Peptides (v.59, #C)

Sequence analysis and feeding responses evoked by the large molecular form of gastrin releasing peptide (GRP) in the rat GRP-29 by Joseph R. Reeve; Martha C. Washington; Karen H. Park; Tanisha Johnson; Jizette Hunt; John E. Shively; Mike Ronk; Terry D. Lee; Yoshi Goto; Peter Chew; Fang-Jen Ho; Ayman I. Sayegh (1-8).
Microisolation techniques utilizing several reverse phase high performance liquid chromatography (HPLC) steps have resulted in the purification of two rat gastrin releasing peptide (GRP) forms suitable for microsequence and mass spectral analysis. The sequence of the larger form is APVSTGAGGGTVLAKMYPRGSHWAVGHLM-amide and the smaller form is GSHWAVGHLM-amide which is the carboxyl terminal decapeptide of the larger peptide. The peptides were synthesized and their feeding patterns e.g. first meal size (MS), intermeal interval (IMI) and satiety ratio (SR, IMI/MS) were determined in overnight food-, but not water deprived, male Sprague Dawley rats. The peptides were administered in the femoral vein (0, 0.21, 0.41 and 1.03 nmol/kg) immediately before presenting the rats with a 10% sucrose solution. We found that (1) GRP-10 (all doses) and GRP-29 (0.41 nmol/kg) reduced first MS, (2) both peptides prolonged IMI length and (3) both peptides increased the SR to similar extents. In conclusion, GRP-10 and GRP-29 are the two endogenous forms of GRP in the rat intestine and they reduce short term feeding to similar extents when administered intravenously.
Keywords: Gastrin releasing peptide-29; Rat; Meal size; Intermeal interval; Intravenous;

Identification of plasma adrenomedullin as a possible prognostic biomarker for aneurysmal subarachnoid hemorrhage by Jian-Yong Cai; Xian-Dong Chen; Hua-Jun Ba; Jian-Hu Lin; Chuan Lu; Mao-Hua Chen; Jun Sun (9-13).
Increased plasma adrenomedullin levels have been reported in critically ill patients. This study tested the hypothesis that plasma adrenomedullin levels are significantly increased in patients with acute spontaneous aneurysmal subarachnoid hemorrhage, and are predictive of clinical outcomes. Plasma adrenomedullin levels from 120 adult patients with spontaneous aneurysmal subarachnoid hemorrhage and 120 healthy volunteers during the study period were evaluated. Mortality and poor long-term outcome (Glasgow Outcome Scale score of 1–3) at 6 months were recorded. Data showed that circulating plasma adrenomedullin levels significantly increased in patients on admission compared with the volunteers. In patients who died or had poor outcome at 6 months, plasma adrenomedullin levels were significantly higher compared with survivors and patients with good outcome. Plasma adrenomedullin levels on presentation were highly associated with clinical severity assessed using World Federation of Neurological Surgeons score and Fisher score, emerged as the independent risk factor of 6-month mortality and poor outcome, and possessed similar predictive value to World Federation of Neurological Surgeons score and Fisher score based on receiver operating characteristic curves. A combined logistic-regression model did not demonstrate the additive benefit of adrenomedullin to World Federation of Neurological Surgeons score and Fisher score. Thus, higher plasma adrenomedullin levels on presentation are associated with clinical severity and worse outcomes in patients with acute spontaneous aneurysmal subarachnoid hemorrhage.
Keywords: Adrenomedullin; Intracranial aneurysmal; Subarachnoid hemorrhage; Functional outcome; Mortality; Biomarker;

