An antimicrobial peptide of the cathelicidin family that provides innate immune defense by killing pathogens and modulating inflammation and wound healing.
Ahmed. Aslaa A; Siman-Tov. Gavriella G; Hall. Grant G; Bhalla. Nishank N; Narayanan. Aarthi A
The paper reviews how human antimicrobial peptides like LL‑37, which are part of our natural immune response, can also fight viruses such as dengue and Zika. It explains that these peptides are quickly produced during infection and can block viruses and calm inflammation, but it doesn’t give specific dosing or treatment plans.
Kulkarni. Nikhil N NN; Takahashi. Toshiya T; Sanford. James A JA; Tong. Yun Y; Gombart. Adrian F AF;...
The study shows that the antimicrobial peptide LL‑37, which is higher in rosacea skin, makes skin blood vessels more sensitive to UV light and promotes inflammation by increasing adhesion molecules that attract immune cells. This effect needs both LL‑37 and double‑stranded RNA released from skin cells after UV exposure, and it works through immune sensors like TLR3. Knocking down these sensors reduces the inflammatory response.
Mücke. Pierre-Alexander PA; Maaß. Sandra S; Kohler. Thomas P TP; Hammerschmidt. Sven S; Be...
The study looked at how the pneumonia‑causing bacteria Streptococcus pneumoniae changes its protein makeup when exposed to the human immune peptide LL‑37. It found that the bugs use known tricks to dodge the peptide and also uncovered a few new proteins that might help them survive.
Zhang. Lulu L; Wei. Xubiao X; Zhang. Rijun R; Petitte. Jim N JN; Si. Dayong D; Li. Zhongxuan Z; Chen...
Scientists created a new hybrid peptide called LTA by mixing parts of the natural antimicrobial peptide LL-37 with a piece of thymosin alpha‑1. In lab tests and mice with gut inflammation caused by bacterial toxins, LTA lowered inflammation markers, protected the gut lining, and was not toxic to cells. It works by binding to the bacterial toxin and blocking the inflammation signaling pathway.
A study in HIV‑positive people gave them high‑dose vitamin D and phenylbutyrate for 16 weeks. While vitamin D levels went up, the combo did not change most gut‑related inflammation markers or the gut microbiome. Only a small subgroup with low vitamin D showed a modest rise in the antimicrobial peptide LL‑37, and this effect disappeared after adjusting for other factors.
In newborn rats exposed to high oxygen, which damages kidneys, giving the natural peptide LL‑37 reduced the injury, lowered oxidative stress and inflammation, and helped the kidneys stay healthier. The study used injections of 4‑8 mg/kg for the first week after birth, showing the peptide can counteract the harmful effects of excess oxygen in this animal model.
Kozhikhova. Ksenia V KV; Shilovskiy. Igor P IP; Shatilov. Artem A AA; Timofeeva. Anastasiia V AV; Tu...
Scientists made several short, positively‑charged peptides and peptide‑dendrimers and tested them against RSV. Two of the new peptides worked better than the natural immune peptide LL‑37, and the dendrimer versions were less toxic to human cells.
Madanchi. H H; Shoushtari. M M; Kashani. H H HH; Sardari. S S
The paper reviews antimicrobial peptides (AMPs) that naturally protect the vagina, highlighting LL-37 as one that can kill both microbes and sperm. It explains why these peptides are interesting as new antibiotics, especially against drug‑resistant sexually transmitted infections, but does not give specific dosing or how to use them in everyday health routines.
McCarthy. Sean D SD; Horgan. Elizabeth E; Ali. Areeba A; Masterson. Claire C; Laffey. John G JG; Mac...
Scientists found that fluid from stem cells can kill common lung bacteria even after being turned into a mist for inhalation, but the specific peptide LL‑37 disappears during that process. The antibacterial effect comes from something larger than 3000 Da, not just LL‑37.
LL-37, a natural human antimicrobial peptide, was shown in lab cells and mice to boost bone‑forming cell growth, cut inflammatory signals, and protect against bone loss caused by bacterial toxins. It works by activating a receptor called P2X7 and turning on specific cell‑signaling pathways (ERK and JNK).
