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PubMed1992

Production of granulocyte-macrophage colony-stimulating factor in two patients with lung cancer, leukocytosis, and eosinophilia.

Leukocytosis in association with malignancy has been well described, but the cause is not known. One potential explanation is production of a colony-stimulating factor by the tumor, and this has been demonstrated in vitro. The authors report two patients with lung cancer, leukocytosis, and eosinophilia. The pleural fluid of both patients contained malignant cells and biologically active granulocyte-macrophage colony-stimulating factor (GM-CSF), as demonstrated by radioimmunoassay, enzyme-linked immunosorbent assay (ELISA), and colony-forming unit-granulocyte-macrophage (CFU-GM) assay. To determine whether GM-CSF is normally detectable in pleural fluid, the authors performed assays on an additional 11 patients with pleural effusions of various origins but without peripheral blood leukocytosis and eosinophilia; only 1 patient had a detectable level of GM-CSF (i.e., greater than or equal to 0.1 ng/ml). Because GM-CSF usually is not present in pleural fluid, the authors postulate that the high levels of GM-CSF found in the pleural fluid of these two patients was produced by their tumors, and production of GM-CSF by their lung cancers likely caused the leukocytosis with eosinophilia.

Adenocarcinoma↗
PubMed1983

Joint fluid leukocytosis of patient with rheumatoid arthritis Computer analysis of possible explanative factors.

The relationship between joint fluid leukocytosis and some clinical and laboratory parameters (disease duration, ESR, maximal titres of rheumatoid factor and of antinuclear factors, blood leukocytosis and sex) was studied in 27 consecutive patients with seropositive rheumatoid arthritis. The concentration of leukocytes was significantly higher in the synovial fluid than in peripheral blood. Variations of joint fluid leukocytosis could, however, not be explained by disease duration, actual ESR, maximal rheumatoid factor or antinuclear factor titres, concentration of blood leukocytes, or sex. It is suggested that a possible correlation between joint fluid leukocytosis and the listed parameters of rheumatoid arthritis may be too complex for analysis by a linear multiple regression model in samples of the present size.

Adult↗
PubMed1988

Fever and leukocytosis: physical manifestations of bipolar affective disorder?

1. Fever and leukocytosis are occasionally observed in patients with psychiatric disorders. A thorough medical evaluation does not always reveal the origin of these abnormalities. 2. We report the case histories of three patients with bipolar affective disorder and an abnormal DST who had fever and leukocytosis during the acute phase of their illness. No organic etiology could be found. 3. All three patients responded to ECT with resolution of the depression, the fever, and the leukocytosis, and normalization of the DST. 4. We propose that fever and leukocytosis may be rare physical manifestations of bipolar affective disorder, particularly in patients with abnormal DST.

Adult↗
PubMed1999

Occult pneumonias: empiric chest radiographs in febrile children with leukocytosis.

STUDY OBJECTIVE: We sought to determine the incidence of radiographic findings of pneumonia in highly febrile children with leukocytosis and no clinical evidence of pneumonia or other major infectious source. METHODS: We conducted a prospective cohort study at a large urban pediatric hospital. Clinical practice guidelines for the use of chest radiography in febrile children were established by the emergency medicine attending staff. All records of emergency department patients with leukocytosis (WBC count >/= 20, 000/mm3), triage temperature 39.0 degreesC or higher, age 5 years or less were reviewed daily for 12 months. Physicians completed a questionnaire to note the diagnosis, the presence of respiratory symptoms and signs, and the reason for the chest radiograph (if one was obtained). Patients were excluded for immunodeficiency, chronic lung disease, or major bacterial sources of infection other than pneumonia. Pneumonia was defined by an attending radiologist's reading of the radiograph. RESULTS: We studied 278 patients. Chest radiographs were obtained in 225 for the following reasons: 79 because of respiratory findings suggestive of pneumonia and 146 because of leukocytosis and no identifiable major source of infection. Fifty-three patients did not undergo radiography. Pneumonia was found in 32 of 79 (40%; 95% confidence interval, 20% to 52%) of those with findings suggestive of pneumonia and in 38 of 146 (26%; 95% confidence interval, 19% to 34%) of those without clinical evidence of pneumonia. If patients who did not have a radiograph are assumed to not have pneumonia, the minimum estimate of occult pneumonia was 38 of 199 patients (19%; 95% confidence interval, 14% to 25%). CONCLUSION: Empiric chest radiographs in highly febrile children with leukocytosis and no findings of pneumonia frequently reveal occult pneumonias. Chest radiography should be considered a routine diagnostic test in children with a temperature of 39 degreesC or greater and WBC count of 20,000/mm3 or greater without an alternative major source of infection.

