The effect of anti-tuftsin antibody on the phagocytosis of bacteria by human neutrophils.

Tuftsin (Thr-Lys-Pro-Arg) is a naturally occurring tetrapeptide which stimulates most known functions of the polymorphonuclear and mononuclear phagocytic cell lines. Although tuftsin is a well characterized bioactive peptide, the exact physiological role tuftsin plays remains unclear. Specific mouse anti-tuftsin antiserum generated in our laboratory, is now available for phagocytosis inhibition studies. Monolayers of human neutrophils were prepared on glass coverslips from a few drops of finger prick blood obtained from a single healthy donor. The monolayers were treated with and without mouse anti-tuftsin antiserum at dilutions of 1:1000 or 1:2000. Exogenous tuftsin (1 microgram/ml) was also added with and without antibody. Treated and untreated neutrophils were subsequently incubated with unopsonized Staphylococcus aureus. The proportion of cells accomplishing phagocytosis (phagocytic index) and the number of bacteria engulfed per cell (avidity index) were recorded. The results showed that exogenous tuftsin increased phagocytosis while the addition of mouse anti-tuftsin antiserum at a 1:1000 dilution inhibited phagocytosis both with and without exogenous tuftsin. This effect was diminished by the antiserum at the 1:2000 dilution. This study reaffirms that tuftsin plays an important physiological role in phagocytosis.     

The Effect of Anti-Tuftsin Antibody on the Phagocytosis of Bacteria by Human Neutrophils

Tuftsin (Thr-Lys-Pro-Arg) is a naturally occurring tetrapeptide which stimulates most known functions of the polymorphonuclear and mononuclear phagocytic cell lines. Although tuftsin is a well characterized bioactive peptide, the exact physiological role tuftsin plays remains unclear. Specific mouse anti-tuftsin antiserum generated in our laboratory, is now available for phagocytosis inhibition studies. Monolayers of human neutrophils were prepared on glass coverslips from a few drops of finger prick blood obtained from a single healthy donor. The monolayers were treated with and without mouse anti-tuftsin antiserum at dilutions of 1:1000 or 1:2000. Exogenous tuftsin (1 μg/ml) was also added with and without antibody. Treated and untreated neutrophils were subsequently incubated with unopsonized Staphylococcus aureus. The proportion of cells accomplishing phagocytosis (phagocytic index) and the number of bacteria engulfed per cell (avidity index) were recorded. The results showed that exogenous tuftsin increased phagocytosis while the addition of mouse anti-tuftsin antiserum at a 1:1000 dilution inhibited phagocytosis both with and without exogenous tuftsin. This effect was diminished by the antiserum at the 1:2000 dilution. This study reaffirms that tuftsin plays an important physiological role in phagocytosis.     

Does tuftsin alter phagocytosis by human polymorphonuclear neutrophils?

The physiological significance of the putative phagocytosis-promoting peptide, tuftsin, was investigated by measurement of chemiluminescence generated during phagocytosis and by assay of the uptake of radiolabeled bacteria. We found no differences in either assay when we compared serum from splenectomized patients (which purportedly lacks tuftsin) with normal serum. Further, there was no difference when serum from splenectomized patients was employed in the presence or absence of exogenous tuftsin. Similar results were obtained under a variety of conditions, utilizing three different challenge particles with varying particle-cell ratios and serum from 20 different splenectomized patients. These results do not agree with the hypothesis that tuftsin plays a major role in promoting phagocytosis.     

Differences in the phagocytosis of four bacteria by channel catfish neutrophils

The purpose of this study was to compare the phagocytosis of Aeromonas hydrophila, Edwardsiella ictaluri, Edwardsiella tarda and Micrococcus luteus by channel catfish neutrophils. Various aspects of opsonization effect and bactericidal ability of channel catfish neutrophils were investigated. Percent phagocytosis ranged from a low of 1% to a high of 91%. The highest percent phagocytosis and phagocytic indices routinely occurred with normal serum and were highest for M. luteus (91.78%, 55.25) and A. hydrophila (87.52%, 43.60). In all cases, the percent phagocytosis and phagocytic index was lowest in assays without serum. Channel catfish neutrophils displayed a bactericidal/static ability for each bacterium tested except E. tarda. Neutrophils exhibited a greater inhibitory capacity for A. hydrophila and M. luteus than for the other bacteria when in the presence of normal or inactivated catfish serum.     

