Imbalance of Circulating Innate Lymphoid Cell Subpopulations in Patients With Septic Shock

Carvelli, Julien; Pipéroglou, Christelle; Bourenne, Jérémy; Farnarier, Catherine; Banzet, Nathalie; Demerle, Clémence; Gainnier, Marc; Vély, Frederic

doi:10.3389/fimmu.2019.02179

Cited by 40 publications

(45 citation statements)

References 65 publications

(70 reference statements)

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“…Similarly, the enhanced expression of T-Bet by the innate lymphocytes of patients with infection but not sepsis provides inferential evidence that human sepsis is linked with a failure to elaborate a robust Th1 response in specific innate lymphocytes. While Carvelli recently reported a decrease in TH17 innate lymphoid cells in patients with sepsis, Carvelli did not include patients with infection, and could not link patient outcome to a specific cellular phenotype [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Innate Lymphocyte Th1 and Th17 Responses in Elderly Hospitalised Patients with Infection and Sepsis

et al. 2020

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Background: the role of innate immunity in human sepsis must be fully clarified to identify potential avenues for novel immune adjuvant sepsis therapies. Methods: A prospective observational study was performed including patients with sepsis (septic group), infection without sepsis (infection group), and healthy controls (control group) in the setting of acute medical wards and intensive care units in a 1000-bed university hospital. A total of 42 patients with sepsis, 30 patients with infection, and 30 healthy controls were studied. The differentiation states of circulating mucosal associated invariant T (MAIT) cells and Natural Killer T (NKT) cells were characterised as naive (CD45RA+, CD197+), central memory (CD45RA−, CD197+), effector memory (CD45RA−, CD197−), or terminally differentiated (CD45RA+, CD197−). The differentiation states of circulating gamma-delta T lymphocytes were characterised as naive (CD45RA+, CD27+), central memory (CD45RA−, CD27+), effector memory (CD45RA−, CD27−), or terminally differentiated (CD45RA+, CD27−). The expression of IL-12 and IL-23 receptors, the transcription factors T-Bet and RORγt, and interferon-γ and IL-17a were analysed. Results: MAIT cell counts were lower in the septic group (p = 0.002) and the infection group (p < 0.001) than in the control group. The MAIT cell T-Bet expression in the infection group was greater than in the septic group (p = 0.012). The MAIT RORγt expression in the septic group was lower than in the control group (p = 0.003). The NK cell counts differed in the three groups (p < 0.001), with lower Natural Killer (NK) cell counts in the septic group (p < 0.001) and in the infection group (p = 0.001) than in the control group. The NK cell counts increased in the septic group in the 3 weeks following the onset of sepsis (p = 0.028). In lymphocyte stimulation experiments, fewer NK cells expressed T-Bet in the septic group than in the infection group (p = 0.002), and fewer NK cells expressed IFN-γ in the septic group than in the control group (p = 0.002). The NKT cell counts were lower in the septic group than both the control group (p = 0.05) and the infection group (p = 0.04). Fewer NKT cells expressed T-Bet in the septic group than in the infection group (p = 0.004). Fewer NKT cells expressed RORγt in the septic group than in the control group (p = 0.003). Fewer NKT cells expressed IFN-γ in the septic group than in both the control group (p = 0.002) and the infection group (p = 0.036). Conclusion: The clinical presentation of infection and or sepsis in patients is linked with a mosaic of changes in the innate lymphocyte Th1 and Th17 phenotypes. The manipulation of the innate lymphocyte phenotype offers a potential avenue for immune modulation in patients with sepsis.

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Section: Discussionmentioning

confidence: 99%

Innate Lymphocyte Th1 and Th17 Responses in Elderly Hospitalised Patients with Infection and Sepsis

et al. 2020

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“…Sepsis is newly defined as a dysregulated host-response to an infection, which leads to life-threatening organ dysfunction due to a lack of immune homeostasis [ 147 , 148 ]. The initial phase of sepsis is characterized by an augmented activation of the innate immune system leading to the “cytokine storm” and ending up in multiple organ failure [ 149 , 150 ]. ILCs mainly reside in tissues close to the mucosal barrier; however, they are also present in human peripheral blood [ 149 ].…”

Section: Systemic Consequences Of Bacterial Infections—the Role Ofmentioning

confidence: 99%

“…The initial phase of sepsis is characterized by an augmented activation of the innate immune system leading to the “cytokine storm” and ending up in multiple organ failure [ 149 , 150 ]. ILCs mainly reside in tissues close to the mucosal barrier; however, they are also present in human peripheral blood [ 149 ]. Recently, still controversial results have been reported that describe the distribution of circulating ILC subsets in septic patients.…”