Child, Preschool↗
PubMed2002

Conditions associated with leukocytosis in a tertiary care hospital, with particular attention to the role of infection caused by clostridium difficile.

Few modern studies have enumerated the conditions associated with leukocytosis. Our clinical experience has implicated Clostridium difficile infection in a substantial proportion of patients with leukocytosis. In a prospective, observational study of 400 inpatients with WBC counts of >/=15,000 cells/mm(3), we documented >/=1 infection in 207 patients (53%). Of these 207 patients, 97 (47%) had pneumonia, 60 (29%) had urinary tract infection, 34 (16%) had soft-tissue infection, and 34 (16%) had C. difficile infection. C. difficile infection was present in 25% of patients with WBC counts of >30,000 cells/mm(3) who did not have hematological malignancy. Other causes of leukocytosis in the 400 patients included physiological stress, in 152 patients (38%); medications or drugs, in 42 (11%); hematological disease, in 22 (6%); and necrosis or inflammation, in 22 (6%). C. difficile infection is a prominent cause of leukocytosis and this diagnosis should be considered for patients with WBC counts of >/=15,000 cells/mm(3), even in the absence of diarrheal symptoms.

Adult↗
PubMed1982

Implications of leukocytosis and fever at conclusion of antibiotic therapy for intra-abdominal sepsis.

Outcomes of 65 patients after operation who had exhibited a clinical response to treatment for intra-abdominal sepsis were compared based on the presence or absence of leukocytosis and fever at the conclusion of antibiotic therapy. Fifty-one patients were afebrile when antibiotics were stopped. Intra-abdominal infection developed in 7 of 21 (33%) who had a persistent leukocytosis, but no intra-abdominal infections developed after operation in 30 patients who had normal WBC counts at the end of antibiotic treatment (p less than 0.005). Nosocomial infections developed in 6 (12%) of the 51 patients, and there was no difference in the incidence between patients with or without leukocytosis. Eleven of 14 (79%) patients who were still febrile when antibiotics were discontinued developed infections after operation. Nosocomial infections occurred in three (21%) and intra-abdominal infections in eight (57%). Of the 15 patients who developed intra-abdominal infection after operation, only four responded to appropriate antibiotic treatment without requiring further surgery. The other patients required surgical management for definitive control within two months of the initial operation. In conclusion, patients at risk of developing infection after operation after exhibiting a clinical response to treatment of intra-abdominal sepsis are those who are afebrile with a persistent leukocytosis or who are still febrile when antibiotics are stopped.

Adult↗
PubMed1996

Establishment of a clonal cell line producing granulocyte colony-stimulating factor and parathyroid hormone-related protein from a lung cancer patient with leukocytosis and hypercalcemia.

Squamous cell lung carcinoma cells obtained from a patient who presented with leukocytosis and hypercalcemia were transplanted into nude mice and a serially transplantable cell line, OKa-N-1, was established. The nude mice transplanted with OKa-N-1 cells displayed leukocytosis and hypercalcemia. Serum levels of granulocyte colony-stimulating factor (G-CSF) and parathyroid hormone-related protein (PTHrP) were both elevated in these mice. In vitro cultivation of this tumor cell line gave rise to a clonal cell line, OKa-C-1. Nude mice transplanted with the OKa-C-1 cell line also showed leukocytosis and hypercalcemia with high serum G-CSF and PTHrP levels. The culture supernatant of OKa-C-1 contained high levels of G-CSF and PTHrP. Immunohistochemical studies showed the expression of PTHrP in OKa-C-1 cells. Reverse transcription polymerase chain reaction revealed the presence of G-CSF and PTHrP mRNA in this cell line. Dexamethasone treatment inhibited the transcription of G-CSF and PTHrP genes. This new human squamous carcinoma cell line, OKa-C-1, would be useful for studying the mechanism of simultaneous production of G-CSF and PTHrP and their control in cancer patients with leukocytosis and hypercalcemia.

Animals↗
PubMed2005

Leukocytosis and ischemic vascular disease morbidity and mortality: is it time to intervene?