Effect of L-arginine on age-related changes in macrophage phagocytic activity

Aging is associated with decline in the functioning of immune cells and reductions in serum L-arginine and excretion of nitric oxide metabolites. Studies have shown that L-arginine plays an important role in many physiological, biological and immunological processes. The present study was performed to determine if treatment with L-arginine could prevent age-related changes in phagocytic function of peritoneal macrophages. The effects of L-arginine on phagocytic activity of peritoneal macrophages were compared between young and middle-aged rats. Studies were performed in four groups of rats for 8 weeks: group 1 (3 month-old) received physiological saline; group 2 (3 month-old) received L-arginine (160 mg/kg/day); group 3 (12 month-old) received physiological saline; group 4 (12 month-old) received L-arginine (160 mg/kg/day). There were no significant differences in percentage of cells which were phagocytized. However, the phagocytosis of activated charcoal by peritoneal macrophages reduced with age. Thus, the phagocytic index was lower in macrophages of middle-aged rats. L-arginine treatment increased phagocytosis by peritoneal macrophages of both young and middle-aged rats. L-arginine-induced augmentation in phagocytosis by macrophages were much higher in the middle-aged rats compared with young rats. In summary, we found that L-arginine prevented the age-related reduction in phagocytic capability of peritoneal macrophages.     

Effect of L-Arginine on Age-Related Changes in Macrophage Phagocytic Activity

Aging is associated with decline in the functioning of immune cells and reductions in serum L-arginine and excretion of nitric oxide metabolites. Studies have shown that L-arginine plays an important role in many physiological, biological and immunological processes. The present study was performed to determine if treatment with L-arginine could prevent age-related changes in phagocytic function of peritoneal macrophages. The effects of L-arginine on phagocytic activity of peritoneal macrophages were compared between young and middle-aged rats. Studies were performed in four groups of rats for 8 weeks: group 1 (3 month-old) received physiological saline; group 2 (3 month-old) received L-arginine (160 mg/kg/day); group 3 (12 month-old) received physiological saline; group 4 (12 month-old) received L-arginine (160 mg/kg/day). There were no significant differences in percentage of cells which were phagocytized. However, the phagocytosis of activated charcoal by peritoneal macrophages reduced with age. Thus, the phagocytic index was lower in macrophages of middle-aged rats. L-arginine treatment increased phagocytosis by peritoneal macrophages of both young and middle-aged rats. L-arginine-induced augmentation in phagocytosis by macrophages were much higher in the middle-aged rats compared with young rats. In summary, we found that L-arginine prevented the age-related reduction in phagocytic capability of peritoneal macrophages.     

实验性哮喘下呼吸道神经激肽B免疫反应纤维

用免疫组织化学方法研究了神经激肽B免疫反应纤维在实验性哮喘豚鼠下呼吸道的变化。在气管和支气管,实验组一抗最佳稀释浓度为1:1500,对照组为1:1000,当两组的一抗浓度均为1:1500时,两者的神经激肽B免疫反应纤维见于平滑肌层,上皮内、上皮和平滑肌交界处以及外膜层,实验组的纤维数量明显多于对照组。在肺组织,实验组一抗最佳稀释浓度为1:2000,对照组为1:1500,当一抗稀释浓度均为1:2000时,两组的神经激肽B免疫反应纤维主要见于肺内各级支气管平滑肌层、血管壁平滑肌层、血管周围结缔组织和肺泡隔内,但实验组的阳性纤维数量明显比对照组多。     

