Menu
Peptide Database
Results
No peptides found
Featured

Use search to browse all 100+ peptides

LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

An antimicrobial peptide of the cathelicidin family that provides innate immune defense by killing pathogens and modulating inflammation and wound healing.

Quick Stats
Studies 2230
Trials 95
Formula C205H340N60O53
Clear All
Utility 2
pubmed Jun 1, 2006

Heterogeneous expression of human cathelicidin hCAP18/LL-37 in inflammatory bowel diseases.

Schauber. Jürgen J; Rieger. Daniel D; Weiler. Frank F; Wehkamp. Jan J; Eck. Matthias M; Fellerm...

The study found that the antimicrobial peptide LL‑37 is higher in the colon tissue of ulcerative colitis patients, but stays the same in Crohn's disease patients. Lab tests showed that common inflammation signals and the short‑chain fatty acid butyrate didn’t change LL‑37 levels in colon cells. This suggests the body’s natural LL‑37 response differs between the two gut diseases.

Utility 2
pubmed Jun 22, 2006

The human cationic host defense peptide LL-37 mediates contrasting effects on apoptotic pathways in different primary cells of the innate immune system.

Barlow. Peter G PG; Li. Yuexin Y; Wilkinson. Thomas S TS; Bowdish. Dawn M E DM; Lau. Y Elaine YE; Co...

LL-37 is a natural protein that helps the immune system. It keeps neutrophils (a type of white blood cell) alive by turning on certain survival signals, but it can also cause airway lining cells to die. This dual action means it could boost defenses against infections, but might also harm lung tissue under some conditions.

Utility 2
pubmed Dec 1, 2007

Host defense peptide LL-37, in synergy with inflammatory mediator IL-1beta, augments immune responses by multiple pathways.

Yu. Jie J; Mookherjee. Neeloffer N; Wee. Kathleen K; Bowdish. Dawn M E DM; Pistolic. Jelena J; Li. Y...

The study shows that the natural peptide LL‑37 can team up with the inflammation signal IL‑1β to make immune cells release more signaling molecules that attract and activate other immune cells. This boost relies on several internal pathways, and it only works with certain signals, not all. The work was done in lab‑grown blood cells, not in people, so it’s more about understanding how the body’s own defenses can be amplified rather than giving a ready‑to‑use supplement plan.

Utility 2
pubmed Mar 1, 2007

Under-expression of VHL and over-expression of HDAC-1, HIF-1alpha, LL-37, and IAP-2 in affected skin biopsies of patients with psoriasis.

Tovar-Castillo. Laura E LE; Cancino-Díaz. Juan C JC; García-Vázquez. Francisco F; Can...

The study found that skin from people with psoriasis shows higher levels of the antimicrobial peptide LL‑37 and other proteins that promote blood vessel growth and block cell death, while a protein that normally suppresses blood vessel growth (VHL) is lower. This pattern may help explain why psoriasis skin cells grow quickly and resist dying.

Utility 2
pubmed Mar 7, 2008

Interaction of LL-37 with model membrane systems of different complexity: influence of the lipid matrix.

Sevcsik. E E; Pabst. G G; Richter. W W; Danner. S S; Amenitsch. H H; Lohner. K K

LL-37, a human antimicrobial peptide, sticks to cell membranes in ways that depend more on how tightly the membrane lipids are packed and their shape than just on the membrane’s electric charge. This means its effects can change a lot depending on the exact mix of fats in the membrane.

Utility 2
pubmed Jun 1, 2006

Antimicrobial peptide LL-37 internalized by immature human dendritic cells alters their phenotype.

Bandholtz. L L; Ekman. G Jacobsson GJ; Vilhelmsson. M M; Buentke. E E; Agerberth. B B; Scheynius. A...

The study shows that the natural antimicrobial peptide LL‑37 can enter young immune cells called dendritic cells, even reaching their nucleus, and makes these cells show more markers that help kick‑start the body’s adaptive immune response. This was seen in lab dishes, not in people, and no dosing or safety info was given.

Utility 2
pubmed Apr 19, 2007

Leukotriene B4 triggers release of the cathelicidin LL-37 from human neutrophils: novel lipid-peptide interactions in innate immune responses.

Wan. Min M; Sabirsh. Alan A; Wetterholm. Anders A; Agerberth. Birgitta B; Haeggström. Jesper Z...

The study shows that a lipid called leukotriene B4 can quickly make immune cells release the antimicrobial peptide LL‑37, and LL‑37 in turn helps cells make more leukotriene B4, boosting the cells' ability to eat bacteria.

Utility 2
pubmed Mar 5, 2008

Cholesterol, lanosterol, and ergosterol attenuate the membrane association of LL-37(W27F) and temporin L.

Sood. Rohit R; Kinnunen. Paavo K J PK

The study found that cholesterol and similar sterols (lanosterol and ergosterol) can lessen how strongly two antimicrobial peptides, LL‑37(F27W) and temporin L, stick into cell membranes, with cholesterol being the most effective. This suggests that the amount of sterols in a membrane can protect cells from the potentially damaging effects of these peptides.

Utility 2
pubmed Mar 3, 2010

The Alzheimer's disease-associated amyloid beta-protein is an antimicrobial peptide.

Soscia. Stephanie J SJ; Kirby. James E JE; Washicosky. Kevin J KJ; Tucker. Stephanie M SM; Ingelsson...

The study shows that the protein amyloid‑beta, which is usually linked to Alzheimer’s disease, also works like an antimicrobial peptide (AMP) similar to the human AMP LL‑37. In lab tests, amyloid‑beta killed a range of common microbes as well as, or better than, LL‑37, and brain tissue from Alzheimer’s patients had higher antimicrobial activity that disappeared when amyloid‑beta was removed.

