Endotoxemia and Sepsis: Important Roles for Lipopolysaccharide Binding Protein and CD14 in Endotoxin Signal Transduction

Bruin, K. F.; Möhlen, M. A. M. Von Der; Deventer, S. J. H. Van

doi:10.1007/978-3-642-85036-3_5

Cited by 3 publications

(1 citation statement)

References 47 publications

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“…Thus, SARS-CoV-2 can invade the intestinal tract causing GI dysfunction which disrupt intestinal barriers, increasing the translocation of microbial products (9,21). Increased systemic endotoxemia has been previously described in several pathological conditions associated with hospitalization, becoming a recognized marker of critical ill who suffer sepsis (22)(23)(24). Furthermore, recent studies described disrupted gut barrier integrity and increased circulating bacteriome in moderate and severe COVID-19 patients (9,16,17).…”

Section: Discussionmentioning

confidence: 99%

Increased LPS levels coexist with systemic inflammation and result in monocyte activation in severe COVID-19 patients

Teixeira

Dorneles

Filho

et al. 2021

Preprint

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This study aimed to evaluate the link between microbial translocation markers and systemic inflammation at the earliest time-point after hospitalization and at the last 72 h of hospitalization in survivors and non-survivors COVID-19 patients. Sixty-six SARS-CoV-2 RT-PCR+ infected patients and nine non-COVID-19 pneumonia controls were admitted in this study. Blood samples were collected at hospital admission (T1) (Controls and COVID-19+ patients) and 0-72 h before hospital discharge (T2, alive or dead) to analyze systemic cytokines and chemokines, LPS concentrations, and soluble CD14 (sCD14) levels. THP-1 human monocytic cell line was incubated with plasma from survivors and non-survivors COVID-19 patients and their phenotype, activation status, TLR4, and chemokine receptors were analyzed by flow cytometry. COVID-19 patients presented higher IL-6, IFN-γ, TNF-α, TGF-β1, CCL2/MCP-1, CCL4/MIP-1β, and CCL5/RANTES levels than controls. Moreover, LPS and sCD14 were higher at hospital admission in SARS-CoV-2-infected patients. Non-survivors COVID-19 patients had increased LPS levels concomitant with higher IL-6, TNF-α, CCL2/MCP-1, and CCL5/RANTES levels at T2. Increased expression of CD16 and CCR5 were identified in THP-1 cells incubated with the plasma of survivor patients obtained at T2. The incubation of THP-1 with T2 plasma of non-survivors COVID-19 leads to higher TLR4, CCR2, CCR5, CCR7, and CD69 expression. In conclusion, increased microbial translocation during hospitalization coexist with the inflammatory condition of SARS-CoV-2 infection and could lead to higher monocyte activation in non-survivors COVID-19 patients.

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Section: Discussionmentioning

confidence: 99%

Increased LPS levels coexist with systemic inflammation and result in monocyte activation in severe COVID-19 patients

Teixeira

Dorneles

Filho

et al. 2021

Preprint

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Is sepsis a mediator-inhibitor mismatch?

Lamy

Deby‐Dupont

1995

Intensive Care Med

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vation appears to precede that of the cellular system, but the sequence of this release of mediators is not well known. In sepsis, however, endotoxins [or lipopolysaccharides (LPS)] or other bacterial toxins seem to be the triggering mechanisms for the acute inflammatory response. Both sepsis and SIRS are the consequence of an excessive host response uncontrolled by natural inhibitors, and certain complications, such as organ dysfunction and shock, are frequently seen after both sepsis and SIRS, when hypotension persists despite adequate fluid resuscitation, leading to tissue hypoperfusion [4][5][6][7].

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Increased LPS levels coexist with systemic inflammation and result in monocyte activation in severe COVID-19 patients

Teixeira¹,

Dorneles²,

Filho³

et al. 2021

International Immunopharmacology

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Mucosal barrier alterations may play a role in the pathogenesis of several diseases, including COVID-19. In this study we evaluate the association between bacterial translocation markers and systemic inflammation at the earliest time-point after hospitalization and at the last 72 h of hospitalization in survivors and non-survivors COVID-19 patients. Sixty-six SARS-CoV-2 RT-PCR positive patients and nine non-COVID-19 pneumonia controls were admitted in this study. Blood samples were collected at hospital admission (T1) (Controls and COVID-19 patients) and 0-72 h before hospital discharge (T2, alive or dead) to analyze systemic cytokines and chemokines, lipopolysaccharide (LPS) concentrations and soluble CD14 (sCD14) levels. THP-1 human monocytic cell line was incubated with plasma from survivors and non-survivors COVID-19 patients and their phenotype, activation status, TLR4, and chemokine receptors were analyzed by flow cytometry. COVID-19 patients presented higher IL-6, IFN-γ, TNF-α, TGF-β1, CCL2/MCP-1, CCL4/MIP-1β, and CCL5/RANTES levels than controls. Moreover, LPS and sCD14 were higher at hospital admission in SARS-CoV-2-infected patients. Non-survivors COVID-19 patients had increased LPS levels concomitant with higher IL-6, TNF-α, CCL2/MCP-1, and CCL5/RANTES levels at T2. Increased expression of CD16 and CCR5 were identified in THP-1 cells incubated with the plasma of survivor patients obtained at T2. The incubation of THP-1 with T2 plasma of non-survivors COVID-19 leads to higher TLR4, CCR2, CCR5, CCR7, and CD69 expression. In conclusion, the coexistence of increased microbial translocation and hyperinflammation in patients with severe COVID-19 may lead to higher monocyte activation, which may be associated with worsening outcomes, such as death.

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Endotoxemia and Sepsis: Important Roles for Lipopolysaccharide Binding Protein and CD14 in Endotoxin Signal Transduction

Cited by 3 publications

References 47 publications

Increased LPS levels coexist with systemic inflammation and result in monocyte activation in severe COVID-19 patients

Increased LPS levels coexist with systemic inflammation and result in monocyte activation in severe COVID-19 patients

Is sepsis a mediator-inhibitor mismatch?

Increased LPS levels coexist with systemic inflammation and result in monocyte activation in severe COVID-19 patients

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