Anti-tumor activities of peptides corresponding to conserved complementary determining regions from different immunoglobulins by Carlos R. Figueiredo; Alisson L. Matsuo; Mariana H. Massaoka; Luciano Polonelli; Luiz R. Travassos (14-19).
Short synthetic peptides corresponding to sequences of complementarity-determining regions (CDRs) from different immunoglobulin families have been shown to induce antimicrobial, antiviral and antitumor activities regardless of the specificity of the original monoclonal antibody (mAb). Presently, we studied the in vitro and in vivo antitumor activity of synthetic peptides derived from conserved CDR sequences of different immunoglobulins against human tumor cell lines and murine B16F10-Nex2 melanoma aiming at the discovery of candidate molecules for cancer therapy. Four light- and heavy-chain CDR peptide sequences from different antibodies (C36-L1, HA9-H2, 1-H2 and Mg16-H2) showed cytotoxic activity against murine melanoma and a panel of human tumor cell lineages in vitro. Importantly, they also exerted anti-metastatic activity using a syngeneic melanoma model in mice. Other peptides (D07-H3, MN20v1, MS2-H3) were also protective against metastatic melanoma, without showing significant cytotoxicity against tumor cells in vitro. In this case, we suggest that these peptides may act as immune adjuvants in vivo. As observed, peptides induced nitric oxide production in bone-marrow macrophages showing that innate immune cells can also be modulated by these CDR peptides. The present screening supports the search in immunoglobulins of rather frequent CDR sequences that are endowed with specific antitumor properties and may be candidates to be developed as anti-cancer drugs.
Keywords: Peptide; CDR; Cytotoxicity; Antitumor activity; Melanoma;

GLP-1(32–36)amide, a novel pentapeptide cleavage product of GLP-1, modulates whole body glucose metabolism in dogs by Dariush Elahi; Franca S. Angeli; Amin Vakilipour; Olga D. Carlson; Eva Tomas; Josephine M. Egan; Joel F. Habener; Richard P. Shannon (20-24).
We have previously demonstrated in human subjects who under euglycemic clamp conditions GLP-1(9–36)amide infusions inhibit endogenous glucose production without substantial insulinotropic effects. An earlier report indicates that GLP-1(9–36)amide is cleaved to a nonapeptide, GLP-1(28–36)amide and a pentapeptide GLP-1(32–36)amide (LVKGR amide). Here we study the effects of the pentapeptide on whole body glucose disposal during hyperglycemic clamp studies. Five dogs underwent indwelling catheterizations. Following recovery, the dogs underwent a 180 min hyperglycemic clamp (basal glucose +98 mg/dl) in a cross-over design. Saline or pentapeptide (30 pmol kg−1  min−1) was infused during the last 120 min after commencement of the hyperglycemic clamp in a primed continuous manner. During the last 30 min of the pentapeptide infusion, glucose utilization (M) significantly increased to 21.4 ± 2.9 mg kg−1  min−1compared to M of 14.3 ± 1.1 mg kg−1  min−1 during the saline infusion (P  = 0.026, paired t-test; P  = 0.062, Mann–Whitney U test). During this interval, no significant differences in insulin (26.6 ± 3.2 vs. 23.7 ± 2.5 μU/ml, P  = NS) or glucagon secretion (34.0 ± 2.1 vs. 31.7 ± 1.8 pg/ml, P  = NS) were observed. These findings demonstrate that under hyperglycemic clamp studies the pentapeptide modulates glucose metabolism by a stimulation of whole-body glucose disposal. Further, the findings suggest that the metabolic benefits previously observed during GLP-1(9–36)amide infusions in humans might be due, at least in part, to the metabolic effects of the pentapeptide that is cleaved from the pro-peptide, GLP-1(9–36)amide in the circulation.
Keywords: Glucagon-like peptide-1; Diabetes; Obesity; Insulin resistance; Glucose utilization;

Peripheral injected cholecystokinin-8S modulates the concentration of serotonin in nerve fibers of the rat brainstem by Kim-Marie Engster; Lisa Frommelt; Tobias Hofmann; Sandra Nolte; Felix Fischer; Matthias Rose; Andreas Stengel; Peter Kobelt (25-33).
Serotonin and cholecystokinin (CCK) play a role in the short-term inhibition of food intake. It is known that peripheral injection of CCK increases c-Fos-immunoreactivity (Fos-IR) in the nucleus of the solitary tract (NTS) in rats, and injection of the serotonin antagonist ondansetron decreases the number of c-Fos-IR cells in the NTS. This supports the idea of serotonin contributing to the effects of CCK. The aim of the present study was to elucidate whether peripherally injected CCK-8S modulates the concentration of serotonin in brain feeding-regulatory nuclei. Ad libitum fed male Sprague-Dawley rats received 5.2 and 8.7 nmol/kg CCK-8S (n  = 3/group) or 0.15 M NaCl (n  = 3–5/group) injected intraperitoneally (ip). The number of c-Fos-IR neurons, and the fluorescence intensity of serotonin in nerve fibers were assessed in the paraventricular nucleus (PVN), arcuate nucleus (ARC), NTS and dorsal motor nucleus of the vagus (DMV). CCK-8S increased the number of c-Fos-ir neurons in the NTS (mean ± SEM: 72 ± 4, and 112 ± 5 neurons/section, respectively) compared to vehicle-treated rats (7 ± 2 neurons/section, P  < 0.05), but did not modulate c-Fos expression in the DMV or ARC. Additionally, CCK-8S dose-dependently increased the number of c-Fos-positive neurons in the PVN (218 ± 15 and 128 ± 14, respectively vs. 19 ± 5, P  < 0.05). In the NTS and DMV we observed a decrease of serotonin-immunoreactivity 90 min after injection of CCK-8S (46 ± 2 and 49 ± 8 pixel/section, respectively) compared to vehicle (81 ± 8 pixel/section, P  < 0.05). No changes of serotonin-immunoreactivity were observed in the PVN and ARC. Our results suggest that serotonin is involved in the mediation of CCK-8's effects in the brainstem.
Keywords: Nucleus of the solitary tract; Cholecystokinin; C-Fos; Dorsal motor nucleus of the vagus; Paraventricular nucleus of the hypothalamus; Serotonin;