Effect of L‐Arginine on Age‐Related Changes in Macrophage Phagocytic Activity

Aging is associated with decline in the functioning of immune cells and reductions in serum L‐arginine and excretion of nitric oxide metabolites. Studies have shown that L‐arginine plays an important role in many physiological, biological and immunological processes. The present study was performed to determine if treatment with L‐arginine could prevent age‐related changes in phagocytic function of peritoneal macrophages. The effects of L‐arginine on phagocytic activity of peritoneal macrophages were compared between young and middle‐aged rats. Studies were performed in four groups of rats for 8 weeks: group 1 (3 month‐old) received physiological saline; group 2 (3 month‐old) received L‐arginine (160 mg/kg/day); group 3 (12 month‐old) received physiological saline; group 4 (12 month‐old) received L‐arginine (160 mg/kg/day). There were no significant differences in percentage of cells which were phagocytized. However, the phagocytosis of activated charcoal by peritoneal macrophages reduced with age. Thus, the phagocytic index was lower in macrophages of middle‐aged rats. L‐arginine treatment increased phagocytosis by peritoneal macrophages of both young and middle‐aged rats. L‐arginine‐induced augmentation in phagocytosis by macrophages were much higher in the middle‐aged rats compared with young rats. In summary, we found that L‐arginine prevented the age‐related reduction in phagocytic capability of peritoneal macrophages.     

Lyn-coupled LacCer-enriched lipid rafts are required for CD11b/CD18-mediated neutrophil phagocytosis of nonopsonized microorganisms

The integrin CD11b/CD18 plays a central role in neutrophil phagocytosis. Although CD11b/CD18 binds a wide range of ligands, including C3bi and beta-glucan, and transmits outside-in signaling, the mechanism of this signaling responsible for phagocytosis remains obscure. Here, we report that lactosylceramide (LacCer)-enriched lipid rafts are required for CD11b/CD18-mediated phagocytosis of nonopsonized zymosans (NOZs) by human neutrophils. Anti-CD11b and anti-LacCer antibodies inhibited the binding of NOZs to neutrophils and the phagocytosis of NOZs. During phagocytosis of NOZ, CD11b and LacCer were accumulated and colocalized in the actin-enriched phagocytic cup regions. Immunoprecipitation experiments suggested that CD11b/CD18 was mobilized into the LacCer-enriched lipid rafts during phagocytosis of NOZs. DMSO-treated, neutrophil-like HL-60 cells (D-HL-60 cells) lacking Lyn-coupled, LacCer-mediated signaling showed little phagocytosis of NOZs. However, loading of D-HL-60 cells with C24 fatty acid chain-containing LacCer (C24-LacCer) reconstructed functional Lyn-associated, LacCer-enriched lipid rafts, and restored D-HL-60 cell NOZ phagocytic activity, which was inhibited by anti-LacCer and anti-CD11b antibodies. Lyn knockdown by small interfering RNA blocked the effect of C24:1-LacCer loading on D-HL-60 cell phagocytosis of NOZs. CD11b/CD18 activation experiments indicated phosphorylation of LacCer-associated Lyn by activation of CD11b. Taken together, these observations suggest that CD11b activation causes translocation of CD11b/CD18 into Lyn-coupled, LacCer-enriched lipid rafts, allowing neutrophils to phagocytose NOZs via CD11b/CD18.     

Apoptosis-dependent and -independent mechanisms mediate the phagocytic recognition/clearance of the HL60-A1 transfectants with prolonged survival

