Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LEUKOCYTOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1981

The leukocytes.

Dogs and cats respond to many diseases by changes in leukocyte numbers. Infectious diseases often cause leukocytosis due to neutrophilia. Left shift may accompany the leukocytosis, indicating that the marrow is mounting a response to the disease. Left shift also indicates that the marrow has fallen somewhat behind the needs of the animal. Degenerative left shift is considered a poor sign. Lymphopenia and eosinopenia also are found in infectious diseases. Lymphocytosis may occur during the recovery or if the disease becomes chronic. The nature and duration of the infection determine the magnitude of the monocyte response. It is erroneous to consider a disease chronic based only upon monocytosis. Trauma, autoimmunity, or any disease with significant tissue destruction can evoke a monocyte response. Leukopenias are relatively common in cats and are found with moderate frequency in dogs. Drugs, viral diseases (such as FeLV, feline enteritis, parvovirus), ehrlichiosis, and hereditary conditions may cause panleukopenias or single leukopenias. Occasionally leukocyte examination provides evidence of a specific etiology (such as with ehrlichiosis). Sometimes changes occur which, although not specific for a disease, may provide a strong evidence of a particular disease (such as in salmon poisoning). Leukocyte evaluation should include not only total count and differential count (with calculation of absolute numbers of the different cells) but also morphologic examination of the cells by qualified people. In many practices the only qualified person is the veterinarian.

Animals↗
PubMed2002

Accelerated telomere length shortening in granulocytes: a diagnostic marker for myeloproliferative diseases.

OBJECTIVE: The telomere in mature myeloid cells derived from abnormal progenitor cells of myeloproliferative diseases (MPDs) may shorten more rapidly than that in T lymphocytes, which are considered to be derived from normal clones. To test this hypothesis, we measured telomere lengths in granulocytes and T lymphocytes from patients with MPDs and compared them with those from normal individuals. MATERIALS AND METHODS: Granulocytes and T lymphocytes were separated from the peripheral blood of 65 patients with MPDs (25 chronic myelogenous leukemia [CML], 16 polycythemia vera, 19 essential thrombocythemia, 5 chronic idiopathic myelofibrosis) and 35 normal individuals. Genomic DNA from each cell fraction was subjected to Southern blot hybridization to determine the mean telomere length. RESULTS: Telomere lengths in granulocytes from patients with MPDs were significantly shorter than those from normal individuals (vs CML, p = 0.002; vs other MPDs, p < 0.0001). However, there was no statistical difference in telomere length in T lymphocytes between MPD patients and normal individuals (vs CML, p = 0.35; vs other MPDs, p = 0.85). DeltaTRF (terminal restriction fragment) in patients with MPDs, which is defined as the difference in telomere length between granulocytes and T lymphocytes, was significantly longer than that in normal individuals. CONCLUSIONS: The results support the disease theory that MPDs result from extensive proliferation of myeloid progenitor cells, leading to accelerated telomere length shortening in mature granulocytes. An increase in DeltaTRF over the standard value (>1.74 kb) may be useful for discriminating leukocytosis due to MPDs from reactive leukocytosis.

Adult↗
PubMed2000

Acute diverticulitis in patients 40 years of age and younger.

Acute colonic diverticulitis typically occurs in patients older than 60 years of age but is uncommon in patients under the age of 40, which may lead to a delay in diagnosis. Because abdominal pain is a very common presenting symptom in emergency department patients, we retrospectively analyzed the cases of 21 patients 40 years of age and younger diagnosed with acute diverticulitis and characterized the presenting signs and symptoms, laboratory and radiographic findings, treatment, and outcome. There were 17 men and 4 women with a mean age of 34.1 +/-5.9 years. All patients had abdominal pain, with 14 (67%) patients noting pain in the left lower quadrant (LLQ) and 5 (24%) patients noting right lower quadrant (RLQ) pain. Nausea was present in 18 (86%) patients and fever in 15 (71%) patients. The mean pulse rate was 103 +/- 16 and the mean temperature was 100.7 +/- 1.4 F. Leukocytosis was present in 19 (90%) patients. Plain abdominal radiographs were obtained in 19 (91%) patients and were normal in 15 (79%) of these cases. Computed tomographic (CT) scans were obtained in 15 (71%) patients which revealed findings consistent with acute diverticulitis in 14 (93%) patients. The admitting diagnosis was diverticulitis in 10 of the 12 patients with LLQ tenderness and appendicitis in 4 of the 6 patients with RLQ tenderness. Overall, six patients were taken to surgery: three patients had cecal diverticulitis and three patients had perforated colonic diverticulitis. General treatment measures included bowel rest in 18 (86%) patients, and intravenous fluids and antibiotics in all patients. All patients survived. In conclusion, acute diverticulitis is uncommon in patients under 40 years of age; however, this condition may be confused with other conditions, usually acute appendicitis. As a result, clinicians should consider acute diverticulitis in young patients with acute abdominal pain, especially if they are male with nausea, fever, tachycardia, and leukocytosis, and consider obtaining a CT scan to aid in the diagnosis.