Section: Systemic Consequences Of Bacterial Infections—the Role Ofmentioning

confidence: 99%

“…Cruz-Zárate et al reported a significant decrease in ILC1 and ILC3 in peripheral blood of such patients, which was related to the expression of an apoptotic marker on the ILC surface [ 151 ]. In contrast, Carvelli et al did not detect a difference in total ILC cell numbers, but reported an increase in ILC1 and decrease in ILC3 in the peripheral blood of patients with septic shock [ 149 ]. They further hypothesized the possible importance of ILC plasticity and an ILC3-ILC1 shift as a reason for the changes in ILC numbers.…”

Section: Systemic Consequences Of Bacterial Infections—the Role Ofmentioning

confidence: 99%

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Innate Lymphoid Cells: Important Regulators of Host–Bacteria Interaction for Border Defense

2020

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Innate lymphoid cells (ILCs) are a recently discovered type of innate immune lymphocyte. They include three different groups classified by the nature of the transcription factors required for their development and by the cytokines they produce. ILCs mainly reside in tissues close to the mucosal barrier such as the respiratory and gastrointestinal tracts. Due to their close proximity to the mucosal surface, ILCs are exposed to a variety of both commensal and pathogenic bacteria. Under non-pathological conditions, ILCs have been shown to be important regulators for the maintenance of tissue homeostasis by mutual interactions with the microbiome. Besides these important functions at homeostasis, several studies have also provided emerging evidence that ILCs contribute to defense against pathogenic bacterial infection by responding rapidly to the pathogens as well as orchestrating other immune cells. In this review, we summarize recent advances in our understanding of the interactions of ILCs and bacteria, with special focus on the function of the different ILC subsets in bacterial infections.

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“…Generally speaking, inflammation is the body's normal defense against the invasion of microorganisms. However, excessive inflammation, such as sepsis, may cause tissue and organ damage and even death (2)(3)(4)(5)(6). The pro-inflammatory cytokines IL-1b and IL-18, mainly from macrophages, play important role in inflammatory diseases.…”

Section: Introductionmentioning

confidence: 99%

Pin1 Promotes NLRP3 Inflammasome Activation by Phosphorylation of p38 MAPK Pathway in Septic Shock

et al. 2021

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Pin1 is the only known peptidyl-prolyl cis-trans isomerase (PPIase) that can specifically recognize and isomerize the phosphorylated Serine/Threonine-Proline (pSer/Thr-Pro) motif, change the conformation of proteins through protein phosphorylation, thus regulate various cellular processes in the body. Pin1 plays an important role in cancer, Alzheimer’s disease, and autoimmune diseases. However, the specific mechanism of Pin1 regulation in LPS-induced septic shock is unclear. Here, we found that lack of Pin1 reduced shock mortality and organ damage in mice, and NLRP3 inflammasome activation also was reduced in this process. We further confirmed that Pin1 can affect the expression of NLRP3, ASC, Caspase1, and this process can be regulated through the p38 MAPK pathway. We analyzed that p38 MAPK signaling pathway was highly expressed in septic shock and showed a positive correlation with Pin1 in the Gene Expression Omnibus database. We found that Pin1 could affect the phosphorylation of p38 MAPK, have no obvious difference in extracellular signal-regulated kinases (ERK) and Jun-amino-terminal kinase (JNK) signaling. We further found that Pin1 and p-p38 MAPK interacted, but not directly. In addition, Pin1 deficiency inhibited the cleavage of gasdermin D (GSDMD) and promoted the death of macrophages with LPS treatment, and reduced secretion of inflammatory cytokines including IL-1β and IL-18. In general, our results suggest that Pin1 regulates the NLRP3 inflammasome activation by p38 MAPK signaling pathway in macrophages. Thus, Pin1 may be a potential target for the treatment of inflammatory diseases such as septic shock.

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Imbalance of Circulating Innate Lymphoid Cell Subpopulations in Patients With Septic Shock

Cited by 40 publications

References 65 publications

Innate Lymphocyte Th1 and Th17 Responses in Elderly Hospitalised Patients with Infection and Sepsis

Innate Lymphocyte Th1 and Th17 Responses in Elderly Hospitalised Patients with Infection and Sepsis

Innate Lymphoid Cells: Important Regulators of Host–Bacteria Interaction for Border Defense

Pin1 Promotes NLRP3 Inflammasome Activation by Phosphorylation of p38 MAPK Pathway in Septic Shock

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