Angiotensin 1–7: A peptide for preventing and treating metabolic syndrome by Sérgio Henrique Sousa Santos; João Marcus Oliveira Andrade (34-41).
Angiotensin-(1–7) is one of the most important active peptides of the renin–angiotensin system (RAS) with recognized cardiovascular relevance; however several studies have shown the potential therapeutic role of Ang-(1–7) on treating and preventing metabolic disorders as well. This peptide achieves a special importance considering that in the last few decades obesity and metabolic syndrome (MS) have become a growing worldwide health problem. Angiotensin (Ang) II is the most studied component of RAS and is increased during obesity, diabetes and dyslipidemia (MS); some experimental evidence has shown that Ang II modulates appetite and metabolism as well as mechanisms that induce adipose tissue growth and metabolism in peripheral organs. Recent articles demonstrated that Ang-(1–7)/Mas axis modulates lipid and glucose metabolism and counterregulates the effects of Ang II. Based on these data, angiotensin-converting enzyme 2 (ACE2)/Ang-(1–7)/Mas pathway activation have been advocated as a new tool for treating metabolic diseases. This review summarizes the new evidence from animal and human experiments indicating the use of Ang-(1–7) in prevention and treatment of obesity and metabolic disorders.
Keywords: Renin–angiotensin system – RAS; Lipid metabolism; Glucose metabolism; ACEi; ARBs;

Hyperalgesic and edematogenic effects of Secapin-2, a peptide isolated from Africanized honeybee (Apis mellifera) venom by D. Mourelle; P. Brigatte; L.D.B. Bringanti; B.M. De Souza; H.A. Arcuri; P.C. Gomes; N.B. Baptista-Saidemberg; J. Ruggiero Neto; M.S. Palma (42-52).
Honeybee stings are a severe public health problem. Bee venom contains a series of active components, including enzymes, peptides, and biogenic amines. The local reactions observed after envenoming include a typical inflammatory response and pain. Honeybee venom contains some well-known polycationic peptides, such as Melittin, Apamin, MCD peptide, Cardiopep, and Tertiapin. Secapin in honeybee venom was described 38 years ago, yet almost nothing is known about its action. A novel, variant form of this peptide was isolated from the venom of Africanized honeybees (Apis mellifera). This novel peptide, named Secapin-2, is 25 amino acid residues long. Conformational analyses using circular dichroism and molecular dynamics simulations revealed a secondary structure rich in strands and turns, stabilized by an intramolecular disulfide bridge. Biological assays indicated that Secapin-2 did not induce hemolysis, mast cell degranulation or chemotactic activities. However, Secapin-2 caused potent dose-related hyperalgesic and edematogenic responses in experimental animals. To evaluate the roles of prostanoids and lipid mediators in the hyperalgesia and edema induced by this peptide, Indomethacin and Zileuton were used to inhibit the cyclooxygenase and lipoxygenase pathways, respectively. The results showed that Zileuton partially blocked the hyperalgesia induced by Secapin-2 and decreased the edematogenic response. In contrast, Indomethacin did not interfere with these phenomena. Zafirlukast, a leukotriene receptor antagonist, blocked the Secapin-2 induced hyperalgesia and edematogenic response. These results indicate that Secapin-2 induces inflammation and pain through the lipoxygenase pathway in both phenomena.
Keywords: Hyperalgesia; Inflammation; Honeybee venom; Secapin; Peptidomics;