Abdominal Pain↗
PubMed2001

Life-threatening capillary leak syndrome after G-CSF mobilization and collection of peripheral blood progenitor cells for allogeneic transplantation.

We report a case of capillary leak syndrome in a 37-year-old female PBPC donor who received G-CSF 900 microg/day for 4 days and underwent leukapheresis. This lady had remained well and stable despite marked leukocytosis during G-CSF treatment, but developed hypotension during leukapheresis, quickly followed by hypoxemia, ascites, pericardial and pleural effusion, shock, edema, neurologic changes and hepatocellular injury. Upon G-CSF withdrawal, dopamine and crystalloid infusion, methylprednisolone treatment and suspension of apheresis, the clinical situation fully reversed. We hypothesize that leukapheresis, in the presence of marked leukocytosis and high doses of G-CSF, may have triggered neutrophil activation and the release of inflammatory mediators, resulting in tissue damage and systemic manifestations of increased capillary permeability.

Adult↗
PubMed1993

[Pseudoleukocytosis in cryoglobulinemia type I].

During routine clinical and laboratory examinations of a symptom-free 54-year-old man a leukocytosis was repeatedly noted, but no cause found. 11 months later a painful spontaneously disappearing cyanosis occurred in two fingers of his right hand. Serum analysis demonstrated monoclonal type IgG-kappa immunoglobulin and an antinuclear antibody titre of 1:160. Skin biopsy suggested scleroderma. 4 months later, after exposure to cold, extensive acral haemorrhages occurred. Serum cryoglobulin concentration in serum was found to be 800 mg/dl. Comparative manual and electronic counts on warm and cooled blood identified the previously diagnosed leukocytosis as a typical artefact associated with cryoglobulinaemia. Treatment with chlorambucil (10-20 mg/d) and prednisolone (25 mg/d), for 14 days every 4 weeks, and finally interferon alpha-2b (5 mill. IU/d) reduced the cryoglobulin concentration to 150 mg/dl. Acral cyanosis and haemorrhages have not recurred since then. No cause of the cryoglobulinaemia has been found.

Biopsy↗
PubMed2000

Prediction of adverse outcomes in children with sickle cell disease.

BACKGROUND: The ability to identify infants with sickle cell anemia who are likely to have severe complications later in life would permit accurate prognostication and tailoring of therapy to match disease-related risks and facilitate planning of clinical trials. We attempted to define the features of such babies by following the clinical course of 392 children with sickle cell disease from infancy to about the age of 10 years. METHODS: We analyzed the records of 392 infants who received the diagnosis of homozygous sickle cell anemia or sickle cell-Beta(0)-thalassemia before the age of six months and for whom comprehensive clinical and laboratory data were recorded prospectively; data were available for a mean (+/-SD) of 10.0+/-4.8 years. Results obtained before the age of two years were evaluated to determine whether they predicted the outcome later in life. RESULTS: Of the 392 infants in the cohort, 70 (18 percent) subsequently had an adverse outcome, defined as death (18 patients [26 percent]), stroke (25 [36 percent]) frequent pain (17 [24 percent]), or recurrent acute chest syndrome (10 [14 percent]). Using multivariate analysis, we found three statistically significant predictors of an adverse outcome: an episode of dactylitis before the age of one year (relative risk of an adverse outcome, 2.55; 95 percent confidence interval, 1.39 to 4.67), a hemoglobin level of less than 7 g per deciliter (relative risk, 2.47; 95 percent confidence interval, 1.14 to 5.33), and leukocytosis in the absence of infection (relative risk, 1.80; 95 percent confidence interval, 1.05 to 3.09). CONCLUSIONS: Three easily identifiable manifestations of sickle cell disease that may appear in the first two years of life (dactylitis, severe anemia, and leukocytosis) can help to predict the possibility of severe sickle cell disease later in life.