Utility 2
pubmed Dec 23, 2007

[Cathelicidin LL-37. A central factor in the pathogenesis of inflammatory dermatoses?].

Schauber. J J; Ruzicka. T T; Rupec. R A RA

The peptide LL‑37, made by skin cells, can either be too low or too high and this imbalance contributes to common skin problems like eczema, rosacea, and psoriasis. Low LL‑37 makes eczema skin prone to infections, while too much or broken‑down LL‑37 fuels inflammation in rosacea and helps trigger an autoimmune reaction in psoriasis. Targeting LL‑37 levels could become a way to treat these conditions, but the study doesn’t give specific how‑to steps.

Utility 2
pubmed Mar 5, 2009

Salivary antimicrobial peptides (LL-37 and alpha-defensins HNP1-3), antimicrobial and IgA responses to prolonged exercise.

Davison. Glen G; Allgrove. Judith J; Gleeson. Michael M

A 2.5‑hour moderate bike ride raised the levels of the antimicrobial peptide LL‑37 (and related defensins) in saliva, even though overall antibacterial activity against E. coli didn’t change. IgA levels stayed the same but its ratio to saliva concentration dropped. This suggests that longer, steady‑state cardio can boost certain innate immune factors in the mouth.

Utility 2
pubmed Sep 1, 2009

Role of reactive oxygen species (ROS) in Mycobacterium bovis bacillus Calmette Guérin-mediated up-regulation of the human cathelicidin LL-37 in A549 cells.

Méndez-Samperio. Patricia P; Pérez. Aline A; Torres. Laura L

When human lung cells are exposed to the BCG vaccine, they quickly produce reactive oxygen species (ROS). This ROS burst is needed for the cells to turn on the antimicrobial peptide LL‑37. Blocking ROS with antioxidants or NADPH‑oxidase inhibitors stops the LL‑37 increase.

Utility 2
pubmed Dec 18, 2007

F2L, a peptide derived from heme-binding protein, inhibits LL-37-induced cell proliferation and tube formation in human umbilical vein endothelial cells.

Lee. Sun Young SY; Lee. Mi-Sook MS; Lee. Ha Young HY; Kim. Sang Doo SD; Shim. Jae Woong JW; Jo. Seon...

Researchers found that a small protein called F2L can stop another molecule, LL‑37, from making blood‑vessel cells grow and form new vessels in lab dishes. While F2L itself makes the cells move a bit, it blocks the growth‑promoting signals of LL‑37, hinting it could be useful for controlling unwanted blood‑vessel formation.

Utility 2
pubmed May 3, 2010

Polyamines can increase resistance of Neisseria gonorrhoeae to mediators of the innate human host defense.

Goytia. Maira M; Shafer. William M WM

The study shows that naturally occurring polyamines (like spermine and spermidine) can make the gonorrhea bacteria more resistant to the body's natural antimicrobial peptide LL-37 and to other similar peptides, but they don't affect resistance to regular antibiotics. This effect depends on how much polyamine is present and can be reversed.

Utility 2
pubmed Sep 1, 2007

Effects of the antimicrobial peptide LL-37 and hyperthermic preconditioning in septic rats.

Torossian. Alexander A; Gurschi. Eugeniu E; Bals. Robert R; Vassiliou. Timon T; Wulf. Hinnerk F HF;...

In a rat study, giving the antimicrobial peptide LL‑37 after a severe abdominal infection boosted survival from 30% to about 70%, and giving it together with a short, high‑heat treatment (41 °C for an hour) raised survival even higher to 90%. The heat treatment alone didn’t help, but the combo lowered harmful inflammation markers. These results are promising but still early and done in animals, so they don’t translate directly into a safe, ready‑to‑use protocol for people.

Utility 2
pubmed Aug 31, 2007

The host defence peptide LL-37/hCAP-18 is a growth factor for lung cancer cells.

von Haussen. Judith J; Koczulla. Rembert R; Shaykhiev. Renat R; Herr. Christian C; Pinkenburg. Olaf...

The study shows that the natural peptide LL‑37, which is part of our immune system, can actually act like a growth signal for lung cancer cells, making them multiply faster and form bigger tumors in mice. This means taking LL‑37 as a supplement could be risky, especially for people who might be prone to cancer.

Utility 2
pubmed Dec 26, 2007

Expression of cathelicidin LL-37 during Mycobacterium tuberculosis infection in human alveolar macrophages, monocytes, neutrophils, and epithelial cells.

Rivas-Santiago. Bruno B; Hernandez-Pando. Rogelio R; Carranza. Claudia C; Juarez. Esmeralda E; Contr...

When lung cells get infected with TB bacteria, they quickly make more of the natural antimicrobial peptide LL‑37, especially the alveolar macrophages. This early boost disappears later when granulomas form, and the peptide can be turned on by activating certain Toll‑like receptors (TLR‑2, TLR‑4, TLR‑9).

Utility 2
pubmed Nov 30, 2009

Expression of factor H binding protein of meningococcus responds to oxygen limitation through a dedicated FNR-regulated promoter.

Oriente. Francesca F; Scarlato. Vincenzo V; Delany. Isabel I

The study shows that a meningococcus protein (fHBP) that helps the bacteria survive attacks by the human antimicrobial peptide LL‑37 is turned on when oxygen levels are low. This activation is controlled by a bacterial regulator called FNR, which binds to a special promoter and boosts fHBP production.