Expression and significance of serum vitamin D and LL-37 levels in infants with bacterial pneumonia

Zhao, Shaojie; He, Yixiu; Pan, Menglan; Chen, Bingzhang; Zhang, Siqi; Zhang, Yufeng; Zhu, Yafei

doi:10.3389/fped.2022.989526

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…Studies reported that LL‐37 exhibits modulation of immune and inflammatory factor secretion in inflammatory diseases, such as chronic obstructive pulmonary disease and pneumonia, 21,22 and neutralizes LPS and thus inhibits TLR4 signaling pathway 23 . Moreover, LL‐37 can also induce septic shock by activating NLRP3 inflammatory vesicles prompting the production of a series of inflammatory factors such as IL‐1β 24 .…”

Section: Discussionmentioning

confidence: 99%

Cathelicidin (LL‐37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4–NF‐κB–NLRP3 signaling

Si,

Lu,

Wen

et al. 2023

Immunity Inflam & Disease

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BackgroundKawasaki disease (KD) is a type of vasculitis with an unidentified etiology. Cathelicidin (LL‐37) may be involved in the development of the KD process; therefore, further research to investigate the molecular mechanism of LL‐37 involvement in KD is warranted.MethodsEnzyme‐linked immunosorbent assay (ELISA) was used to detect the levels of tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, NLRP3, and LL‐37 in the sera of healthy subjects, children with KD, and children with pneumonia. Subsequently, human recombinant LL‐37 or/and toll‐like receptors 4 (TLR4)‐specific inhibitor TAK‐242 stimulated human coronary artery endothelial cells (HCAECs), CCK‐8 was used to detect cell proliferation, flow cytometry to detect apoptosis, transmission electron microscopy to observe cytoskeletal changes, Transwell to measure cell migration ability, ELISA to detect inflammatory factor levels, Western blot analysis to analyze protein levels of toll‐like receptors 4 (TLR4) and NF‐κB p‐65, and quantitative real‐time polymerase chain reaction (qRT‐PCR) to determine LL‐37, NLRP3 mRNA levels.ResultsIn this study, we found that the level of LL‐37 was highly expressed in the serum of children with KD, and after LL‐37 stimulation, apoptosis was significantly increased in HCAECs, and the expression levels of TLR4, NLRP3 and inflammatory factors in cells were significantly enhanced. Intervention with the TLR4‐specific inhibitor TAK‐242 significantly alleviated the LL‐37 effects on cellular inflammation, TLR4, NLRP3 promotion effect.ConclusionsOur data suggest that LL‐37 induces an inflammatory response in KD coronary endothelial cells via TLR4‐NF‐κB‐NLRP3, providing a potential target for the treatment of KD.

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Section: Discussionmentioning

confidence: 99%

Cathelicidin (LL‐37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4–NF‐κB–NLRP3 signaling

Si,

Lu,

Wen

et al. 2023

Immunity Inflam & Disease

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show abstract

“…Studies reported that LL-37 exhibits modulation of immune and inflammatory factor secretion in inflammatory diseases, such as chronic obstructive pulmonary disease and pneumonia (20,21), and neutralizes LPS and thus inhibits TLR4 signaling pathway (22).…”

Section: Ll-37 Stimulates Immune Inflammatory Responses In Hcaecs Cel...mentioning

confidence: 99%

Cathelicidin (LL-37) causes coronary artery lesions in Kawasaki disease by activating TLR4-NF-κB-NLRP3 signaling

Si,

Lu,

Wen

et al. 2024

Preprint

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Background: Kawasaki disease (KD) is a kind of vasculitis with an unidentified etiology. Cathelicidin (LL-37) may be involved in the development of the KD process; therefore, further research to investigate the molecular mechanism of LL-37 involvement in KD is warranted. Methods: Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of TNF-α, IL-1β, NLRP3, and LL-37 in the sera of healthy subjects, children with KD, and children with pneumonia. Subsequently, human recombinant LL-37 or/and TLR4-specific inhibitor TAK-242 stimulated HCAECs cells, CCK-8 was used to detect cell proliferation, flow cytometry to detect apoptosis, transmission electron microscopy to observe cytoskeletal changes, Transwell to measure cell migration ability, ELISA to detect inflammatory factor levels, Western blotting to analyze protein levels of TLR4 and NF-κB p-65, and qRT-PCR to determine LL-37, NLRP3 mRNA levels. Results: In this study, we found that the level of LL-37 was highly expressed in the serum of children with KD, and after LL-37 stimulation, apoptosis was significantly increased in HCAECs, and the expression levels of TLR4, NLRP3 and inflammatory factors in cells were significantly enhanced. Intervention with the TLR4-specific inhibitor TAK-242 significantly alleviated the LL-37 effects on cellular inflammation, TLR4, NLRP3 promotion effect. Conclusions: Our data suggest that LL-37 induces an inflammatory response in endothelial cells via TLR4-NF-κB, leading to coronary artery injury in KD, providing a potential target to treat KD.

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Outcomes of High-Dose Versus Low-Dose Vitamin D on Prognosis of Sepsis Requiring Mechanical Ventilation: A Randomized Controlled Trial

Ashoor,

Abd Elazim,

Mustafa

et al. 2024

J Intensive Care Med

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Background: Critically ill patients with sepsis have a high incidence of vitamin D deficiency. Vitamin D promotes the synthesis of human cathelicidin antimicrobial peptide, a precursor of LL-37, which is a part of the innate immune system. This study investigated the effectiveness and safety of the early administration of high-dose enteral vitamin D3 in comparison with low-dose vitamin D3 in patients with sepsis requiring mechanical ventilation (MV). Methods: Eighty adult patients with sepsis requiring MV with known vitamin D deficiency were randomly assigned to receive either an enteral 50 000 IU (Group I) or 5000 IU (Group II) vitamin D supplementation. Clinical and laboratory parameters were evaluated at baseline and on days 4 and 7 between the study groups. The change in serum procalcitonin (PCT) levels on day 7 was the primary outcome, while the change in serum LL-37 levels on day 7, changes in sequential organ failure assessment (SOFA) score, and clinical pulmonary infection score on day 7, MV duration, and hospital length of stay (LOS) were the secondary outcomes. Results: The (day 7-day 0) change in serum PCT and LL-37 levels and SOFA score were significantly different in Group I ( P = .010, P < .001, and P < .001, respectively). The SOFA score was significantly different on days 4 and 7 in Group I ( P < .001 and P < .001, respectively). The incidence of early ventilator-associated pneumonia was significantly different between both treatment groups ( P = .025). The hospital LOS was shorter in Group I ( P < .001). No 25-hydroxyvitamin-D toxicity was observed in either group. Conclusions: Early enteral administration of high-dose vitamin D3 in critically ill patients with sepsis requiring MV along with standard treatment for sepsis decreased serum procalcitonin levels, increased serum LL-37 levels, and ameliorated illness severity scores.

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Expression and significance of serum vitamin D and LL-37 levels in infants with bacterial pneumonia

Cited by 3 publications

References 27 publications

Cathelicidin (LL‐37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4–NF‐κB–NLRP3 signaling

Cathelicidin (LL‐37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4–NF‐κB–NLRP3 signaling

Cathelicidin (LL-37) causes coronary artery lesions in Kawasaki disease by activating TLR4-NF-κB-NLRP3 signaling

Outcomes of High-Dose Versus Low-Dose Vitamin D on Prognosis of Sepsis Requiring Mechanical Ventilation: A Randomized Controlled Trial

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