Anemia↗
PubMed2002

Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta.

BACKGROUND: A small proportion of patients with chronic myeloproliferative diseases have constitutive activation of the gene for platelet-derived growth factor receptor beta (PDGFRB), which encodes a receptor tyrosine kinase. The gene is located on chromosome 5q33, and the activation is usually caused by a t(5;12)(q33;p13) translocation associated with an ETV6-PDGFRB fusion gene. The tyrosine kinase inhibitor imatinib mesylate specifically inhibits ABL, PDGFR, and KIT kinases and has impressive clinical efficacy in BCR-ABL-positive chronic myeloid leukemia. METHODS: We treated four patients who had chronic myeloproliferative diseases and chromosomal translocations involving 5q33 with imatinib mesylate (400 mg daily). Three of the four patients presented with leukocytosis and eosinophilia; their leukemia cells carried the ETV6-PDGFRB fusion gene. The fourth patient had leukocytosis, eosinophilia, and a t(5;12) translocation involving PDGFRB and an unknown partner gene; he also had extensive raised, ulcerated skin lesions that had been present for a long time. RESULTS: In all four patients, a normal blood count was achieved within four weeks after treatment began. In the patient with skin disease, the lesions began to resolve shortly after treatment began. The t(5;12) translocation was undetectable by 12 weeks in three patients and by 36 weeks in the fourth patient. In the three patients with the ETV6-PDGFRB fusion gene, the transcript level decreased, and in one patient, it became undetectable by 36 weeks. All responses were durable at 9 to 12 months of follow-up. CONCLUSIONS: Imatinib mesylate induces durable responses in patients with chronic myeloproliferative diseases associated with activation of PDGFRB.

Adult↗
PubMed1999

Tumor necrosis factor alpha is a determinant of pathogenesis and disease progression in mycobacterial infection in the central nervous system.

The pathogenesis of tuberculous meningitis, a devastating complication of tuberculosis in man, is poorly understood. We previously reported that rabbits with experimental tuberculous meningitis were protected from death by a combination of antibiotics and thalidomide therapy. Survival was associated with inhibition of tumor necrosis factor alpha (TNF-alpha) production by thalidomide. To test whether cerebrospinal fluid (CSF) levels of TNF-alpha correlated with pathogenesis, the response of rabbits infected in the central nervous system (CNS) with various mycobacterial strains was studied. CNS infection with Mycobacterium bovis Ravenel, M. bovis bacillus Calmette-Guérin (BCG) Pasteur, and M. bovis BCG Montreal were compared. M. bovis Ravenel induced the highest levels of TNF-alpha in the CSF in association with high leukocytosis, protein accumulation, and severe meningeal inflammation. BCG Pasteur had intermediate effects, and BCG Montreal was the least virulent. In addition, M. bovis Ravenel numbers were highest in the brain and CSF and the bacilli also disseminated more efficiently to distant organs, compared with BCG Pasteur and BCG Montreal. In subsequent experiments, rabbits were infected with either recombinant M. bovis BCG Montreal (vector), or BCG Montreal expressing the murine gene for TNF-alpha (BCG mTNF-alpha). BCG Montreal was rendered virulent by the expression of murine TNF-alpha, as demonstrated by high CSF leukocytosis, high protein accumulation, severe meningeal inflammation, persistent bacillary load, and progressive clinical deterioration. Taken together, these results demonstrate that the level of TNF-alpha produced during mycobacterial CNS infection determines, at least in part, the extent of pathogenesis.

Animals↗
PubMed2006

Paraneoplastic production of granulocyte colony-stimulating factor in a bladder carcinoma.

We report the case of a 51-year-old female with poorly differentiated bladder carcinoma who presented with leukocytosis and hypercalcemia. Granulocyte colony-stimulating factor was noted to be twice the normal level. Paraneoplastic leukocytosis in bladder carcinoma is rare, is often associated with paraneoplastic hypercalcemia, and appears to represent a particularly aggressive form of the disease.

