Neonatal NET-inhibitory factor and related peptides inhibit neutrophil extracellular trap formation

Yost, Christian C.; Schwertz, Hansjörg; Cody, Mark J.; Wallace, Jared; Campbell, Robert A.; Vieira‐de‐Abreu, Adriana; Araujo, Claudia V. de; Schubert, Sebastian; Harris, Estelle S.; Rowley, Jesse W.; Rondina, Matthew T.; Fulcher, James; Koening, Curry L.; Weyrich, Andrew S.; Zimmerman, Guy A.

doi:10.1172/jci83873

Cited by 120 publications

(144 citation statements)

References 75 publications

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“…This impairment was recently attributed to a neonatal NETinhibitory factor present in cord blood plasma, which blunts in vitro and in vivo NET formation. 145 In summary, we report that amniotic fluid neutrophils undergo NET formation in women with intra-amniotic infection. This finding provides a new immune defense mechanism whereby amniotic fluid neutrophils can kill microbes invading the amniotic cavity.…”

Section: Discussionmentioning

confidence: 70%

“…This finding suggests that amniotic fluid neutrophils form NETs when bacteria invade the amniotic cavity. Yet, there is a possibility that NETs are formed in the setting of sterile intra-amniotic inflammation as alarmins (eg, high-mobility group box 1, 143 monosodium urate crystals, 144 and heme 145 ) and cytokines (eg, IL- It is worth mentioning that neonatal neutrophils formed fewer NETs than maternal neutrophils upon PMA stimulation. This impairment was recently attributed to a neonatal NETinhibitory factor present in cord blood plasma, which blunts in vitro and in vivo NET formation.…”

Section: Discussionmentioning

confidence: 99%

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Neutrophil Extracellular Traps in the Amniotic Cavity of Women with Intra-Amniotic Infection: A New Mechanism of Host Defense

Gomez‐Lopez

Romero

et al. 2017

Reprod. Sci.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Neutrophil Extracellular Traps in the Amniotic Cavity of Women with Intra-Amniotic Infection: A New Mechanism of Host Defense

Gomez‐Lopez

Romero

et al. 2017

Reprod. Sci.

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“…NETs did not directly induce coagulation of human plasma in recent in vitro studies, however, suggesting that there may be species differences or other relevant variables (125). Agents with the ability to inhibit NETosis or dismantle NETs after their formation have been identified (55,59,123,124,126), suggesting potential adjuvant therapeutic approaches in sepsis and septic ARDS.…”

Section: Translational Reviewmentioning

confidence: 99%

“…(DAMP) that mediates tissue injury (52) and modifies experimental sepsis (53), induces NET deployment by human and murine PMNs (54,55). NETs mediate damage to lung cells in vitro and contribute to lung injury and dysfunction in vivo in experimental models (12,44).…”

Section: Platelets Are Inflammatory and Immune Effector Cells In The mentioning

confidence: 99%

Amicus or Adversary Revisited: Platelets in Acute Lung Injury and Acute Respiratory Distress Syndrome

Middleton

Rondina

Schwertz

et al. 2018

Am J Respir Cell Mol Biol

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Platelets are essential cellular effectors of hemostasis and contribute to disease as circulating effectors of pathologic thrombosis. These are their most widely known biologic activities. Nevertheless, recent observations demonstrate that platelets have a much more intricate repertoire beyond these traditional functions and that they are specialized for contributions to vascular barrier integrity, organ repair, antimicrobial host defense, inflammation, and activities across the immune continuum. Paradoxically, on the basis of clinical investigations and animal models of disease, some of these newly discovered activities of platelets appear to contribute to tissue injury. Studies in the last decade indicate unique interactions of platelets and their precursor, the megakaryocyte, in the lung and implicate platelets as essential effectors in experimental acute lung injury and clinical acute respiratory distress syndrome. Additional discoveries derived from evolving work will be required to precisely define the contributions of platelets to complex subphenotypes of acute lung injury and to determine if these remarkable and versatile blood cells are therapeutic targets in acute respiratory distress syndrome.

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“…We examined whether the absence of MAIT cells altered survival outcomes in vivo during experimental sepsis. In the CLP model of polymicrobial sepsis (20,21), we saw that MR1-deficient mice (MR1 -/-) which lack MAIT cells, had significantly increased sepsis-related mortality compared to WT mice (Figure 2A). The majority (11/15, ~73%) of MR1 -/mice died 24 to 48 hours following induction of sepsis, while the majority (13/15, ~87%) of WT mice survived up to 100 hours after sepsis (Figure 2A).…”

Section: Mait Deficiency Increases Bacterial Burden and Mortality Durmentioning

confidence: 99%

Mucosal-associated invariant T (MAIT) cells mediate protective host responses in sepsis

Trivedi

Labuz

Anderson

et al. 2020

Preprint

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Sepsis is a systemic inflammatory response to infection and a leading cause of death. Mucosal-associated invariant T (MAIT) cells are innate-like T cells enriched in mucosal tissues that recognize bacterial ligands. We investigated MAIT cells during clinical and experimental sepsis, and their contribution to host responses. In experimental sepsis, MAIT-deficient mice had significantly increased mortality and bacterial load, and reduced tissue-specific cytokine responses. MAIT cells of WT mice expressed lower levels of IFN-γ and IL-17a during sepsis compared to sham surgery, changes not seen in non-MAIT T cells. MAIT cells of patients presenting with sepsis were significantly reduced in frequency, more activated, and had decreased IFN-γ production when stimulated, compared to healthy donors and paired 90-day post-sepsis samples. Our data suggest that MAIT cells are highly activated and become dysfunctional during clinical sepsis, and contribute to tissue-specific cytokine responses that are protective against mortality during experimental sepsis.

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Neonatal NET-inhibitory factor and related peptides inhibit neutrophil extracellular trap formation

Cited by 120 publications

References 75 publications

Neutrophil Extracellular Traps in the Amniotic Cavity of Women with Intra-Amniotic Infection: A New Mechanism of Host Defense

Neutrophil Extracellular Traps in the Amniotic Cavity of Women with Intra-Amniotic Infection: A New Mechanism of Host Defense

Amicus or Adversary Revisited: Platelets in Acute Lung Injury and Acute Respiratory Distress Syndrome

Mucosal-associated invariant T (MAIT) cells mediate protective host responses in sepsis

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