome can shape disease outcomes in cutaneous leishmaniasis and suggest pathways toward host-directed therapies to mitigate the inflammatory consequences.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Multiomic profiling of cutaneous leishmaniasis infections reveals microbiota-driven mechanisms underlying disease severity

Farias Amorim,

Lovins,

Singh

et al. 2023

Sci. Transl. Med.

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“… 29 In contrast, there is attenuation in S. aureus virulence in irg1 -deficient mice. 30 Future studies are needed to further examine the role of irg1 in wound healing and host defense against infection to determine if irg1 could be a potential target for treating infected wounds. It is critical to identify inflammatory targets that do not link to host defense.…”

Section: Discussionmentioning

confidence: 99%

Infection induced inflammation impairs wound healing through IL-1β signaling

Shen,

Miskolci,

Dewey

et al. 2024

iScience

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“…Since then, several seminal studies have demonstrated how diverse metabolites function as signaling intermediates that dictate the immune response [10,35,[42][43][44] . Interestingly, it is increasingly being recognized that bacterial pathogens can subvert immunometabolism to promote infection [12,45,46] .…”

Section: Immunometabolismmentioning

confidence: 99%

Immunometabolic control by Klebsiella pneumoniae

Prince

Lung

2023

Immunometabolism

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Klebsiella pneumoniae is a common Gram-negative pathogen associated with community-acquired and healthcare-associated infections. Its ability to acquire genetic elements resulted in its rapid development of resistance to virtually all antimicrobial agents. Once infection is established, K. pneumoniae is able to evade the host immune response and perhaps more importantly, undergo metabolic rewiring to optimize its ability to maintain infection. K. pneumoniae lipopolysaccharide and capsular polysaccharide are central factors in the induction and evasion of immune clearance. Less well understood is the importance of immunometabolism, the intersection between cellular metabolism and immune function, in the host response to K. pneumoniae infection. Bacterial metabolism itself is perceived as a metabolic stress to the host, altering the microenvironment at the site of infection. In this review, we will discuss the metabolic responses induced by K. pneumoniae, particularly in response to stimulation with the metabolically active bacteria versus pathogen-associated molecular patterns alone, and their implications in shaping the nature of the immune response and the infection outcome. A better understanding of the immunometabolic response to K. pneumoniae may help identify new targets for therapeutic intervention in the treatment of multidrug-resistant bacterial infections.

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Staphylococcus aureus stimulates neutrophil itaconate production that suppresses the oxidative burst

Cited by 45 publications

References 55 publications

Multiomic profiling of cutaneous leishmaniasis infections reveals microbiota-driven mechanisms underlying disease severity

Multiomic profiling of cutaneous leishmaniasis infections reveals microbiota-driven mechanisms underlying disease severity

Infection induced inflammation impairs wound healing through IL-1β signaling

Immunometabolic control by Klebsiella pneumoniae

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