Keywords: In silico analysis; Metabolic syndrome; Meat proteins; Blood peptides; ACE-I; DPP-IV;

Angiotensin IV induced contractions in human jejunal wall musculature in vitro by M. Malinauskas; E. Stankevičius; A. Casselbrant (63-69).
Angiotensin II (AngII) has been reported to mediate contractile actions in rats and human jejunal wall musculature. However, except for one report showing the angiotensin IV (AngIV) contractile effects on the internal anal sphincter of rats, no data is available describing the action of AngIV on smooth muscle in human small intestine. The aim of this study was to investigate the expression and localization of the enzymes responsible to AngIV formation, as well as the receptor, and to elucidate the contractile function of AngIV in the muscular layer of human jejunum in vitro. Jejunal smooth muscle was taken from 23 patients undergoing Roux-en-Y gastric bypass surgery and was used to record isometric tension in vitro in response to AngIV alone and in the presence of losartan or PD123319. ELISA, western blot and immunohistochemistry were used to investigate the expression and localization of key components for AngIV formation: the enzymes aminopeptidases-A, B, M, and the AngIV receptor insulin-regulated aminopeptidase (IRAP). AngIV elicited concentration-dependent contraction in both longitudinal and circular smooth-muscle preparation. Presence of losartan abolished AngIV-induced contraction, but not PD123319. The main peptide AngII, as well as the enzymes aminopeptidases-A, B and M was detected in all muscle samples. Immunohistochemistry localized the enzymes and IRAP in the myenteric plexus between longitudinal and circular muscle layers. The present study indicates that all enzymes necessary for AngIV formation exist in human jejunal smooth muscle and that the contractile action elicited by AngIV is primarily mediated through the AngII type 1 receptor.
Keywords: Angiotensin III; Angiotensin IV; IRAP; Human jejunal wall musculature;

Postoperative plasma copeptin levels independently predict delirium and cognitive dysfunction after coronary artery bypass graft surgery by Sheng Dong; Chun-Lai Li; Wan-Dong Liang; Mao-Hua Chen; Yun-Tian Bi; Xing-Wang Li (70-74).
Copeptin can reflect individual's stress state and are correlated with poor outcome of critical illness. The occurrence of postoperative delirium (POD) and cognitive dysfunction (POCD) is associated with worse outcome after coronary artery bypass graft (CABG) surgery. The present study aimed to investigate the ability of postoperative plasma copeptin level to predict POD and POCD in patients undergoing CABG surgery. Postoperative plasma copeptin levels of 108 patients were measured by an enzyme-linked immunosorbent assay. It was demonstrated that plasma copeptin levels were substantially higher in patients with POD than without POD (1.8 ± 0.6 ng/mL vs. 1.1 ± 0.3 ng/mL; P  < 0.001) and in patients with POCD than without POCD (1.9 ± 0.6 ng/mL vs. 1.1 ± 0.4 ng/mL; P  < 0.001). Plasma copeptin level and age were identified as independent predictors for POD [odds ratio (OR), 67.386; 95% confidence interval (CI), 12.031–377.426; P  < 0.001 and OR, 1.202; 95% CI, 1.075–1.345; P  = 0.001] and POCD (OR, 28.814; 95% CI, 7.131–116.425; P  < 0.001 and OR, 1.151; 95% CI, 1.030–1.285; P  = 0.003) using a multivariate analysis. For prediction of POD, the area under receiver operating characteristic curve (AUC) of the copeptin concentration (AUC, 0.883; 95% CI, 0.807–0.937) was markedly higher than that of age (AUC, 0.746; 95% CI, 0.653–0.825; P  = 0.020). For prediction of POCD, the AUC of the copeptin concentration (AUC, 0.870; 95% CI, 0.792–0.927) was markedly higher than that of age (AUC, 0.735; 95% CI, 0.641–0.815; P  = 0.043). Thus, postoperative plasma copeptin level may be a useful, complementary tool to predict POD and POCD in patients undergoing CABG surgery.
Keywords: Copeptin; Delirium; Cognitive dysfunction; Postoperative; Coronary artery bypass graft surgery;