The association between leukocytosis and increased morbidity and mortality of ischemic vascular disease has been observed for more than half a century, and recent studies in >350,000 patients confirm the robustness of the association and the dramatically higher relative and absolute acute and chronic mortality rates in patients with high versus low leukocyte counts. Although there is reason to believe that the association is not causal (that is, that leukocytosis is simply a marker of inflammation), there is also reason to believe that the leukocytosis directly enhances acute thrombosis and chronic atherosclerosis. Leukocytosis also is associated with poor prognosis and vaso-occlusive events in patients with sickle cell disease, and experimental data suggest a direct role for leukocytes in microvascular obstruction. The only way to test whether leukocytes contribute directly to poor outcome in ischemic cardiovascular disease is to assess the effect of modifying leukocyte function or number. Because selective blockade of leukocyte integrin alphaMbeta2 and P-selectin have thus far been disappointing as therapeutic strategies in human cardiovascular and cerebrovascular disease, I discuss the potential risks and benefits of short-term treatment with hydroxyurea to decrease the leukocyte count in select populations of patients at the highest risk of short-term death.

Humans↗
PubMed1991

Evidence that tumor necrosis factor plays a pathogenetic role in the paraneoplastic syndromes of cachexia, hypercalcemia, and leukocytosis in a human tumor in nude mice.

Recently, we have established a human squamous cell carcinoma of the maxilla (called MH-85) associated with hypercalcemia, leukocytosis, and cachexia in culture. MH-85 tumor cells caused the same paraneoplastic syndromes in tumor-bearing nude mice. We found that there was a sixfold increase in splenic size in MH-85 tumor-bearing mice. This increase paralleled tumor growth and was reversed by surgical removal of the tumor. Splenectomy in nude mice 1 wk before or 6 wk after tumor inoculation resulted in a decrease in tumor growth, and impairment of hypercalcemia, leukocytosis, and cachexia. In MH-85 tumor-bearing animals that had been pretreated by splenectomy, intravenous injection of fresh normal spleen cells caused an immediate reversal of leukocytosis, hypercalcemia, and cachexia. Since the presence of cachexia in both the patient and the mice carrying the tumor suggested tumor necrosis factor (TNF) may be overproduced, we injected polyclonal neutralizing antibodies raised against murine TNF into tumor-bearing mice. There was a rapid and reproducible decrease in blood ionized calcium, accompanied by suppression of osteoclast activity. No changes in blood ionized calcium were seen in mice injected with normal immune sera. In addition, there was an increase in body weight and decrease in white cell count. Plasma immunoreactive TNF was increased almost fourfold in tumor-bearing nude mice compared with control nude mice. Although TNF activity was undetectable in MH-85 culture supernatants, cells of the macrophage lineage, including spleen cells, released increased amounts of TNF when cultured with MH-85 tumor-conditioned media. These results suggest that splenic cytokines such as TNF may influence the development of the paraneoplastic syndromes of hypercalcemia, leukocytosis, and cachexia in these animals, as well as tumor growth. They also show that paraneoplastic syndromes may be due to factors produced by normal host cells stimulated by the presence of the tumor.

Animals↗
PubMed2006

Leukocytosis is a risk factor for thrombosis in essential thrombocythemia: interaction with treatment, standard risk factors, and Jak2 mutation status.

Leukocytes contribute to the pathogenesis of thrombosis in essential thrombocythemia (ET) through recently discovered mechanisms of activation and interaction with platelets and endothelial cells. To evaluate whether an increased leukocyte count was associated with thrombosis and whether this effect can be modulated by therapy, we analyzed the clinical course of 439 patients with ET followed at the Ospedali Riuniti di Bergamo. The strength of the association was measured at diagnosis or before thrombotic events by multivariable analyses carried out using data at baseline as well as time-varying covariates. The results showed that (1) an increased leukocyte count at diagnosis was associated with thrombosis during follow-up ("baseline analysis," relative risk [RR] 2.3, 95% confidence interval [CI] 1.4-3.9, P = .001); (2) hydroxyurea (HU) lowered leukocytosis and reduced the strength of the association between leukocytosis and thrombosis ("time-dependent analysis," RR 1.6, 95% CI 0.9-2.0, not significant [NS]); (3) the association of leukocytosis and thrombosis was more evident in untreated low-risk patients (RR 2.7, 95% CI 1.2-6.4, P = .01) compared with HU-treated high-risk patients (RR 1.6, 95% CI 0.8-3.2, NS); and (4) the presence of JAK2 V617F was not identified as a risk factor for thrombosis during follow-up despite a significant association between the mutation and leukocytosis. We suggest validation of these findings in prospective clinical studies.