Objective: The phagocytic recognition and clearance of the recruited inflammatory cells with prolonged survival play a pivotal role in relieving tissue inflammation and maintaining tissue homeostasis. Transgenic mice expressing Bcl-2 in mature neutrophils demonstrated that Bcl-2 attenuated neutrophil apoptosis, while the homeostasis of the neutrophil population was essentially unaffected. This result suggests that clearance of neutrophils with prolonged survival operates independently from apoptosis. Owing to the constitutive and inducible expression of Bcl-2 homologue, A1 in human neutrophils and the intolerance of preparation for the isolated human neutrophils with prolonged survival, the human promyelocytic HL60-A1 transfectants were established to study the mechanism of phagocytic recognition/clearance of the cells with prolonged survival. Materials and Methods: The non-apoptotic cells with prolonged survival were enriched by serum withdrawal for five days and negatively isolated by annexin V-binding beads. Then, the cells were labeled with a fluorogenic marker. Monocyte-derived macrophages (MDM) were co-cultured to perform the phagocytosis assay, and flow cytometry was employed to determine the phagocytic index. Results: In the serum-free condition, the phagocytic index of HL60-A1 transfectants was little different from that of the HL60-EGFP control, despite showing a significantly lower degree of apoptosis. While the phagocytic index of HL60-EGFP control was significantly correlated with the degree of apoptosis, the index of the HL60-A1 transfectants was less relevant to it. The phagocytic index for the annexin V-positive cells did not distinguish the two cell types. However, the phagocytic index for the annexin V-negative cells from the HL60-A1 transfectants was increased with age in days. Preincubation of MDM with the scavenger receptor inhibitor, Oxi-LDL, and the inhibitory antibodies against αvβ3, CD14 and CD36 surface molecules could attenuate the phagocytic recognition of the annexin V-positive HL60 cells but not the annexin V-negative A1 transfectants with prolonged survival. Conclusions: This study thus suggests that a mechanism unrelated to apoptosis exists, which mediates the phagocytic clearance of the non-apoptotic cells with prolonged survival and may be associated with A1 function in the myeloid cells. Received 2 August 2006; returned for revision 7 September 2006; accepted by G. Wallace 29 November 2006 C.-L. Chou and L.-L. Chiang contributed equally to the work on this project as first authors.     

Effects of chemotactic peptide f-met-leu-phe (FMLP) on C3b receptor (CR1) expression and phagocytosis of microspheres by human neutrophils

FMLP caused maximal upregulation of CR1 on neutrophils at a concentration of 10^–8 M but caused maximal enhancement of CR1-dependent phagocytosis of C3b · IgG-coated microspheres only at a concentration of 10^–6 M. There were positive correlations between FMLP-mediated upregulation of CR1 and FMLP-mediated enhancement of phagocytosis (correlation coefficient=0.73, slope=2.2) and between FMLP-mediated upregulation of CR1 and FMLP-mediated increase in total cell-associated microspheres (correlation coefficient=0.88, slope=1.3). The phagocytic capacity of both untreated and 10^–6 M FMLP-treated neutrophils was completely inhibited by fluid phase C3b and partially inhibited by aggregated IgG. The data suggest that CR1 upregulation is required but is not sufficient for maximal phagocytosis by the leukocytes. The data also suggest that FMLP at the higher concentrations may impart a phagocytic function to CR1, activate other phagocytic receptors, elicit phagocytosis—inducing mediators or may elicit a separate mechanism of phagocytosis. During the study, it was observed that there was considerable individual variation among different neutrophil preparations with respect to CR1 expression and binding and phagocytic capacity.     

Roles of antibody and complement in the bactericidal activity of mouse peritoneal exudate neutrophils.