Female↗
PubMed2003

Efficacy and morbidity of therapeutic renal embolization in the spectrum of urologic disease.

PURPOSE: We report the largest series of renal embolizations performed for a variety of indications. PATIENTS AND METHODS: A retrospective analysis was performed on embolizations performed in our institution from 1997 to 2002 encompassing 36 patients who underwent 44 procedures. RESULTS: Embolization was successful on the first attempt in 87% of the patients. A second embolization was performed in four of the five unsuccessful cases, three successfully, increasing the success rate to 95%. The mean postoperative narcotic use was 27.2 mg of morphine equivalent, and 10 mg or less was required by 45% of the patients. In the 14 patients who had not also undergone a surgical procedure, the mean narcotic use was 21 mg, and 64% required 10 mg or less. Only 15% of the patients developed fever, which resolved within 2 days in all cases. Leukocytosis was seen in 47%. Follow-up creatinine and hypertension information was available in 16 and 18 patients, respectively. After a mean follow-up of 269 days, only one patient had a clinically significant rise in the creatinine concentration. After a mean follow-up of 496 days, two patients had new-onset hypertension. There was no statistically significant difference in the success rate, narcotic use, complications, creatinine concentrations, or the likelihood of fever, leukocytosis, or hypertension according to the indication for embolization or the agent used. Use of a microcatheter was associated with less parenchymal loss, and decreased parenchymal loss was associated with a significant reduction of narcotic use. CONCLUSIONS: Renal embolization is a highly effective and well-tolerated procedure in a variety of urologic conditions. The indications and material used did not have a significant effect on the outcome. Reducing parenchymal loss can significantly reduce morbidity.

Analgesics↗
PubMed1980

Bordetella pertussis respiratory tract infection in the mouse: pathophysiological responses.

The influence of living Bordetella pertussis on the induction and duration of pathophysiological reactions in mice infected intranasally with graded doses of culture was studied. Lethally infected mice showed loss of body weight, spleen atrophy, pronounced hypothermia and hypoglycemia, and highly elevated levels of leukocytes and serum immunoreactive insulin. Sublethally infected mice showed normal weight gain, practically normal temperature, spleen enlargement, lesser pronounced hypoglycemia, lower but significantly elevated levels of leukocytes and serum immunoreactive insulin, and histamine sensitization. Intensity of each reaction was related to the degree of lung infectivity. Hypothermia and leukocytosis were highly correlated. Concentration of serum immunoreactive insulin was closely related to the level of leukocytosis but not to the level of glucose. The strain and age of mice significantly affected the degree and duration of the reactions. The results suggest that the intranasally infected mouse may provide a useful model for investigations on whooping cough.

Aging↗
PubMed1989

Inhibition of complement-factor-5a-induced inflammatory reactions by prostaglandin E2 in experimental meningitis.

The possible role of complement factor 5a (C5a) and prostaglandin E2 (PGE2) in cerebrospinal fluid (CSF) pleocytosis and protein accumulation was assessed in a rabbit model of meningitis. Intracisternally administered C5a caused a rapid, early influx of leukocytes into CSF that peaked at 1 h after injection; by 6 h, cell counts were slightly higher than those in controls. Administration of PGE2 or saline did not induce detectable CSF leukocytosis. Coadministration of PGE2 with C5a decreased CSF leukocytosis in a dose-related fashion. Protein concentration increased 30 min after administration of C5a, peaked after 1 h, and remained elevated for 6 h. PGE2 caused a dose-related increase in protein content after 2 h, whereas coadministration caused an inversely dose-related inhibition of the C5a-induced protein influx into CSF. These data suggest that PGE2 in the subarachnoid space exerts an inhibitory action on the C5a-mediated response that is probably not related to its direct effects on protein extravasation.

Animals↗
PubMed1998

Production of granulocyte-macrophage colony-stimulating factor in a patient with metastatic chest wall large cell carcinoma.

Recent reports of cancers that produce colony-stimulating factors (CSF) and which are associated with leukocytosis indicate that most are granulocyte CSF-producing tumors. A 71-year-old man with metastatic chest wall tumors from large cell lung cancer with marked leukocytosis and eosinophilia was reported. His maximal leukocyte count was 48300/microliter with 37.5% eosinophils. Granulocyte-macrophage CSF (GM-CSF) activity detected by enzyme-linked immunosorbent assay (ELISA) in serum was 112 pg/ml (normal range < 2.0 pg/ml), but G-CSF was normal. Immunohistochemical detection of GM-CSF protein on a chest wall tumor sample was positive. Irradiation of the chest wall tumor was performed and the leukocyte count decreased temporally. However, he died of respiratory failure due to progressive tumor growth 56 days after admission. Based on these results it appears that autocrine production of GM-CSF is a possible cause of this leukemoid reaction.

