LL-37 Dosing Protocol: Antimicrobial Research Guide

Mechanistically, LL-37-induced CXCL10 production relied on the Jak1/signal transducer and activator of transcription 1 signaling pathway. In summary, our findings provide a crucial link to keratinocyte-T-cell crosstalk, and blockade of the CXCL10:CXCR3 axis or Jak1/signal transducer and activator of transcription 1 pathways can be an effective anti-inflammatory strategy to reduce rosacea inflammation by restricting pathogenic T-cell infiltration.

Limitations: No placebo control reported.

These immunomodulatory actions occurring at concentrations lower than those microbicidal uncover a new guise for cathelicidin modulating the epithelial barrier against A/E pathogens. Recognizing native cathelicidin's functions in a specified disease setting (e.g., colitis) will help establish it as an anti-infectious immunomodulator.

Limitations: No placebo control reported.

Finally, the LL-37-induced EndMT was inhibited by Akt and nuclear factor-kappa B (NF-κB) inhibitors, suggesting that LL-37 induces EndMT by activating Akt and NF-κB. These observations speculate a role of LL-37 in the pathogenesis of atherosclerosis as an EndMT inducer.

Limitations: No placebo control reported.

LL-37 was expressed in macrophages and myofibroblasts of capsular tissue in 10 (34%) and nine (31%) of the specimens, respectively. In eight cases (27.5%), it was expressed by both macrophages and myofibroblasts of the same specimen.

Limitations: No placebo control reported.

The effect of LL-37 is time-dependent. As a result, LL-37 may provide rapid and affordable therapies for RVFV infection in Egypt, both during outbreaks and as a preventive strategy.

Limitations: No placebo control reported.

Interestingly, synthetic LL-37, at this concentration, reduces viability of human osteoblast-like MG63 cells, whereas the THP-1 cells are less sensitive as demonstrated by the MTT assay. In summary, we show that vitamin D enhances hCAP18/LL-37 production, and that this effect can be of physiological/pathophysiological relevance for LL-37-induced human osteoblast toxicity.

Limitations: No placebo control reported.

This review provides a comprehensive discussion of research highlighting the beneficial health effects of LL-37/nucleic acid complexes, as well as discussing observed detrimental effects. We will emphasize why it is important to investigate and elucidate structural characteristics, such as condensation patterns of nucleic acids within complexation, and their mechanisms of action, to shed light on the intricate physiological effects of LL-37 and the seemingly contradictory role of LL-37/nucleic acid complexes in the innate immune response.

Limitations: No placebo control reported. Review article — no new primary data.

Oral LL-37 expression is an important factor in oral homeostasis that maintains the physiological microbiota but is also involved in the development of oral dysbiosis, infectious diseases (including viral, bacterial, and fungal infections), autoimmune diseases, and oral carcinomas. This peptide has also been proposed as a marker of inflammation severity and treatment outcome.

Limitations: Animal study only — human translation uncertain. Review article — no new primary data.

In addition, cathelicidin LL-37 inhibited the cell cycle and accumulated cells in the S phase. Therefore, these results specify the potential of cathelicidin LL-37 for developing a new and effective anti-Candida agent.

Limitations: In-vitro study — may not reflect in-vivo effects.

Interestingly, the LL-37‒induced distribution of tight junction proteins and improvement in the tight junction barrier were inhibited in autophagy-deficient keratinocytes and keratinocytes and skin models treated with autophagy inhibitors, indicating that the LL-37‒mediated tight junction barrier is associated with autophagy activation. Collectively, these findings suggest that LL-37 is a potential therapeutic target for skin diseases characterized by dysfunctional autophagy and skin barriers.

Limitations: No placebo control reported.

coli load in the liver and spleen (P&#xa0;<&#xa0;0.01) and restored the structure of the liver and kidney. Taken together, LL-37 conferred protection in a EHEC O157:H7-induced mouse model by reducing intestinal inflammation, enhancing intestinal barrier function, and restoring the balance of the intestinal microbiota, which indicates the therapeutic potential of LL-37 against pathogen infection.

Limitations: No placebo control reported.

In terms of its efficacy and safety in vivo, there are still many questions to be answered. Undoubtedly, LL-37 can open up new windows of opportunity to prevent and treat obstinate biofilm-mediated infections.

Limitations: No placebo control reported. Review article — no new primary data.

Taken together, these observations suggest that LL-37 induces autophagy in endothelial cells but enhances cell death in autophagy-dysfunctional conditions, in which the intracellular degradation of LL-37 is disturbed. Thus, LL-37 may exert an adverse action on autophagy-dysfunctional endothelial cells to induce cell death in the pathogenesis of atherosclerosis.

Limitations: No placebo control reported.

In addition, it has been postulated that LL-37 can directly bind the S1 domain of SARS-CoV-2, mask angiotensin converting enzyme 2 (ACE2) receptors, and limit SARS-CoV-2 infection. Purposeful upregulation of LL-37 could also serve as a preventative and therapeutic strategy for SARS-CoV-2 infections.

Limitations: No placebo control reported. Review article — no new primary data.