Copeptin as a diagnostic biomarker for sepsis-related deaths by Cristian Palmiere; Marc Augsburger (75-78).
Copeptin has been shown to increase in patients with sepsis, severe sepsis and septic shock. In the study herein described, copeptin was measured in a series of sepsis-related fatalities and control cases that underwent medico-legal investigations. No age-dependent differences in copeptin levels in either sepsis or control cases were observed. No correlation between copeptin concentrations and postmortem interval was identified in either group. Copeptin levels were significantly higher in sepsis cases. Moreover, copeptin concentrations in septic cases correlated with procalcitonin, C-reactive protein and interleukin 6 values. These preliminary findings seem to indicate that copeptin can be reliably measured in biological samples collected during postmortem investigations. These results also suggest that hemodynamic instability associated with sepsis and septic shock can be characterized by copeptin measurement also in the forensic casework.
Keywords: Copeptin; Sepsis; Autopsy; Postmortem biochemistry;

Orexin A enhances food intake in bullfrog larvae by Shunsuke Shimizu; Tomoya Nakamachi; Norifumi Konno; Kouhei Matsuda (79-82).
Orexin is a potent orexigenic peptide implicated in appetite regulation in rodents. However, except for teleost fish, the involvement of orexin in the regulation of feeding in non-mammalian vertebrates has not been well studied. Anuran amphibian larvae feed and grow during the pre- and prometamorphic stages. Therefore, orexigenic factors seem to play important roles in growing larvae. Indeed, our recent studies have demonstrated that neuropeptide Y and ghrelin exert orexigenic actions in bullfrog larvae during the prometamorphic stages. In this study, we examined the effect of intracerebroventricular (ICV) administration of synthetic orexin A on food intake in bullfrog larvae at the prometamorphic stages. Food intake was significantly increased by ICV administration of orexin A (at 6 pmol/g BW) during a 15-min observation period. The orexigenic action of orexin A at 6 pmol/g BW was blocked by treatment with an orexin receptor antagonist, SB334867, at 60 pmol/g BW. These results indicate that orexin A acts as an orexigenic factor in bullfrog larvae.
Keywords: Bullfrog; Prometamorphic larvae; Orexin A; Food intake; Orexigenic action;

Physiological fluctuations of human plasma total salusin-β, an endogenous parasympathomimetic/proatherosclerotic peptide by Akifumi Ogawa; Kazumi Fujimoto; Akinori Hayashi; Shoma Chida; Kengo Sato; Kuninobu Takai; Tsuguto Masaki; Akihiko Suzuki; Yuji Kamata; Koji Takano; Takatoshi Koyama; Masayoshi Shichiri (83-88).
Salusin-β is an endogenous bioactive peptide that systemically exerts acute parasympathomimetic hemodynamic actions and locally induces atherogenesis. Due to its unique physicochemical characteristics to immediately adhere to all types of plastic and glassware, its plasma concentrations have only been successfully determined very recently. Using a total of 50 healthy adults (median age 28 years, range 24–57 years), we evaluated whether circulating salusin-β levels are affected by the autonomic nervous functions. Plasma total salusin-β levels obtained during daytime ambulatory monitoring of heart rate variability showed strong negative correlations with variables reflecting parasympathetic nervous activity, high frequency amplitude (HF; r  = −0.27, p  = 0.0018) and the square root of the mean squared differences of successive normal-to-normal intervals (RMSSD; r  = −0.19, p  = 0.0292), but did not with low frequency amplitude (LF) or LF/HF, variables influenced by sympathetic nervous activity. Because early morning nadir in the diurnal variation of plasma total salusin-β levels appeared to follow the nighttime parasympathetic nervous activity peak as quantified by HF and RMSSD, we determined whether parasympathetic stimulation reduces plasma salusin-β levels. Both Valsalva maneuver (p  < 0.05) and urination (p  < 0.05) significantly reduced plasma total salusin-β levels. Despite the fact that salusin-β is the sole endogenous parasympathomimetic peptide identified to date, the current results argue against the contention that physiological parasympathetic augmentation is the consequences of upregulated circulating salusin-β. Rather, circulating salusin-β levels are suppressed following physiological parasympathetic stimulation and appear to constitute a negative feedback relationship with the parasympathetic nervous system.
Keywords: Salusin-β; Parasympathetic stimulation; Valsalva maneuver; Urination; Plasma; Autonomic nervous function;