Aged↗
PubMedDate not supplied

Tumor necrosis factor monoclonal antibody prevents alterations in leukocyte populations during cardiopulmonary bypass.

Tumor necrosis factor-alpha (TNF-alpha) has been implicated as causing the systemic inflammatory response to cardiopulmonary bypass (CPB) that contributes to the postoperative sequelae of coagulopathy, increased capillary permeability, leukocytosis, fever, and multiple organ dysfunction. To define the role of TNF-alpha on leukocyte populations during CPB, pigs (n = 6) were pretreated with 20 mg TNF-alpha monoclonal murine antibody before normothermic CPB (2 hr) in a blinded prospective randomized study with saline used as a control (n = 6). The leukocyte response to CPB was measured at 10, 30, 60, and 120 min during CPB and at 60 and 120 min after CPB. Repeated measures analysis of variance was performed and the null hypothesis was discarded at the 5% level. The control group displayed the typical leukocyte profile associated with CPB: and initial leukopenia (36% reduction) followed by leukocytosis (11% increase, P = 0.0001). The initial leukopenia was due to a fall in both polymorphonuclear neutrophils (33% reduced, P < 0.05) and monocytes (37% reduced, P < 0.05). In the TNF-alpha monoclonal murine antibody group the total leukocyte profile did not change significantly from baseline, (8.7% reduction to a 16% increase, P = 0.24) nor were there significant changes in populations including neutrophils and lymphocytes. In the treatment group the initial reduction in monocytes was prevented and total circulating monocytes increased during bypass. The experimental data suggest that TNF-alpha may play an important role in the early alterations in leukocyte populations associated with CPB, and TNF-alpha monoclonal murine antibody pretreatment ameliorates the leukocyte response.

Animals↗
PubMed1999

Delayed intracranial hypertension: relationship to leukocyte count.

OBJECTIVE: Secondary intracranial hypertension has been linked to leukocytosis. We examined our data bank containing physiologic recordings and outcome data of severely head injured patients to investigate the relationship between delayed increases in intracranial pressure (ICP), defined as occurring after a 12-hr period of normal ICP values, and leukocytosis. DESIGN: A retrospective study of observational data. SETTING: Regional neurosurgical unit and intensive care unit. PATIENTS: Sixty-four patients suffered increased ICP >20 mm Hg. Thirty-five patients fulfilled selection criteria for delayed increases in ICP (group 1). Twenty-nine patients with increased ICP with no preceding or intervening periods of normal ICP were selected as a comparison group (group 2). MEASUREMENTS AND MAIN RESULTS: Comparison of 12-month outcome revealed that 11% of group 1 patients died, with 49% remaining severely disabled, in contrast to group 2, where 35% of patients died and 14% were left severely disabled (p = .021). The pattern of outcome was independent of monitoring time, or injury severity. Regression modeling was performed for prediction of delayed increase in ICP. Of 46 patients with an initial increase then decrease in leukocyte count in the first 48 hrs, 65% experienced delayed increases in ICP, as compared with 18% of the 11 patients without this pattern p = .01 1). CONCLUSIONS: Patients with delayed increases have a significantly different pattern of outcome. Change in leukocyte count from admission to day 2 is a significant predictor of such a delayed increase.

Adult↗
PubMed1993

Predicting severity of trauma by admission white blood cell count, serum potassium level, and arterial pH.

Traumatized patients frequently have leukocytosis, hypokalemia, and acidosis. The purpose of this study was to determine whether the admission serum potassium level (K+), white blood cell count (WBC), and arterial pH predicted the severity of injury in trauma patients. The injury severity score (ISS), total length of stay in the hospital (tLOS), and length of stay in the intensive care unit (LOS-ICU) were used to measure the severity of the injury. The charts of 156 consecutive trauma patients admitted to a level II trauma center were reviewed. Acidosis (arterial pH < 7.35) was associated with an increased mean ISS, tLOS, and LOS-ICU. Leukocytosis (WBC > or = 10,500/mm3) correlated with a higher mean ISS, and LOS-ICU. Patients with hypokalemia (K+ < 3.6 mEq/L) had an increased mean ISS and tLOS. Our findings suggest that the admission white blood cell count, serum potassium level, and arterial pH have a predictive value as to the severity of injury.