Adolescent↗
PubMed2005

Delayed leukocytosis and cytokine response to high-force eccentric exercise.

PURPOSE: Delayed leukocytosis after strenuous exercise is well documented, but the underlying mechanisms are not clear. In this study, we investigated the relationship between exercise-induced muscle damage and delayed leukocytosis, by utilizing an extreme eccentric exercise protocol. METHODS: We obtained blood samples from 11 healthy men before and after 300 maximal eccentric actions with m. quadriceps. Maximal force-generating capacity was tested before and regularly during the 7 d after exercise. Blood was analyzed for leukocytes, growth hormone (GH), cortisol, granulocyte colony-stimulating factor (G-CSF), macrophage colony-stimulating factor (M-CSF), interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1beta (MIP-1beta), creatine kinase (CK), C-reactive protein (CRP), complement activation products (C3bc and the terminal complement complex (TCC)), and chemotactic activity in plasma. RESULTS: The force-generating capacity was reduced by 47 +/- 5% (mean +/- SEM) immediately after exercise. Blood concentration of neutrophils and monocytes and the plasma concentration of G-CSF, IL-6, and MCP-1 peaked 6 h after exercise, whereas M-CSF peaked immediately after exercise. Serum concentration of GH and cortisol also peaked immediately after exercise, whereas the serum concentration of CRP and CK peaked after 2 and 4 d, respectively. At 1 h after exercise, chemotactic activity in plasma was increased; at the same time, concentration of C3bc and TCC were decreased. A positive correlation was found between the acute loss of force and the delayed leukocytosis (r = 0.66; P < 0.05), between peak G-CSF and the delayed neutrophilia (r = 0.65, P < 0.05), between acute loss of force and changes in CK (r = 0.65, P < 0.05), between acute loss of force and changes in CRP (r = 0.65, P < 0.05), and between changes in GH and monocyte blood concentrations (r = 0.68, P < 0.05). CONCLUSION: The degree of exercise-induced muscle damage seems to be reflected by the magnitude of the subsequent delayed leukocytosis. The signal between the exercised muscle and bone marrow must be investigated further, but G-CSF and GH are putative mobilizing factors.

Adult↗
PubMed2002

Clinicopathological study of involvement of granulocyte colony stimulating factor and granulocyte-macrophage colony stimulating factor in non-lymphohematopoietic malignant tumors accompanied by leukocytosis.

Involvement of granulocyte colony stimulating factor (G-CSF) and granulocyte-macrophage colony stimulating factor (GM-CSF) in non-lymphohematopoietic malignant tumors accompanied by leukocytosis was clinicopathologically investigated. Among 1,778 autopsy cases in the last 20 years, 485 lesions of 439 cases with non-lymphohematopoietic malignant tumors accompanied by leukocytosis with a white blood cell count of 10,000/mm3 or greater during the course were immunohistologically examined for G-CSF and GM-CSF. Three (0.7%) and two cases (0.5%) were G-CSF- and GM-CSF-positive, respectively. GM-CSF mRNA was confirmed by using non-fixed cryopreserved tumor tissues in one case positive for GM-CSF. G-CSF-positive cases were large cell carcinoma of the lung, adenocarcinoma of the colon, and adenocarcinoma of the stomach, and GM-CSF-positive cases were spindle cell carcinoma of the lung and malignant thymoma. In the case with stomach carcinoma, the primary lesion showing moderately differentiated adenocarcinoma was negative, but the lung metastatic lesion showing less differentiated adenocarcinoma was G-CSF-positive. The survival period was six months or less in four out of five positive cases. The highest white blood cell count in five CSF-positive cases was markedly elevated: 29,400-103,500/mm3 (mean: 59,700/mm3). In four cases, excluding one case which may have been markedly affected by chemotherapy, the bone marrow showed hyperplasia, and the number of the granulocyte series cells significantly increased. There were three cases (0.7%) negative for both G-CSF and GM-CSF, although they showed marked leukocytosis (60,000/mm3 or higher) which were higher than the mean count of CSF-positive cases and was not observed in autopsy cases with non-tumorous diseases. Other stimulating factors may be involved in the development of leukocytosis in such cases.