The contributions of complement and antibody to phagocytosis and, as a separate process, intracellular killing of Proteus mirabilis, were investigated using mouse peritoneal exudate neutrophils. Phagocytosis of P. mirabilis was promoted by both immune mouse (IMS) and normal mouse (NMS) sera. Opsonization by IMS promoted significantly greater phagocytosis than did NMS, as did NMS compared with heated IMS (HIMS). The ability of NMS to opsonize P. mirabilis for both phagocytosis and phagocytic killing was diminished by chelation with EGTA and abolished by chelation with EDTA. This suggested that fixation of complement by both alternative and classical pathways provided optimal opsonization of this organism in NMS. In order to study intracellular killing as a process separate from phagocytosis, peritoneal exudate cell suspensions were exposed to P. mirabilis, previously incubated with 1% NMS, 1% IMS, 10% HNMS (heated normal mouse serum) or 10% HIMS, followed by centrifugation of the phagocyte-bacteria mixtures on Percoll density gradients. Populations of neutrophils containing viable intracellular bacteria, and relatively free of extracellular bacteria (less than 7% of total) were recovered in washed suspensions of cells fractionated at densities greater than 1.069 g/ml. For P. mirabilis that had been opsonized with 1% NMS before phagocytosis, the continued presence of extracellular serum was necessary for intracellular killing. NMS stimulated significantly greater intracellular killing than did HNMS, which stimulated some intracellular killing compared with the absence of serum, in which no killing occurred. IMS was similar to NMS in its ability to stimulate intracellular killing. EGTA partially blocked the stimulation of intracellular killing by NMS, and EDTA abolished it. These findings suggested that (as for optimal opsonization) complement activated via both alternative and classical pathways was responsible for optimal stimulation of intracellular killing.     

Localization on encapsulated Cryptococcus neoformans of serum components opsonic for phagocytosis by macrophages and neutrophils.

Previous studies have shown that the cryptococcal capsule inhibits phagocytosis of Cryptococcus neoformans by macrophages and neutrophils. In this study, the binding sites of potential serum opsonins in immune and nonimmune sera were determined by immunoelectron microscopy, and the results were compared with the results of phagocytosis of the yeasts by mouse peritoneal macrophages and human neutrophils. Immunoglobulin G (IgG) from normal human serum showed low-density binding at the capsular surface and at sites throughout the capsule. Complement component C3 from normal serum bound heavily at the capsular surface. IgG from rabbit capsular antiserum showed relatively dense deposition at the capsular surface and at sites throughout the capsule. Cells opsonized with heat-inactivated human serum were engulfed poorly by both macrophages and neutrophils, indicating that the low-density deposition of IgG produced by normal serum was not adequate for opsonization. Yeasts opsonized with normal human serum were engulfed in large numbers by neutrophils and to a lesser extent by macrophages, indicating that neutrophils in particular were able to effectively utilize the opsonically active C3 which normal human serum deposited at the capsular surface. Yeasts opsonized with rabbit anticapsular serum were engulfed by both macrophages and neutrophils, indicating that the high density of surface IgG produced by capsular antiserum is an effective opsonin for both cells. These results suggest that the complement-neutrophil system is a possible defense mechanism in the nonimmune host.     

Lipopolysaccharide inhibits macrophage phagocytosis of apoptotic neutrophils by regulating the production of tumour necrosis factor α and growth arrest-specific gene 6

Removal of apoptotic cells from inflammatory sites by macrophages is an important step in the resolution of inflammation. However, the effect of inflammatory modulators on phagocytic clearance of apoptotic cells remains to be clarified. In this paper, we demonstrate that lipopolysaccharide (LPS), a potent inflammatory agent, inhibits the phagocytosis of apoptotic neutrophils by mouse peritoneal macrophages. This inhibition can be attributed to both LPS-mediated induction of tumour necrosis factor (TNF-α) and suppression of growth arrest-specific gene 6 (Gas6) in macrophages. We found that LPS-induced TNF-α production inhibited phagocytic ability of macrophages in an autocrine manner. In contrast, Gas6 expression in macrophages was blocked by LPS, which also contributes to the inhibition of macrophage phagocytosis by LPS. Our data suggest that phagocytic clearance of apoptotic neutrophils by macrophages can be regulated by local pro- and anti-inflammatory factors in two opposite states.     