Plasma copeptin as a predictor of intoxication severity and delayed neurological sequelae in acute carbon monoxide poisoning by Li Pang; He-Lei Wang; Zhi-Hao Wang; Yang Wu; Ning Dong; Da-Hai Xu; Da-Wei Wang; Hong Xu; Nan Zhang (89-93).
The present study was designed to assess the usefulness of measuring plasma levels of copeptin (a peptide co-released with the hypothalamic stress hormone vasopressin) as a biomarker for the severity of carbon monoxide (CO) poisoning and for predicting delayed neurological sequelae (DNS). Seventy-two patients with CO poisoning and 72 sex and age matched healthy individuals were recruited. Plasma copeptin levels were measured on admission from CO poisoning patients and for healthy individuals at study entry by using a sandwich immunoassay. The CO poisoning patients were divided into two groups according to severity (unconscious and conscious) and occurrence of DNS. The mean plasma copeptin levels (52.5 ± 18.5 pmol/L) in the unconscious group were significantly higher than in the conscious group (26.3 ± 12.7 pmol/L) (P  < 0.001). Plasma copeptin levels of more than 39.0 pmol/L detected CO poisoning with severe neurological symptoms e.g. unconsciousness (sensitivity 84.6% and specificity 81.4%). The plasma copeptin levels were higher in patients with DNS compared to patients without DNS (52.2 ± 20.6 pmol/L vs. 27.9 ± 14.8 pmol/L, P  < 0.001). Plasma copeptin levels higher than 40.5 pmol/L predicted the development of DNS (sensitivity 77.8%, specificity 82.1%). Plasma copeptin levels were identified as an independent predictor for intoxication severity [odds ratio (OR) 1.261, 95% confidence interval (CI) 1.112–1.638, P  = 0.002] and DNS (OR 1.313, 95% CI 1.106–1.859, P  = 0.001). Thus, plasma copeptin levels independently related to intoxication severity and were identified as a novel biomarker for predicting DNS after acute CO poisoning.
Keywords: Biomarker; Carbon monoxide poisoning; Copeptin; Delayed neurological sequelae; Severity;

Bacterial toxin-inducible gene expression of cathelicidin-B1 in the chicken bursal lymphoma-derived cell line DT40: Functional characterization of cathelicidin-B1 by Asuna Takeda; Takashi Tsubaki; Nozomi Sagae; Yumiko Onda; Yuri Inada; Takuya Mochizuki; Kazuo Okumura; Sakae Kikuyama; Tetsuya Kobayashi; Shawichi Iwamuro (94-102).
Chicken cathelicidin-B1 (chCATH-B1) is a major host defense peptide of the chicken bursa of Fabricius (BF). To investigate the mechanisms of chCATH-B1 gene expression in the BF, we focused on the DT40 cell line derived from chicken bursal lymphoma as a model for analysis. A cDNA encoding chCATH-B1 precursor was cloned from DT40 cells. The nucleotide sequence of the cDNA was identical with that of the BF chCATH-B1. A broth dilution analysis showed that the synthetic chCATH-B1 exhibited a significant defensive activity against both Escherichia coli and Staphylococcus aureus. A scanning microscopic analysis demonstrated that chCATH-B1 inhibited bacterial growth through membrane destruction with formation of blebs and spheroplasts. Limulus amoebocyte lysate assay and electromobility shift assay results revealed that chCATH-B1 bound to lipopolysaccharide (LPS) and lipoteichoic acid (LTA), which are the surface substances of the E. coli and S. aureus cell, respectively. A chemotactic assay results revealed that chCATH-B1 showed mouse-derived P-815 mastocytoma migrating activity dose-dependently but with a higher concentration, resulting in a loss of the activity. A semi-quantitative real-time RT-PCR analysis revealed that LPS stimulated chCATH-B1 gene expression in a dose-dependent manner and that the LPS-inducible chCATH-B1 gene expression was inhibited by the administration of dexamethasone. The chCATH-B1 mRNA levels in DT40 cells were also increased by the administration of bacterial LTA. The results indicate that bacterial toxins induce chCATH-B1 gene expression in the chicken BF and the peptide expressed in the organ would act against pathogenic microorganisms not only directly but also indirectly by attracting mast cells.
Keywords: Bursa of Fabricius; Cathelicidin; Chemotaxis; DT40 cells; Host defense peptides; Membrane destruction;