Bone Marrow↗
PubMed1988

A paraneoplastic syndrome of hypercalcemia and leukocytosis associated with solid tumors: production of interleukin 1 alpha (IL-1 alpha) and granulocyte colony-stimulating factor (G-CSF) by clonal squamous cell carcinoma cells.

We have demonstrated that T3M-1 cells and T3M-5 cells, derived from squamous carcinomas of patients with leukocytosis and hypercalcemia, produced excessively G-CSF, IL-1 alpha and a small amount of PTH-like factor. We confirmed that G-CSF and IL-1 alpha (hemopoietin 1) enhanced granulocytopoiesis and caused marked leukocytosis in vivo. Furthermore, we also demonstrated that PTH-rP and IL-1 alpha (a potent osteoclast-activating factor) synergistically stimulated bone resorption in vitro and also synergistically increased serum calcium concentration in vivo. Since we have demonstrated that at least two clonal cell lines derived from patients with hypercalcemia and leukocytosis produced G-CSF and IL-1 alpha, we presume that hypercalcemia and leukocytosis associated with some solid tumors may constitute a new paraneoplastic syndrome.

Adult↗
PubMed1999

Clinical outcome and associated diseases in dogs with leukocytosis and neutrophilia: 118 cases (1996-1998)

OBJECTIVE: To describe diseases, prognosis, and clinical outcomes associated with leukocytosis and neutrophilia in dogs. DESIGN: Retrospective study. ANIMALS: 118 dogs with leukocytosis and neutrophilia. PROCEDURE: Medical records from 1996 to 1998 were examined for dogs with WBC > or = 50,000 cells/microliter and neutrophilia > or = 50%. Signalment, absolute and differential WBC counts, body temperature, clinical or pathologic diagnosis, duration and cost of hospitalization, and survival time were reviewed. RESULTS: Mean age was 7.7 years, WBC count was 65,795 cells/microliter, and absolute neutrophil count was 53,798 cells/microliter. Mean duration of hospitalization was 7.4 days and cost of hospitalization was $2,028.00. Forty (34%) dogs were febrile, and 73 (62%) dogs died. Overall median survival time was 17 days. Dogs with neoplasia or fever were more likely to die than dogs that were hospitalized or had systemic or local infections. CLINICAL IMPLICATIONS: Leukocytosis and neutrophilia were associated with high mortality rate and have prognostic value. Given the mean duration and cost of hospitalization, frank discussion with an owner at first recognition of leukocytosis and neutrophilia may be warranted.

Animals↗
PubMed2001

New insights in the regulation of leukocytosis and the role played by leukocytes in septic shock.

Leukocytosis is the result of white blood cell production in the bone marrow, margination onto the blood and lymph vessels and elimination of leukocytes in the peripheral tissues and the spleen. The regulation of the exit of leukocytes from the circulation at peripheral inflammatory sites is well known as the four-step paradigm of rolling, adhesion, diapedesis and chemotaxis. The entry of white blood cells into the circulation is less well studied. In the bone marrow, immature myeloid cells adhere to the stromal network by means of interactions between oligosaccharides and lectins and between adhesion molecules. During the maturation process, cell surface molecules are altered and the possibilities for multivalent binding to stroma components or cells are gradually lost. Mature cells produce matrix metalloproteinases (MMPs) that solubilise the basement membranes of the bone marrow sinuses. Hematogenic signals of inflammation activate mature granulocytes in the bone marrow and cause an increase in the circulating pool of leukocytes. The so-called shift-to-the-left, i.e. the presence of precursor forms of differentiating neutrophils, appears during full blown reactions. In the latter situation, immature cells, positive for the CD34 cell surface marker, enter the circulation. The activities of gelatinase B and integrin interactions are indispensable to induce leukocytosis and stem cell mobilization. Indeed, with the use of neutralizing antibodies against gelatinase B and against lymphocyte-associated functional antigen-1 (LFA-1), experimentally induced leukocytosis and stem cell mobilization were blocked. What is the role of adhesion molecules and proteases in septic shock syndromes? In the early phase of endotoxinaemia or bacteraemia, the bone marrow will be activated, which leads to leukocytosis. Neutrophils secrete considerable amounts of latent MMPs, including neutrophil procollagenase (MMP-8) and progelatinase B (MMP-9). In addition, these granulocytes activate the enzymes chemically and these cells are not able to produce tissue inhibitors of metalloproteinases (TIMPs). As a result, an intensive degradation of endothelial basement membranes occurs and results in vascular leakage and shock. These observations raise the hope that inhibition of proteases might constitute a new strategy for the treatment of septic shock.