Influence of Glucose Levels on the In Vitro Phagocytosis of Bacteria by Human Neutrophils

A previously developed in vitro method for studying the phagocytosis of bacteria and particles by human neutrophils was used to investigate the influence of different glucose levels on phagocytosis. It was found that high glucose levels (200, 400, and 800 mg of glucose/100 ml) significantly depressed the phagocytosis of Staphylococcus epidermidis, S. aureus, and Escherichia coli. At very low glucose levels, a somewhat decreased phagocytic activity was noted. The strongest phagocytic activity occurred at glucose concentrations of 50 and 100 mg/100 ml. A second effect noted at the higher (200, 400 and 800 mg/100 ml) glucose concentrations was a decreased adhesiveness of the neutrophils to solid surfaces. The mechanism of the decrease in phagocytosis and in neutrophil adhesiveness at higher glucose levels is unknown, but it is not linked to increased osmotic pressures due to the presence of glucose, as ethanol, at the same and even higher osmolal concentrations, had no effect on the phagocytosis. These results show that not only the phagocytic activity of those neutrophils that do adhere to a solid surface is diminished at higher glucose concentrations but also that fewer neutrophils adhere to solid surfaces at higher glucose levels. These two phenomena combined may provide at least part of the explanation for the well-known decrease in resistance to bacterial infections of diabetics.     

Impact of Interleukin-17 on Macrophage Phagocytosis of Apoptotic Neutrophils and Particles

There is now substantial evidence that the cytokine interleukin-17 orchestrates the accumulation of neutrophils in mammals and thereby contributes to host defense. However, the role of IL-17 in controlling neutrophil turnover is not fully understood. Here, we demonstrate that IL-17 stimulates the apoptosis of mouse neutrophils and, simultaneously, the release of the microbicidal compound, myeloperoxidase. IL-17 also stimulates mouse macrophages to phagocytose aged neutrophils and latex beads, and it induces an increase in a soluble form of the phagocytic receptor, lectin-like oxidized low-density lipoprotein receptor-1 as well. In contrast, IL-17 does not markedly increase the release of the archetype neutrophil-recruiting cytokine, macrophage inflammatory protein-2 in mouse macrophages. Importantly, IL-17 also stimulates the phagocytosis of latex beads in human monocyte-derived macrophages. Thus, IL-17 bears the potential to control both phagocytosis and neutrophil turnover during activation of host defense.     

Senescence in innate immune responses: reduced neutrophil phagocytic capacity and CD16 expression in elderly humans.

Elderly humans are more susceptible to bacterial infections because of declining immune status. We have investigated the effect of aging on neutrophil bactericidal responses, comparing neutrophil function in healthy, young (23-35 years) and elderly (>65 years) volunteers. Superoxide generation in response to fMLP was slightly increased in neutrophils from elderly donors, and serum from the elderly was able to opsonize E. coli efficiently. In contrast, phagocytic index was significantly lower in neutrophils from the elderly, compared with young donors (P<0.005). CD11a and CD11b expression was not affected by age, but CD16 was significantly reduced in neutrophils from elderly donors (P<0.0001). CD16 expression and phagocytic index were measured in the same neutrophils using FITC-labeled E. coli, PE-conjugated anti-CD16 antibody, and CD16 expression correlated with phagocytic index (r=0.83; P<0.05). In elderly patients with bacterial infection, CD16 expression remained low. We propose that reduced neutrophil CD16 expression and phagocytosis contribute to human immunesenescence.     

Roles of antibody and complement in the bactericidal activity of mouse peritoneal exudate neutrophils