Altogether, our results suggest a "carpet" membrane dissolution followed by a detergent-like membrane disruption mechanism upon LL-37 activity. This research gives a novel insight into the understanding of LL-37 influence on multicomponent model membranes and a promising contribution to the development of LL-37-derived therapeutic agents against drug-resistant bacteria.

Limitations: No placebo control reported.

Pretreatment with the FPRL1 antagonist inhibited LL-37-induced phosphorylation of ERK and Akt proteins and attenuated LL-37-induced HDLEC migration and tube-like formation. These data indicated that LL-37 induces lymphangiogenesis in lymphatic endothelial cells via FPRL1, and the activation of the ERK and Akt-dependent signaling pathways.

Limitations: No placebo control reported.

Diseased sites had significantly (P <0.05) higher levels of LL-37 and lower levels of HNP 1-3 than healthy sites in both smokers and non-smokers. Diseased sites of smokers presented significantly lower levels of LL-37 and HNP 1-3 when compared with diseased sites of non-smokers.

Limitations: No placebo control reported.

Between others, they demonstrate high clinical potential as antimicrobial, anti-cancer, immunomodulatory and regenerative agents. Due to continuous research, knowledge on pleiotropic character of natural antibacterial peptides and their mimics is growing, and it is justifying to stay that the therapeutic potential of nanosystems containing membrane active compounds has not been exhausted yet.

Limitations: No placebo control reported. Review article — no new primary data.

LL-37 treatment dramatically increased IFN&#x3b2;1 expression in treated cells in a time-dependent manner. Our results establish LL-37 as a relevant and novel potential therapeutic strategy for the treatment of VEEV infections.

Limitations: No placebo control reported.

Also discussed are other application strategies, including peptide formulation, antimicrobial implants, and peptide-inducing factors such as vitamin D and sunlight. Finally, we summarize what we learned from peptide design based on human LL-37.

Limitations: No placebo control reported. Review article — no new primary data.

Given that the phenotypic and functional properties of immune compartments are different and significantly impacted by the anatomical sites, tissue-specific factors of host origin and microbial communities play important roles in the regulation of LL-37. This review summarizes the expression and biological functions of LL-37 and discusses its significant roles in the innate immune system based on its anatomical distribution.

Limitations: No placebo control reported. Review article — no new primary data.

Meanwhile, the findings that vitamin D-dependent induction of cathelicidin in human macrophages activates the anti-cancer activity of tumor-associated macrophages (TAMs) and enhances antibody-dependent cellular cytotoxicity (ADCC) support critical roles of vitamin D-dependent induction of cathelicidin in cancer progression. This review describes novel advances involving the roles and mechanisms of human cathelicidin LL-37 in cancer.

Limitations: No placebo control reported. Review article — no new primary data.

EGCG killed 100&#xa0;% of planktonic S. mutans within 5&#xa0;h, inhibited biofilm formation within 24&#xa0;h, and reduced bacteria cells in preformed biofilms within 3&#xa0;h at a concentration of 0.2&#xa0;mg/mL.

Limitations: No placebo control reported.

Sixty-three post-infectious BO patients and 65 healthy children (median age 73&#x2009;&#xb1;&#x2009;55 and 78.74&#x2009;&#xb1;&#x2009;36.32 months, respectively) were enrolled in the study. The mean of hBD2 levels in patients and the control group were 1.06&#x2009;&#xb1;&#x2009;0.24 and 0.67&#x2009;&#xb1;&#x2009;0.72 ng/mL, respectively (P&#x2009;<&#x2009;0.001).

Limitations: Standard limitations apply. Check original paper for full discussion.

We analyzed the main molecular pathways dependent on human cathelicidin and related them to specific diseases. We conclude that LL-37 shows a great potential to be further investigated and developed as a drug with clinical use.

Limitations: No placebo control reported. Review article — no new primary data.

Cathelicidin peptides could serve as a template for the development of modern anti-microbial and anti-viral drugs. LL-37 is an excellent candidate to develop into therapeutics for infected wounds.

Limitations: No placebo control reported. Review article — no new primary data.

We also consider its different membrane-dependent effects on our own cells, which underlie many of its other activities in host defence. This article is part of a Special Issue entitled: Pore-Forming Toxins edited by Mauro Dalla Serra and Franco Gambale.

Limitations: No placebo control reported. Review article — no new primary data.

Furthermore, LL-37 reduced phosphorylation of Src kinase and Akt(Ser473), decreased platelet spreading on immobilized fibrinogen and inhibited P-selectin expression on platelets. These results demonstrate that LL-37 has antiplatelet and antithrombotic actions.

Limitations: No placebo control reported.

This discrepancy can be attributed to peptide-based factors, host membrane-based factors, and signal regulation. Here, we describe the association between AMPs and cancer with a focus on anticancer peptide functions and selectivity in an effort to understand potential therapeutic implications.

Limitations: In-vitro study — may not reflect in-vivo effects. Review article — no new primary data.

The mechanistic results from this study suggest that regulation of immune-mediated inflammation by these peptides may be controlled by the dual phosphatase MKP-1. We speculate that LL-37 and its derivatives may contribute to the control of immune-mediated inflammatory diseases.

Limitations: No placebo control reported.