Acidosis↗
PubMed2006

Hematologic abnormalities within the first week after acute isolated traumatic cervical spinal cord injury: a case-control cohort study.

STUDY DESIGN: Case-control cohort study. OBJECTIVE: To evaluate 1) the hematologic abnormalities within the first week following isolated acute cervical spine trauma or spinal cord injury (SCI); and 2) the influence of age, sex, and severity of SCI on these hematologic abnormalities. SUMMARY OF BACKGROUND DATA: Given that autonomic nervous system has a critical role in the regulation of the hematopoietic system, we sought to evaluate the potential association between hematologic abnormalities within the first week posttrauma and the severity of SCI. METHODS: All consecutive individuals with isolated acute cervical spine trauma admitted to our institution from 1998 to 2000 were reviewed. Exclusion criteria included preexisting medical comorbidities and polytrauma. The study population was divided into a SCI group and a control group (individuals with spine trauma without neurologic impairment). The SCI group was subdivided into patients with motor complete SCI (American Spinal Injury Association [ASIA] Grades A/B) and individuals with motor incomplete SCI (ASIA Grades C/D). RESULTS: There were 21 SCI individuals (15 male, 6 female; ages 17-83 years; mean, 57 years) and 11 controls (6 male, 5 female; ages 18-75 years; mean, 41 years). When controlled for age, SCI individuals showed a significantly higher frequency of reduced hemoglobin concentration (RHC), leukocytosis, lymphopenia, and thrombocytopenia than controls within the first week posttrauma. Blood hemoglobin concentration, lymphocyte, and platelet counts in the SCI group were significant lower than the controls. The SCI group showed a significant higher leukocyte count than the controls. The degree of RHC and lymphopenia was significantly correlated with the severity of SCI. CONCLUSION: Our results indicate that patients with isolated cervical SCI have significantly greater frequency of RHC, leukocytosis, lymphopenia, and thrombocytopenia than controls during the first week posttrauma. The degree of RHC and lymphopenia was significantly associated with the severity of SCI. While the mechanisms underlying these clinically important hematologic consequences of SCI remain undetermined, evidence from the literature suggests that acute autonomic denervation of the hematopoietic system could play a key role.

Adolescent↗
PubMed2002

Establishment and characterization of a new lung cancer cell line (MI-4) producing high levels of granulocyte colony stimulating factor.

We established a human lung cancer cell line, MI-4 from the pleural effusion of a 69-year-old male with advanced large cell undifferentiated carcinoma of the lung complicated by leukocytosis. The culture supernatant of MI-4 contained high levels of granulocyte colony stimulating factor (G-CSF). The intracellular localization of the G-CSF was identified by immunocytochemistry. Reverse transcription-polymerase chain reaction (RT-PCR) revealed G-CSF mRNA expression in this cell line. The cell line was successfully transplanted into nude mice. The transplanted nude mice also showed leukocytosis with a high serum G-CSF level. Southern blot analysis did not show amplification or rearrangement of the G-CSF gene in MI-4 cells. Spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) analyses revealed that this cell line has an additional chromosome 17 attached to a segment of chromosome 10 besides two intact chromosomes 17, and that each of these three chromosomes 17 has a G-CSF gene on chromosome 17q. Inflammatory cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta, significantly enhanced G-CSF expression at both the protein and mRNA levels in MI-4. However, these cytokines did not stimulate the growth of MI-4 cells, regardless of abundant G-CSF production. TNF-alpha rather suppressed it, in a dose-dependent manner. Exogenous recombinant human G-CSF and anti-G-CSF antibody did not promote or inhibit the growth of MI-4 cells at any concentration examined. In addition, RT-PCR analysis did not show G-CSF receptor mRNA expression. These results suggest that this cell line does not have an autocrine growth loop for G-CSF. This cell line should be very useful for understanding the biological activity of G-CSF in G-CSF-overproducing lung cancer.

Aged↗