Recombinant Mouse Cathelicidin antimicrobial peptide (Camp) - E.coli

1. Mice treated with BMMNCs pre-incubated with CRAMP had smaller scars, enhanced cardiac recovery and less adverse remodeling. Histologically, this group had higher capillary density. Similarly, sustained CRAMP release from hydrogels enhanced the therapeutic effect of SDF-1, leading to enhanced functional recovery
2. LL-37/CRAMP represents an important mediator of platelet activation and thrombo-inflammation.
3. CRAMP deficiency impairs phagocytosis in cultured microglia cells after exposure to N. meningitides.
4. Immunoblotting, qPCR, ChIP and siRNA-mediated gene knockdown studies revealed that the activation of phosphatidylinositol 3-kinase/protein kinase C zeta pathways in poly(I:C)-stimulated cells underlies Sp1 phosphorylation and recruitment to the mCRAMP promoter, leading to enhanced transcription
5. The effect on insulin resistance found in Cramp-/- mice is solely due to leukocyte infiltration and not due to inflammatory phenotype of macrophages. Therefore we conclude that cathelicidin causes insulin resistance by the recruitment of myeloid cells into the adipose tissue.
6. Cathelicidin is required for innate resistance to M. tuberculosis in a relevant animal model and is a key mediator in regulation of the levels of pro-inflammatory cytokines by calcium and cyclic nucleotides.
7. Histological examination confirmed that CRAMP deficiency worsened the pancreatic inflammatory condition. These results indicate that CRAMP may be considered a novel modulatory mediator in mouse experimental AP.
8. promotes olfactory epithelium inflammation
9. overexpressed CRAMP in prostate tumor initially chemoattracts early myeloid progenitors to tumor microenvironment and mediates differentiation and polarization of early myeloid progenitors into protumorigenic M2 macrophages during PCa progression
10. critical role in prevention of RSV-mediated disease postinfection exogenously applied LL-37 is protective against RSV-mediated disease in vivo.
11. The aim of this project was to examine the functional impact of the human cathelicidin LL-37 and the mouse cathelicidin-related AMP (CRAMP) on the pathogenesis of lupus and arthritis.
12. pancreatic beta-cells' production is controlled by short-chain fatty acids produced by the gut microbiota, and is defective in non-obese diabetic (NOD) mice
13. Data indicate the role of cathelicidin-related antimicrobial peptide (CRAMP) as part of the innate immune defense against pathogens in bacterial CNS infections.
14. Hypoxia-inducible factor-1alpha (HIF-1alpha), a transcription factor important for activating innate immune effectors, and the antimicrobial peptide LL-37 (CRAMP in mice) are key determinants of C. albicans colonization resistance.
15. Specific structural motifs in syndecan-1 HS promote Staphylococcus aureus corneal infection by inhibiting neutrophil CRAMP.
16. these findings show that the production of an antimicrobial peptide Camp by adipocytes is an important element for protection against S. aureus infection of the skin
17. Cathelicidin-deficient (Cnlp(-/-)) mice produce much less LTB4 and TXB2 in vivo in response to TNF-alpha compared with control mice.
18. observations indicate a nonredundant role for Fpr2 and its agonist CRAMP in DC maturation in immune responses.
19. Expression of the antimicrobial peptide cathelicidin in the context of inflammation and in non-tumorous cells is an important factor for lung tumor growth.
20. Citrullination alters immunomodulatory function of LL-37 essential for prevention of endotoxin-induced sepsis.
21. visfatin enhances CAMP, hBD-2, hBD-3, and S100A7 production in human keratinocytes and their orthologs in murine imiquimod-treated psoriatic skin.
22. These data demonstrated that Salmonella Typhimurium PhoQ can sense cationic antimicrobial peptides and CRAMP serves as a putative direct PhoPQ activation signal in the mouse intestine.
23. suppresses osteoclastogenesis induced by LPS and flagellin
24. Collectively, these findings indicate that cathelicidin protects against H. pylori infection and its associated gastritis in vivo. Our study also demonstrates the feasibility of using the transformed food-grade bacteria to deliver cathelicidin.
25. this investigation revealed an indispensable role for BD3, BD4, and CRAMP in defense against F. solani-induced keratitis
26. Neutrophil-derived cathelicidin promotes adhesion of classical monocytes.
27. TLR9 can induce the expression of antimicrobial peptides such as CRAMP in response to bacterial DNA motifs in primary glial cells.
28. LL-37 activates caspase-1 in murine macrophages, resulting in release of active IL-1beta & IL-18. LL-37 activation of the NLRP3 inflammasome utilizes P2X7 receptor-mediated potassium efflux.
29. CRAMP may exert important immunomodulatory effects that regulate lung injury and Gram-negative bacterial dissemination.
30. CRAMP promotes atherosclerosis by enhancement of the recruitment of inflammatory monocytes.
31. The role of the Src family kinase Lyn in the immunomodulatory activities of cathelicidin peptide LL-37 on monocytic cells
32. Cathelicidin signaling via the Toll-like receptor (TLR9) protects against colitis in mice.
33. results suggest that mCRAMP differentially regulates B- and T-cell function and implicate mCRAMP in the regulation of adaptive immune responses.
34. ER stress increases CAMP expression via NF-kappaB-C/EBPalpha activation, independent of VDR, illuminating a novel VDR-independent role for ER stress in stimulating innate immunity.
35. The presence of pronounced host inflammatory infiltration in lesions and lymph nodes of Leishmania-infected animals was CAMP-dependent.
36. LL-37 induces apoptosis in CTLs via multiple different mechanisms, initiated by the LL-37-induced leakage of granzymes from cytolytic granules
37. Data show that cathelicidin is highly produced during experimental pulmonary tuberculosis from diverse cellular sources and could have significant participation in its pathogenesis.
38. Data show flagellin-induced protection was partially abrogated in cathelicidin-related antimicrobial peptide-deficient mice.
39. CRAMP, the unique antimicrobial peptide derived from cathelin in mouse inhibited all the responses coupled to P2X(7) receptors in macrophages from wild type mice.
40. an important native component of innate host defence in mice and provide protection against necrotic skin infection caused by Group A Streptococcus (GAS).
41. solution structure in TFE/H2O solution determined by CD and NMR spectroscopy
42. Cathelicidins are localized in the cytoplasmic granules of murine bone marrow-derived mast cells and directly participate in the mast cell immune response.
43. cathelicidin expression (CRAMP) in the skin is 10- to 100-fold greater in the perinatal period than adult
44. Intracellular reactive oxygen intermediates and proteases regulate macrophage CRAMP expression and activity to impair the replication of an intracellular bacterial pathogen.
45. cathelicidin antimicrobial peptides are expressed in murine mammary glands
46. Mig-14 and VirK inhibit binding of CRAMP to Salmonella typhimurium and thus promote bacterial resistance to CRAMP
47. important component of innate antimicrobial defense in the colon
48. CRAMP functions as both a chemoattractant for phagocytic leukocytes and an enhancer of adaptive immune response.
49. role of cathelicidin in host susceptibility to HSV infection
50. Data describe the production and function of the cathelicidin antimicrobial peptides LL-37, its precursor hCAP-18 and its ortholog CRAMP in epithelial cells of human and mouse urinary tract, respectively.

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