Cell Adhesion↗
PubMed1992

Histamine leukocytosis. I. Effect of histamine on peripheral leukocyte counts.

The effect of chronic administration of histamine on the number of cells in peripheral blood of dogs, rabbits and guinea pigs was tested by single and consecutive intramuscular injections of histamine in a beeswax-sesame oil mixture. Leukocytosis due to increased numbers of neutrophils occurred in all animals after single injections of histamine in beeswax, although erythrocytes and hematocrit values were unaffected in all species. When injection of histamine was repeated on consecutive days, the extent of leukocytosis subsided in some cases; however, the simultaneous administration of aminoguanidine restored leukocytosis. Single or daily injections of the beeswax-sesame oil mixture without histamine had none of these effects in any animals tested. Although simultaneous injections of histamine and H1 receptor antagonists did not alter histamine effects, the combined administrations of histamine and H2 receptor blocking agents suppressed histamine-induced leukocytosis.

Animals↗
PubMed1987

Production of interleukin 1 alpha-like factor and colony-stimulating factor by a squamous cell carcinoma of the thyroid (T3M-5) derived from a patient with hypercalcemia and leukocytosis.

In order to elucidate the pathogenesis of humoral hypercalcemia and leukocytosis in a 71-year-old patient with squamous cell carcinoma of the thyroid, bone-resorbing activity (BRA) and colony-stimulating activity in the conditioned medium of T3M-5 cells, a clonal cell line established from the tumor, were studied. Gel chromatography of the concentrated conditioned medium revealed respective single peaks of colony-stimulating activity (Mr approximately 27,000) and BRA (Mr 15,000-20,000). BRA did not elicit parathyroid-hormone-like activity but greatly enhanced phytohemagglutinin-induced thymocyte proliferation. This interleukin 1 (IL-1)-like activity exactly coeluted with BRA upon gel chromatography, DEAE-Sepharose ion-exchange chromatography, and isoelectric focusing (pI, 4.7-5.2). BRA was partially inhibited by indomethacin and hydrocortisone, and completely inhibited by anti-IL-1 alpha antiserum, whereas anti-IL-1 beta antiserum had no effect. Furthermore, transplantation of T3M-5 cells into nude mice caused marked hypercalcemia as well as leukocytosis. These findings suggested that excessive production of colony-stimulating factor and IL-1 alpha-like factor by the squamous cell carcinoma was responsible for leukocytosis and hypercalcemia, respectively, in the tumor-bearing nude mice and in the patient. Since several similar cases have been reported in Japan, the syndrome of leukocytosis and hypercalcemia associated with certain solid tumors may constitute a new paraneoplastic syndrome.

Aged↗
PubMed1985

A synthetic nonapeptide corresponding to the NH2-terminal sequence of C3d-K causes leukocytosis in rabbits.

Numerous biologically active fragments have been described that are derived from the C3 molecule. Recently, a polypeptide (Mr 41,000) generated from the alpha chain of human iC3b by limited proteolysis with plasma kallikrein was shown to exhibit several biological functions. This C3-derived cleavage product, C3d-K, suppresses mitogen- and antigen-induced proliferation of human T-lymphocytes and induces leukocytosis in rabbits. We have identified and synthesized a portion of C3d-K that is associated with the leukocytosis phenomenon. A nonapeptide corresponding to the amino-terminal nine residues of C3d-K was synthesized using conventional Merrifield solid-phase peptide chemistry; the structure of this peptide is Thr-Leu-Asp-Pro-Glu-Arg-Leu-Gly-Arg (TLDPERLGR). At a final concentration of 4 X 10(-6) M, both the nonapeptide and the des-Arg octapeptide (TLDPERLG) were capable of inducing leukocytosis in rabbits. Additionally, both peptides enhance vascular permeability when injected in guinea pig skin. These activities are similar to those previously attributed to a C3 fragment identified as C3e by Ghebrehiwet and Müller-Eberhard (Ghebrehiwet, B., and Müller-Eberhard, H.J. (1979) J. Immunol. 123, 616-621). We conclude that the nonapeptide TLDPERLGR represents the active center of the C3-derived leukocytosis factors C3e and C3d-K. This active synthetic analogue of C3d-K should prove valuable in elucidating the mechanism of action for complement-dependent leukocyte mobilization in vivo.

Amino Acid Sequence↗