Scientists made mice that constantly produce the natural antimicrobial peptide LL-37 and also transplanted stem cells engineered to release LL-37 into damaged lungs. The mice cleared a dangerous lung infection (Pseudomonas aeruginosa) better and survived with less breathing trouble. Human lung stem cells were also shown to be able to be engineered the same way, hinting at future treatments.
In mice, giving the natural peptide LL-37 (called CRAMP in mice) before a kidney injury caused by loss of blood flow helped protect the kidneys. It reduced inflammation, cell death, and a specific immune alarm system called NLRP3, and it needed the EGF receptor to work. Humans with acute kidney injury had lower LL-37 levels, hinting the peptide might matter in people too.
Wu. Yan Y; Zhang. Yacheng Y; Zhang. Jie J; Zhai. Tingting T; Hu. Jingping J; Luo. Hairong H; Zhou. H...
In mice, the natural antimicrobial peptide cathelicidin (LL‑37 in humans) makes heart damage worse after a temporary blockage of blood flow. The peptide comes mainly from neutrophils (a type of white blood cell) that rush into the heart, and it triggers strong inflammation through TLR4 and the P2X7/NLRP3 inflammasome, leading to more cell death and higher heart‑damage markers.
Qin. Xiuchuan X; Zhu. Guangfa G; Huang. Lixue L; Zhang. Wenwei W; Huang. Yan Y; Xi. Xin X
In a mouse study, giving the natural peptide LL‑37 or a similar version (sLL‑37) after sepsis reduced inflammation and lung damage by stopping immune cells called neutrophils from moving into the lungs. The effect was linked to blocking specific signaling proteins (FAK, ERK, and P38).
Hacioglu. Mayram M; Oyardi. Ozlem O; Bozkurt-Guzel. Cagla C; Savage. Paul B PB
The study tested the natural antimicrobial peptide LL‑37 (along with other peptides) against stubborn mixed fungal‑bacterial biofilms and found it didn’t work at the doses they tried, while synthetic compounds called ceragenins were much better at killing these biofilms.
Liu. Tangxiele T; Deng. Zhili Z; Xie. Hongfu H; Chen. Mengting M; Xu. San S; Peng. Qinqin Q; Sha. Ke...
The study found that the skin‑irritating peptide LL‑37 triggers higher levels of a protein called ADAMDEC1, which pushes immune cells (macrophages) toward a pro‑inflammatory M1 state and worsens rosacea‑like skin inflammation in mice and humans.
LL-37, a natural antimicrobial peptide, helps immune cells stay alive and can calm down an over‑active immune response by slowing T‑cell growth and boosting the number of regulatory T‑cells that keep inflammation in check. However, its effects change depending on whether the immune system is already activated, and the study only looked at cells in a lab dish, not in people.
Nordström. Randi R; Andrén. Oliver C J OCJ; Singh. Shalini S; Malkoch. Michael M; Davoudi....
Scientists tested tiny, biodegradable gel particles (nanogels) that can hold the antimicrobial peptide LL‑37. The gels stick to the peptide but don’t let it go inside, so the peptide is released quickly and still kills bacteria. The gels themselves aren’t toxic to red blood cells, but they don’t make LL‑37 work any better than the free peptide.
Nordström. Randi R; Browning. Kathryn L KL; Parra-Ortiz. Elisa E; Damgaard. Liv Sofia Elinor LS...
The study looked at how the antimicrobial peptide LL‑37 interacts with cell‑like membranes when it’s delivered free versus when it’s packed inside tiny gel particles (microgels). It found that the peptide itself does the heavy lifting – it binds to and disrupts membranes, especially at higher concentrations – while the gel particles barely stick to the membrane. Loading LL‑37 into the microgels slows its release, which in turn slows the peptide’s ability to insert into the membrane and form its usual helix shape.
Ribon. Matthieu M; Seninet. Sarra S; Mussard. Julie J; Sebbag. Mireille M; Clavel. Cyril C; Serre. G...
The study shows that neutrophil traps (NETs) can both ramp up and calm down inflammation in rheumatoid arthritis, and that the peptide LL‑37 together with complement protein C1q changes how NETs affect immune cells. While LL‑37 can boost some anti‑inflammatory signals, it also makes certain immune cells more active, so its effects are context‑dependent.