The contributions of complement and antibody to phagocytosis and, as a separate process, intracellular killing of Proteus mirabilis, were investigated using mouse peritoneal exudate neutrophils. Phagocytosis of P. mirabilis was promoted by both immune mouse (IMS) and normal mouse (NMS) sera. Opsonization by IMS promoted significantly greater phagocytosis than did NMS, as did NMS compared with heated IMS (HIMS). The ability of NMS to opsonize P. mirabilis for both phagocytosis and phagocytic killing was diminished by chelation with EGTA and abolished by chelation with EDTA. This suggested that fixation of complement by both alternative and classical pathways provided optimal opsonization of this organism in NMS. In order to study intracellular killing as a process separate from phagocytosis, peritoneal exudate cell suspensions were exposed to P. mirabilis, previously incubated with 1% NMS, 1% IMS, 10% HNMS (heated normal mouse serum) or 10% HIMS, followed by centrifugation of the phagocyte-bacteria mixtures on Percoll density gradients. Populations of neutrophils containing viable intracellular bacteria, and relatively free of extracellular bacteria (less than 7% of total) were recovered in washed suspensions of cells fractionated at densities greater than 1.069 g/ml. For P. mirabilis that had been opsonized with 1% NMS before phagocytosis, the continued presence of extracellular serum was necessary for intracellular killing. NMS stimulated significantly greater intracellular killing than did HNMS, which stimulated some intracellular killing compared with the absence of serum, in which no killing occurred. IMS was similar to NMS in its ability to stimulate intracellular killing. EGTA partially blocked the stimulation of intracellular killing by NMS, and EDTA abolished it. These findings suggested that (as for optimal opsonization) complement activated via both alternative and classical pathways was responsible for optimal stimulation of intracellular killing.     

Novel Microtechnique for Assessment of Postnatal Maturation of the Phagocytic Function of Neutrophils and Monocytes

We describe a simple test for the evaluation of phagocytosis and provide a chart of reference values to evaluate normal phagocytosis by age. We assessed the postnatal maturation of phagocytic function of neutrophils and monocytes. Phagocytosis was evaluated in newborn children delivered vaginally or by cesarean section, infants, preschool children, schoolchildren, and adult subjects. Two drops of blood were placed on a microscope slide and incubated with Saccharomyces cerevisiae yeasts, and phagocytosis was evaluated by microscopy. Our technique showed results comparable to or better than those obtained by other usual techniques. The neutrophils of newborn children delivered by cesarean section showed a phagocytic capacity 45% higher than those of neonates delivered vaginally, whereas neutrophils from children in the latter group showed the lowest phagocytic capacity of all age groups. Phagocytosis by neutrophils reached the levels seen in adults at about the first year of life, while there were no important variations in phagocytosis by monocytes in the different age groups. The technique described is reliable and fast, uses only a few drops of blood, and allows better preservation of cell function due to the minimal manipulation to which the cells are submitted. The delayed maturation of the phagocytic function by neutrophils may account for the high levels of susceptibility of newborn and infant children to bacterial infections. This practical method of assessment of phagocytosis may allow the diagnosis of primary or secondary phagocytic deficiencies to be made more easily and may allow better monitoring and treatment of those with dysfunctions of these cells.     

Peptides and their constituent amino acids influence the immune response and phagocytosis in different ways.

To elucidate the role of immunoactive amino acids (which are capable of stimulating the immune response) in the peptide regulation of antibody production and phagocytic processes we have studied the influence of some fragments of natural peptides and the amino acids included in them on the thymus-dependent immune response to sheep red blood cells (SRBC) and on the phagocytosis of Staphylococcus by murine peritoneal neutrophils. It has been found that the effects of amino acids, as well as of peptides that they form, on the immune response and on phagocytosis were diverse. Glutamic and aspartic acids, threonine and valine stimulated both the immune response and phagocytosis. Glycine and isoleucine influenced neither the immune response nor phagocytosis, whereas lysine, proline, tyrosine and leucine did not influence the immune response, but enhanced the phagocytic activity of neutrophils. Arginine inhibited the immune response but stimulated phagocytosis. Peptide TTKD section (the fragment 77-80 of murine Thy-1-antigen) contained in C- and N-terminus amino acids (T and D) which stimulated the antibody production and phagocytosis, and lysine (K) which stimulated phagocytosis only, enhanced both processes. Peptides LGIP and PYIK (the fragments 49-53 and 66-69 of murine Thy-1 antigen) which contained both immunologically inert amino acids (L, G, I, P, Y, K) and phagocytosis stimulating amino acids (L, Y, P, K) influenced neither the immune response nor the phagocytic activity of neutrophils.(ABSTRACT TRUNCATED AT 250 WORDS)